Ifc Week 8

Front 1

3 basic elements of breath control:

Back 1

1. sensors (input to CC)

2. Central Controller (BS)

3. effectors (output of CC)

Front 2

respiratory effectors are really just:

Back 2

respiratory muscles

Front 3

VRG:

(3)

Back 3

1. contains both inspiratory and expiratory neurons

2. projects to phrenic nerve, IC, and abdominal MN's

3. contains pre-Botzinger Complex

Front 4

Botzinger Complex =

Back 4

pacemaker of respiration

- originates normal breathing rhythm

Front 5

Dorsal Respiratory Group:

(3)

Back 5

1. main sensory nucleus for breathing

2. contains mainly inspiratory neurons

3. includes NTS

Front 6

pneumotaxic and apneustic center of the BS:

(2)

Back 6

1. located in the pons

2. modulates respiratory rhythm

Front 7

"pneumotaxic" ~~

Back 7

rhythm

Front 8

apneustic ~~

Back 8

gasping type of breathing

- prolonged inspiration, short expiration

Front 9

3 effectors of respiration:

Back 9

1. phrenic MN's

2. thoracic MN's

3. Lumbar MN's

Front 10

phrenic MN's:

(2)

Back 10

1. located in C2-C5

2. project to diaphragm

Front 11

thoracic MN's:

(2)

Back 11

1. located in T1-T12

2. project to IC's

Front 12

Lumbar MN's project to:

Back 12

abdominal muscles

Front 13

5 sensors of respiration:

Back 13

1. peripheral chemoreceptors

2. central chemoreceptors

3. pulmonary stretch receptors

4. irritant receptors

5. J receptors

Front 14

peripheral chemoreceptors are located in:

Back 14

each common carotid bifurcation, and in the aortic arch

(3 total)

Front 15

***main stimulus of peripheral chemoreceptors = ***

Back 15

low O2

(<60 mmHg)

- minor response to CO2 or pH

Front 16

what is the afferent of ALL respiratory sensors?

(except for central chemoreceptors - no need to travel)

Back 16

the vagus nerve

Front 17

each carotid body:

(2)

Back 17

1. extremely well-vascularized

2. **turns on or off very quickly**

Front 18

a carotid body can be tricked into sensing hypoxemia by:

Back 18

constriction of the SM surrounding it

Front 19

normal PaCO2 =

Back 19

40

Front 20

***main stimulus for central chemoreceptors = ***

Back 20

PaCO2 and H+

Front 21

central chemoreceptors are located in:

Back 21

the BS

Front 22

CSF is NOT a good buffer; a small change in H+ concentration will result in:

Back 22

a HUGE change in pH

Front 23

the blood-brain barrier is highly permeable to CO2; changes in arterial CO2 are quickly:

Back 23

reflected in the CSF

Front 24

increasing CSF CO2 => lower CSF pH =>

Back 24

**increased ventilation**

Front 25

in people with severe lung disease, hypoxemia becomes:

Back 25

the main drive for ventilation

(instead of PCO2)

Front 26

administering 100% O2 removes the hypoxemia sensed by peripheral chemoreceptors; => =>

Back 26

sharp increase in PaCO2 because chemoreceptors no longer driving ventilation

=> death

Front 27

need to administer just enough:

Back 27

O2

- no more, no less

Front 28

***changes in CO2 ~~

Back 28

a slower, more gradual change in ventilation than changes in O2

Front 29

pulmonary stretch receptors are located in:

Back 29

airway SM

Front 30

pulmonary stretch receptors participate in:

Back 30

the Hering-Breuer reflex

Front 31

Hering-Breuer reflex =

Back 31

stimulation of pulm. stretch receptors tell the brain to stop inspiration

- prevents overinflation

Front 32

**pulmonary stretch receptors are:**

Back 32

slowly-adapting

- continue to fire for as long as lung is stretched too much

Front 33

severing the vagus nerve => increase in:

Back 33

TV, because vagus no longer carries stretch receptor signal to brain

Front 34

pulmonary irritant receptors are located:

Back 34

b/w airway epithelial cells

Front 35

pulm. irritant receptors are stimulated by:

(4)

Back 35

1. noxious gases

2. cig smoke

3. inhaled dust

4. cold air

Front 36

activation of irritant receptors increases:

(3)

Back 36

ventilation, bronchoconstriction, and coughing,

to eliminate the stimulate

Front 37

irritant receptors are also stimulated by:

Back 37

**histamine in asthma attacks**

Front 38

***irritant receptors are rapidly-adapting;***

Back 38

desensitize even while stimulus remains

Front 39

J receptors are located in:

Back 39

the external wall of the pulmonary caps

Front 40

J receptors respond rapidly to:

(3)

Back 40

1. blood-borne substances

2. vascular congestion

3. edema

Front 41

activation of J receptors causes:

Back 41

transient apnea, followed by:

shallow breathing, bronchoconstriction, and mucous secretion

Front 42

change in ventilation due to exercise is NOT caused by:

Back 42

either O2, CO2, or pH

- but an unknown, multifactorial cause

Front 43

causes of hypoventilation:

(3)

Back 43

1. problems with BS/SC/MN's

2. drugs

3. upper airway obstruction (as with obesity)

Front 44

lamina propria = the layer beneath:

Back 44

tracheal epithelium

Front 45

submucousa = layer beneath:

Back 45

lamina propria

- contains mucous glands to line throat

Front 46

**the posterior portion of the trachea does NOT have:

Back 46

cartilage

Front 47

what's found in the posterior portion of the trachea?

Back 47

the trachealis muscle

Front 48

trachealis muscle:

(2)

Back 48

1. SM

2. used for coughing, swallowing

Front 49

***defining feature of bronchus =

Back 49

islands of cartilage

Front 50

bronchi also have:

(2)

Back 50

1. lots of SM

2. submucousa layer

Front 51

the trachea and bronchi have lots of:

Back 51

goblet cells

Front 52

***bronchioles have NO:

Back 52

cartilage***

Front 53

bronchioles:

(3)

Back 53

1. no cartilage

2. no goblet cells

3. simple columnar

Front 54

the epithelium of airways above the bronchioles is:

Back 54

**pseudostratified**

Front 55

lymphoid tissue is:

Back 55

dark

Front 56

the respiratory bronchioles have less epithelium than:

Back 56

terminal bronchioles

Front 57

the terminal bronchioles have no goblet cells; instead, they have:

Back 57

clara cells

Front 58

clara cells:

(4)

Back 58

1. non-ciliated

2. secretory - produce a component of SFT

3. act as stem cells, to replace damaged epithelium

4. secrete enzymes to destroy noxious substances

Front 59

clara cells have a __________ look

Back 59

balloon

Front 60

***respiratory bronchioles are broken up, meaning:***

Back 60

they have an **incomplete** circle of SM

Front 61

alveoli are lined by:

Back 61

Type I pneumocytes

Front 62

Type I pneumocytes are:

Back 62

loooooong

Front 63

underneath the Type I cells are:

Back 63

caps

Front 64

Type II cells:

(2)

Back 64

1. round

2. contain lamellar bodies

Front 65

lamellar bodies store:

Back 65

SFT

Front 66

Wheezing ~~

Back 66

turbulent flow in the small airways

Front 67

what drives ventilation?

Back 67

**CO2**

Front 68

FRC = Functional Residual Capacity; occurs at:

Back 68

bottom of normal tidal breath

Front 69

Normal expiration/inspiration ratio =

Back 69

2:1

Front 70

nicotinic receptors are:

Back 70

ionotropic

Front 71

roles of the kidneys:

(6)

Back 71

1. solute balance

2. water balance

3. electrolyte balance

4. acid balance

5. excretion

6. hormone production

Front 72

why is electrolyte balance so important?

Back 72

ions determine AP's

=> heart beat, CNS, etc.

Front 73

what 3 hormones do the kidneys produce?

Back 73

1. renin

2. EPO

3. VitD3

Front 74

main extracellular fluid ions =

(2)

Back 74

Na+ and Cl-

Front 75

osmolarity =

Back 75

**concentration** of dissolved particles

Front 76

150 mM of NaCl =

Back 76

300 mOsm

Front 77

**high osmolarity =

Back 77

little free water

Front 78

coloid osmotic pressute =

Back 78

osmolarity of plasma proteins

Front 79

changes in salt or water intake => changes in ECF =>

Back 79

changes in ICF,

b/c ECF and ICF equilibrate quickly

Front 80

osmotic changes can perturb a cell's:

(2)

Back 80

size and function

Front 81

hyposmolar = hypotonic; cell will:

Back 81

swell as water rushes in

Front 82

tonicity and osmolarity measure:

Back 82

the relative concentration of a call/fluid

Front 83

amount of water is indirectly proportional to:

Back 83

osmolarity

- decreasing osmolarity means increasing water

Front 84

positive balance =

Back 84

intake > output

Front 85

negative balance =

Back 85

output > intake

Front 86

what is the functional unit of the kidney?

Back 86

the nephron

Front 87

kidneys excrete only:

Back 87

1% of water and solutes that are filtered

Front 88

ultrafiltrate =

Back 88

fluid going from arterioles to caps of Bowman's capsule

Front 89

secretion ~~

Back 89

going straight from the plasma to the kidney tubules

- not filtrate

~ both water and solutes

Front 90

excretion equation:

Back 90

excretion = filtration + secretion - reabsorption

Front 91

the kidneys are highly vascularized; nephrons have 2:

Back 91

capillary beds

- 1 at the glomerulus

- 1 surrounding the tubules

Front 92

GFR =

Back 92

volume of fluid filtered across ALL the glomeruli

Front 93

GFR value =

Back 93

120 ml/min

Front 94

normal RBF =

Back 94

1000 ml/min

Front 95

normal RPF =

Back 95

600 ml/min

Front 96

***urine flow = V =

Back 96

volume of urine *excreted* per min

- ml/min

Front 97

filtered load of a substance =

Back 97

GFR x Py

Front 98

Py =

Back 98

plasma concentration of a substance y

Front 99

excreted load of a substance =

Back 99

V x Uy

Front 100

Uy =

Back 100

urine concentration of substance y

Front 101

reabsorption =

Back 101

filtered load - excreted load

Front 102

secretion =

Back 102

excreted load - filtered load

Front 103

***clearance =

Back 103

volume of plasma cleared of a substance, in ml/min

Front 104

***Cy =

Back 104

V x Uy / Py

Front 105

ultimately, clearance = net effect of:

Back 105

filtration, reabsorption, and secretion

Front 106

***when clearance = GFR, there is NO:

Back 106

secretion or reabsorption

Front 107

no secretion or reabsorption means filtered load =

Back 107

excreted load

Front 108

2 examples where clearance = GFR:

Back 108

inulin, creatinin

Front 109

maximum clearance ~

Back 109

RPF, 600 ml/min

Front 110

RPF is measured by:

Back 110

PAH

Front 111

PAH is almost completely:

Back 111

removed in one pass through the kidneys

Front 112

when clearance is less than GFR, what must be occurring?

Back 112

reabsorption

Front 113

GFR is about 20% of:

Back 113

RPF

Front 114

inulin is rarely:

Back 114

used to measure GFR

Front 115

creatinin slightly ________________ GFR

Back 115

overestimates

Front 116

***plasma creatinin increases in proportion to:***

Back 116

a decrease in GFR

- as one goes up, the other comes down

Front 117

dark spots in the kidney cortex =

Back 117

corpuscles

Front 118

renal corpuscle =

(2)

Back 118

glomerulus + Bowman's capsule

Front 119

glomerulus =

Back 119

ball of caps

Front 120

juxtamedullary neprhons give off:

Back 120

vasa recta

Front 121

vasa recta are thin, straight arteries that supply:

Back 121

the renal medulla

Front 122

medullary rays are located in the cortex but:

Back 122

are composed of the collecting tubules that make up the medulla

Front 123

3 unique features of renal blood flow:

Back 123

1. glomerulus is flanked by 2 arterioles

2. efferent arterioles are flanked by 2 cap beds

3. vasa recta are long and straight

Front 124

urinary pole =

Back 124

PCT end of the corpuscle

Front 125

Bowman's capsule =

Back 125

parietal (outside) layer + visceral layer of podocytes

Front 126

visceral layer of podocytes surrounds:

Back 126

glom. caps

Front 127

what kind of epithelium is the parietal layer of Bowman's capsule?

Back 127

simple squamous

Front 128

what is the main diffusion barrier for the glomeruli?

Back 128

the basement membrane of Bowman's capsule

Front 129

what are pedicles?

Back 129

processes of podocytes, overlying basement membrane

Front 130

4 resident cells of the renal corpuscle:

Back 130

1. parietal Bowman's cells

2. podocytes

3. cap. endothelial cells

4. mesangial cells

Front 131

what do mesangial cells do?

(2)

Back 131

1. hold glomeruli together (contractile)

2. phagocytose

Front 132

PCT histology:

(3)

Back 132

1. prominent brush border

2. lots of mit.

3. basal striations

Front 133

DCT histology:

(2)

Back 133

1. NO brush border

2. but also has basal striations

Front 134

what kind of epithelium is the loop of Henle?

Back 134

squamous

Front 135

what kind of epithelium are the collecitng ducts?

(2)

Back 135

1. classic cuboidal for the most part

2. then columnar in the deep medulla

Front 136

3 cells of the JG apparatus:

Back 136

1. macula densa cells

2. lacis (mesangial) cells

3. JG cells

Front 137

macula densa cells:

(2)

Back 137

1. next to DCT

2. sense NaCl concentration

Front 138

what do JG cells do?

Back 138

produce renin

Front 139

medullary papilla =

Back 139

final stop before calyx and excretion

Front 140

the ureter is shaped like a:

Back 140

star

Front 141

what does transitional epithelium look like when stretched?

(2)

Back 141

1. layers look stratified

2. apical surface is irregular

Front 142

urethra: begins with transitional epithelium, =>

Back 142

stratified columnar

=> stratified squamous at the end

Front 143

****anatomical shunt ~~

Back 143

blood goes through the lung w/o being exposed to alveolar gas- bypassing any chance to exchange gas.

Front 144

physiological dead space =

Back 144

more ventilation than the perfusion can handle- so called "wasted" ventilation.

Front 145

****physiological shunt =

Back 145

Q > V

Front 146

in general, glomerular filtration depends on:

(2)

Back 146

1. filtration barrier

2. high Pgc

Front 147

Bowman's space is filled with:

Back 147

filtrate, which continues to the PCT

Front 148

what do glomerular caps have that aids in filtration?

Back 148

fenestrations

Front 149

the basement membrane under glomerular cap. endothelium is the main:

Back 149

diffusion barrier

- very selective

Front 150

what do podocytes do?

Back 150

stabilize the basement membrane

Front 151

***the basement membrane has a strong _____________ charge***

Back 151

negative;

keeps negative mlcls out of Bowman's space

Front 152

****what kind of mlcls are NOT filtered from the glom. caps?***

(2)

Back 152

1. large mlcls

2. negative mlcls

Front 153

how big is a "large" mlcl?

Back 153

greater than or equal to 40 A

Front 154

mlcls less than ___ Angstroms are freely filtered

Back 154

20

Front 155

filtration of mlcls between 20 and 40 Angstroms is determined by:

Back 155

their charge

Front 156

glucose is freely filtered b/c it's a:

Back 156

small mlcl

Front 157

should never see _____ or __________ in the urine

Back 157

RBC's;

albumin

Front 158

****Pgc is greater than:****

Back 158

Pc of all other caps

Front 159

****Pgc is _______________ throughout the length of the glomerular cap****

Back 159

CONSTANT

Front 160

***Pgc is ALWAYS greater than ______________ in the glomerular capillaries***

Back 160

COP

Front 161

**what's the significance of Pgc being greater than COP at every point of the glom. cap?**

Back 161

***there is ALWAYS net filtration at the glom. caps***

Front 162

Kf of the glom caps is ___________x's greater than in other caps

Back 162

100-200x

Front 163

why is Kf of glom caps so much greater?

Back 163

b/c of fenestrations

Front 164

how does COP change along glom caps?

Back 164

it **increases** steadily

Front 165

why does COP increase along the length of the glom cap?

Back 165

b/c water is leaving

=> increased concentration of plasma proteins

Front 166

GFR = Kf x ______

Back 166

MFP

Front 167

MFP = mean filtration pressure =

Back 167

average filtration pressure along the length of the caps

Front 168

factors that alter GFR:

(4)

Back 168

1. change in Pgc

2. change in Resistance of afferent or efferent arterioles => change in Pgc

3. change in COP

4. change in Kf

Front 169

**to increase GFR:**

(2)

Back 169

1. increase Pgc

2. decrease COP

Front 170

2 constrictors of renal arterioles:

Back 170

1. increased sympathetic tone

2. increased ANG II

(both decrease Pgc)

Front 171

5 dilators of the renal arterioles:

Back 171

1. NO

2. bradykinin

3. prostaglandins

4. dec. sympathetic tone

5. dec. ANG II

Front 172

what inhibits prostaglandins?

Back 172

NSAIDS/ibuprofen

Front 173

most mediators of renal arterioles affect:

Back 173

the **afferent** arteriole,

Front 174

why do most mediators of renal arterioles affect the afferent arteriole?

Back 174

b/c of its greater thickness/more SM

Front 175

****changes to afferent arterioles => changes in:****

Back 175

Pgc, GFR, and RBF,

all in the SAME DIRECTION

Front 176

****changes to the efferent arterioles => changes in:****

Back 176

Pgc and GFR in the

OPPOSITE direction

from RBF

Front 177

example: increasing afferent arteriole R =>

(3)

Back 177

1. dec. Pgc,

2. dec. GFR,

and

3. dec. RBF

Front 178

another example: increasing efferent arteriole R =>

(3)

Back 178

1. increased Pgc

and

2. increased GFR

but

3. decreased RBF

Front 179

normal plasma concentration of Na+ =

Back 179

140

Front 180

normal plasma concentration of Cl- =

Back 180

100

Front 181

normal plasma concentration of HCO3- =

Back 181

24

Front 182

normal plasma concentration of glucose =

Back 182

100

Front 183

Na+, water, and glucose are readily ________________ at the PCT

Back 183

reabsorbed

Front 184

what 2 substances are readily secreted at the PCT?

(2)

Back 184

1. PAH

2. many drugs

Front 185

overall, the **nephrons** (not just PCT) reabsorb:

(2)

Back 185

1. 99% of Na+ and water

2. ALL of glucose and AA's in the filtrate

Front 186

water movement in the kidneys:

(4)

Back 186

1. NEVER pumped, always passive

2. depends on concentration or osmotic gradients

3. passes through pores formed by aquaporins

4. can move paracellularly

Front 187

Na+/K+ ATPases create the Na+ gradient necessary for:

Back 187

all other movement/transport

Front 188

Na+ reabsorption uses both:

Back 188

symports and antiports

Front 189

Na+ symports ~~

Back 189

**reabsorption**

Front 190

cotransporter =

Back 190

symport

Front 191

Na+ antiports ~~

Back 191

**secretion**

Front 192

Na+ can also move:

Back 192

paracellularly, through **leaky epithelium**

- movement depends on electrochemical gradient

Front 193

***what makes epithelium leaky?***

Back 193

whether Na+ or H20 can move easily, in a paracellular fashion

Front 194

water generally moves through *leaky epithelium*, via constitutively-expressed:

Back 194

aquaporin 1

Front 195

sometimes water can move through tight epithelium, via:

Back 195

hormonally-expressed aquaporin 2

Front 196

**there is NO change in the ____________________ of the PCT, despite the movement of solutes**

Back 196

osmolarity

Front 197

PCT reabsorbs:

(4 percents)

Back 197

1. 67% of NaCl, water, and K+

2. most HCO3

3. all glucose/AA's

Front 198

6 apical transporters/pumps of the PCT:

Back 198

1. Na+/glucose symport

2. Na+/AA symport

3. Na+/Cl symport

4. Na+/H+ antiport

5. AQ1

6. ROMK

Front 199

3 basolateral transporters/pumps of the PCT epithelium:

Back 199

1. Na+/K+ ATPase

2. glucose transporter

3. aquaporin 1

Front 200

water moves despite isosmolar nature of the PCT b/c:

Back 200

a series of small pockets of solute transport occur,

and water follows

Front 201

***what is the maximum activity of the Na+ / glucose transport?***

Back 201

180 mg/dL

Front 202

plasma glucose [ ] =

Back 202

filtrate glucose concentration

Front 203

even a meal of straight sugar won't raise plasma glucose (and thus filtrate glucose) past:

Back 203

180 mg/dL

Front 204

when plasma glucose exceeds 180 mg/dL, some of it remains in:

Back 204

the PCT => keeps going through tubules

=> **retains water** => polyuria, thirst

Front 205

polyuria =

Back 205

high urine output

Front 206

What are the steps to reclaiming HCO3 in the PCT?

(5)

Back 206

1. CA generates HCO3 and H+ from intracellular Co2 and H20

2. H+ gets sent into tubular lumen via Na+/H+ antiport

3. combines with HCO3 in filtrate to make CO2 and H2O

4. CO2 enters cell, combines w/ H2O to form HCO3 and H+

5. HCO3 is sent out to peritubular caps via Na+/HCO3 symports on the basolateral surface

Front 207

Renal Tubular Acidosis =

Back 207

systemic acidosis due to failure of kidneys to balance acids-bases properly

Front 208

proximal RTA =

Back 208

failure to reclaim filtered HCO3

=> loss of HCO3 to urine

Front 209

Franconis Syndrome =

Back 209

general PCT dysfunction = impaired reabsorption of solutes (glucose, AA's, bicarb)

Front 210

Franconis Syndrome =>

(2)

Back 210

glucosuria, proximal RTA, etc

Front 211

urea in the PCT: ___% of it is passively reabsorbed

Back 211

50%

Front 212

plasma urea [ ] =

Back 212

filtered urea [ ]

Front 213

H2O reabsorption in the PCT concentrates urea =>

Back 213

urea moves out of PCT due to this concentration gradient

Front 214

the LOH **always** reabsorbs more:

Back 214

salt than water

Front 215

because the LOH always reabsorbs more salt than water, fluid at the end of the LOH is:

Back 215

hyposmolar

Front 216

hyposmolar fluid =

Back 216

dilute fluid

- the fluid has less solutes/more water than the interstitium

Front 217

concentration of fluid entering the LOH is _____ mOsm/L

Back 217

300 mOsm/L

Front 218

***what does the ascending limb ACTIVELY do?***

Back 218

it actively ***reabsorbs NaCl***

Front 219

what does the ascending limb use to reabsorb NaCl?

Back 219

NKCC transporters

Front 220

what is the ascending limb **impermeable to**?

Back 220

**water**

Front 221

because it's impermeable to water, the ascending limb is called the:

Back 221

diluting segment

=> makes the fluid mostly water

Front 222

NKCC transporters are located in:

Back 222

the thick portion of the ascending limb of the LOH

Front 223

NKCC transporters *always* reabsorb:

Back 223

1 Na+, 1 K+, and 2 Cl's

Front 224

what's the significance of the NKCC transporters reabsorbing 4 ions?

Back 224

they create a **future gradient for water** to be reabsorbed

Front 225

what drives NKCC transporters?

Back 225

tubular K+

(NKCC's are secondary active transporters)

Front 226

how does K+ enter the tubules?

Back 226

via ROMK's

(apical K+ channels)

Front 227

what do you absolutely need for NKCC's to work?

Back 227

a high concentration of K+ in the tubular lumen

Front 228

diuretics ~~ both:

Back 228

water AND solute excretion

Front 229

best example of a diuretic =

Back 229

Lasix

Front 230

***what do diuretics block?***

Back 230

**NKCC transporters**

=> less water reabsorption, b/c that future gradient isn't created

Front 231

Barter's syndrome =

Back 231

mutations of NKCC transporters

Front 232

Barter's syndrome presents as if:

Back 232

loop diuretic is always present

Front 233

2 results of Barter's syndrome:

Back 233

1. hypokalemia

2. dehydration

Front 234

the descending LOH is ________;

Back 234

leaky;

salt and water pass freely, equilibrate b/w the lumen and the interstitium

Front 235

b/c the ascending limb is impermeable to water, but actively reabsorbs NaCl, fluid in the lumen is _______________, while it's ________________ in the interstitium

Back 235

dilute in the lumen;

concentrated in the interstitium

Front 236

***NKCC's of the ascending limb always create a gradient (i.e. difference) of _________***

Back 236

200 mOsm/L

(between the lumen and the intersititum)

Front 237

horizontal gradient ~~

(2)

Back 237

1. the concentration difference between the interstitium and the ascending limb, created by the NKCC's

2. how the descending limb will equilibrate with the interstitium after the NKCC's do their work

Front 238

pump-equilibrate step =

Back 238

fluid comes down and around LOH, and NKCC's create a gradient of 200 between the interstitium and the ascending limb,

followed by descending limb equilibrating with the interstitium

Front 239

shift step =

Back 239

more filtrate coming in from the PCT moves osmolaritys around the bend and up in to the ascending limb

=> horizontal gradient is no longer 200

=> pump-equilibrate again

Front 240

vasa recta =

Back 240

*peritubular* caps of the renal medulla


fall and ascend with LOH

Front 241

**main role of the vasa recta:**

Back 241

prevent the dissipation of longitidunal gradients surrounding the LOH

- it *matches* the interstitum concentrations/exchanges at the LOH

Front 242

the descending portion of the vasa recta ~

(2)

Back 242

1. solutes enter it

2. water exits it

Front 243

the ascending portion of the vasa recta ~

(2)

Back 243

1. solutes exit

2. water enters VR

Front 244

3 transport mechanisms of the VR:

Back 244

1. NaCl and water by passive diffussion

2. paracellular water via AQ1

3. urea via UT3

Front 245

600-1200 mOsm/L is considered:

Back 245

hyperosmolar

Front 246

the high osmolarity at the turn of the LOH ~ high concentrations of:

(2)

Back 246

**Na+ and urea**

Front 247

the LOH **always** reabsorbs more:

Back 247

salt than water

Front 248

hyposmolar =

Back 248

dilute

Front 249

100 mOsm/L is considered:

Back 249

hyposmolar

Front 250

early DCT:

(2)

Back 250

1. **further dilutes** tubular fluid

2. = TIGHT epithelium

Front 251

how does the early DCT further dilute tubular fluid?

Back 251

by **further Na+ reabsorption**

Front 252

what transporters does the early DCT use to reabsorb Na+?

Back 252

NCC's

(Na/Cl Co-transporters)

Front 253

b/c of the early DCT, osmolarity of the fluid goes from:

Back 253

100 Osm to 80 Osm

Front 254

the early DCT is made of tight epithelium, which means it's **impermeable to:**

Back 254

water

Front 255

the late DCT's role =

Back 255

Na+ reabsorption

Front 256

how does the late DCT reabsorb Na+?

Back 256

**via ENaC's**

Front 257

Na+ reabsorption is coupled to:

(2)

Back 257

K+ or H+ *secretion*

Front 258

thiazide diuretics inhibit:

Back 258

*NCC's*

Front 259

inhibiting NCC's => dec. Na+ reabsorption =>

Back 259

dec. water reabsorption => increased Na+ and water excretion

Front 260

Gitelman's syndrome =

Back 260

loss of function of NCC

Front 261

Gordon's syndrome =

Back 261

opposite of Gitelman's

Front 262

Liddle's syndrome =

Back 262

**gain of function of EnaC's**

Front 263

what does gain of function of EnaC's cause?

(2)

Back 263

1. hypokalemia

2. hypertension

Front 264

why does increasing the reabsorption of Na+ cause an increase in BP?

Back 264

b/c water follows Na+

Front 265

the decision to absorb water or not is made at the:

Back 265

DCT

Front 266

fluid at the beginning of the DCT is:

Back 266

hyposmolar

(dilute)

Front 267

whether or not the DCT reabsorbs water depends on:

Back 267

the presence or absence of ADH

Front 268

high *urine* osmolarity ~~

Back 268

little water ~~ ADH is *present and active in the body*

Front 269

hyposmolar fluid leaving the LOH presents a favorable gradient for reabsorbing water at the DCT, if:

Back 269

ADH is around

Front 270

50% of urea is reabsorbed at:

Back 270

the PCT

Front 271

from the DCT through the medullary CD, which segments of the kidney are *permeable* to urea?

Back 271

only the medullary CD

Front 272

**the medullary CD absorbs urea only if:**

Back 272

***ADH is present***

Front 273

as water leaves the medullary CD (in presence of ADH), the urea gradient:

Back 273

increases

=> urea moves down concentration gradient and out of lumen

Front 274

with ADH present, ___% of urea is reabsorbed at the medullary CD

Back 274

40%

Front 275

without ADH, ___% of urea is reabsorbed at the medullary CD

Back 275

0% - none of it

=> excreted

Front 276

ADH present => ____________ urine

Back 276

concentrated

Front 277

ADH does NOT alter _______________________ by the DCT or CD's

Back 277

Na+ reabsorption;

ADH only alters water reabsorption

Front 278

high flow rate through the LOH => less:

Back 278

Na+ reabsorption => higher osmolarity of tubular fluid

Front 279

how much water do you lose per day?

Back 279

1.5 L

Front 280

how much of the 1.5 L lost per day is lost as urine?

Back 280

0.5 L

Front 281

you *must* excrete ______ mOsm of solute as waste product every day, b/c that's how much you create

Back 281

600 mOsm

Front 282

ADH = dipsogen:

Back 282

stimulates thirst

Front 283

what do osmoreceptors of the hypothalamus sense?

Back 283

**plasma** osmolarity

Front 284

if plasma osmolarity is too high, osmoreceptors cause:

Back 284

the posterior pituitary to release ADH

Front 285

ADH = VP:

(3)

Back 285

1. constricts blood vessels

2. via V1/ADH receptors

3. => inc. BP

Front 286

ADH's antidiuretic effects occur via binding to:

Back 286

V2/ADH receptors

Front 287

***what's the effect of ADH on amount of solute excreted in the urine?***

Back 287

***NONE***

- amount of solute excreted never changes due to ADH

Front 288

ADH has a short:

Back 288

half-life

Front 289

***how does ADH change the urine flow rate?***

Back 289

***it decreases urine flow rate***

(in inverse proportion to urine osmolarity)

Front 290

what are 3 stimuli for ADH release?

Back 290

1. change in plasma osmolarity (either direction)

2. dec. blood volume

3. dec. BP

Front 291

what is the primary stimulus for ADH release?

Back 291

change in plasma osmolarity

Front 292

what is decreased BV sense by?

Back 292

atrial stretch receptors

Front 293

what is dec. BP sensed by?

Back 293

baroreceptors

Front 294

what transporters do V2/ADH receptors activate in the medullary CD?

Back 294

UT1's

Front 295

**drinking water does NOT change:**

(2)

Back 295

GFR or solute excretion

Front 296

hyponatremia = dec. plasma Na+, ~~

Back 296

too much water in plasma ~~ ADH is too high

Front 297

diabetes insipidus ~~

Back 297

**too little ADH**

=> abnormal loss of water

Front 298

polydipsia =

Back 298

excessive thirst

Front 299

diabetes insipidus comes in 2 forms:

Back 299

1. central

2. nephrogenic

Front 300

central DI~~ problem with:

Back 300

ADH synthesis or release

Front 301

how does central DI occur?

(2)

Back 301

via trauma, CNS tumor

Front 302

nephrongenic DI ~~

Back 302

*resistance* to ADH

Front 303

how does nephrogenic DI occur?

(2)

Back 303

via kidney injury, Lithium meds

Front 304

Glomerulotubular balance (GT) =

Back 304

how the nephron reabsorbs a constant *percentage* of Na+ and water, no matter how the GFR changes

=> Na+ and water reabsorption always changes proportionally to GFR

Front 305

inc. GFR => inc. COP in the peritubular caps =>

Back 305

inc. driving force for the reabsorption of water => inc. Na+ reabsorption (as it follows water)/ dec. back leak of Na+

Front 306

if GFR dec, => dec. COP =>

Back 306

decreased reabsorption of water/Na+

Front 307

GT balance can be *reset* by:

Back 307

ECV

Front 308

when ECV increases, the percent of Na+ and water reabsorbed _____________

Back 308

**decreases**

in other words, *more Na+ and water is excreted* than normal

Front 309

when ECV decreases, what happens to Na+ and water excretion?

Back 309

they both get *excreted less*

i.e. more is reabsorbed

Front 310

increased salt intake => increased water retention =>

Back 310

increased ECV =>

*increased salt excretion by the kidney*

Front 311

what happens if you decrease Na+ intake after having a high-salt diet?

Back 311

kidney starts excreting *less* Na+ until you're back at steady state

Front 312

(negative balance =

Back 312

excretion > intake)

Front 313

(steady state means:

Back 313

excretion = intake)

Front 314

macula densa cells are found within:

Back 314

the walls of the DCT

Front 315

the DCT is right next to:

Back 315

both glomerular arterioles

Front 316

JG cells secrete:

Back 316

renin

Front 317

atrial natriuretic peptide (ANP):

(5)

Back 317

1. made in the atria

2. released during increased ECV

3. **inhibits** Na+ reabsorption

4. inhibits renin secretion

5. increases dilation of *afferent* arterioles => inc. GFR

Front 318

***net effect of ANP =***

Back 318

inc. natriuresis

Front 319

natriuresis =

Back 319

excretion of Na+

Front 320

what do renal sympathetic efferent nerves do?

(3)

Back 320

1. constrict glom. arterioles (afferent more than efferent)
=> dec. GFR

2. stimulate PCT's Na+/H+ antiport

3. inc. renin secretion

Front 321

***net effect of renal sympathetics:***

Back 321

*increase Na+ reabsorption in the PCT*

/conserve water

Front 322

**renal sympathetics are activated during:**

Back 322

**decreased ECV**

(hemorrhage, etc)

Front 323

renin converts:

Back 323

angiotensinogen into AI

Front 324

AI is converted to AII via:

Back 324

ACE

Front 325

***what activates renin release?***

(5)

Back 325

1. dec. ECV

2. dec. BP

3. dec GFR

4. inc. symp activity

5. dec. Na+ concentration at the macula densa

Front 326

***net effect of RAAS = ***

Back 326

reabsorb Na+ AND water

Front 327

major difference between ADH and RAAS =

Back 327

ADH deals with water, while AII deals with both water AND Na+

Front 328

what is the most potent vasoconstrictor?

Back 328

AII

=> inc. TPR, inc. MAP

Front 329

***AII acts in concert with:***

Back 329

renal sympathetics

Front 330

***net effect of AII + renal sympathetics = ***

Back 330

greater constriction of afferent arteriole than efferent

=> dec. Pgc, dec. GFR, dec. RBF

Front 331

other AII effects:

(4)

Back 331

1. inc. Na+/H+ antiport at PCT

2. inc. aldosterone secretion

3. inc. ADH

4. inc. thirst

Front 332

***ultimate effect of AII:***

Back 332

***bring ECV back up***

(if it had decreased)

Front 333

aldosterone:

(2)

where?

Back 333

1. inc. Na+ reabsorption ***in the DCT***

2. inc. K+ secretion in the DCT

Front 334

what's the mechanism by which aldosterone reabsorbs Na+?

Back 334

via **rapid activation of EnaC's** =>

Front 335

b/c aldosterone is a steroid hormone, it also causes:

Back 335

synthesis of ENaC's

Front 336

**release of aldosterone is stimulated by:**

(4)

Back 336

1. elevated plasma AII

2. elevated plasma K+

3. dec. Na+ in plasma

4. dec ECV

Front 337

ADH modifies water excretion _________________ of salt

Back 337

independent

Front 338

normal plasma concentration of H+ =

Back 338

40 nM

Front 339

maximum H+ concentration =

Back 339

100 nM => pH of 7 => acidotic

Front 340

minimum plasma concentration of H+ =

Back 340

16 nM => pH of 7.8 => alkalotic

Front 341

***50% of short-term buffering is achieved by:***

Back 341

intracellular proteins, which take on excess H+

- but eventually, you *need* HCO3 to take over

Front 342

body pH =

(equation)

Back 342

6.1 x log [HCO3] / [CO2]

Front 343

lung expelling CO2 isn't enough to prevent acidosis by itself, b/c:

Back 343

every time we produce a CO2, we knock out a bicarb to do it

=> => ruins the HH balance

Front 344

what gets rid of H+ in the long term?

Back 344

the kidneys

Front 345

H+ comes from:

(4)

Back 345

1. metabolism

2. GI secretions

3. changes in CO2 production

4. anaerobic exercise

Front 346

***kidneys recover_____ HCO3 from the filtrate***

Back 346

ALL

(in normal circumstances)

Front 347

***the kidneys do NOT generate:

Back 347

new HCO3***

Front 348

**how kidneys shape acid-base balance:**

(4)

Back 348

1. reclaim HCO3 from filtrate

2. secrete H+ to be excreted

3. attach H+ to P buffers, which are excreted

4. secrete H+ as ammonium (NH4+)

Front 349

we need to get rid of about 100 mmol of H+, b/c that's how much:

Back 349

we produce

Front 350

secreting H+ by itself and secreting it with the P buffer is:

Back 350

not enough

Front 351

**attaching H+ to something other than HCO3, like the P buffer, effectively gives us:**

Back 351

another HCO3

Front 352

how do we get NH4?

Back 352

glutamine is taken up by the PCT cells;

glutaminase splits it into NH4 and aKG

- NH4 is secreted

Front 353

**aKG is converted into**:

Back 353

2 HCO3's !

Front 354

there is no limit to the amount of NH4 that can be:

Back 354

excreted

Front 355

during acidosis, renal glutaminase is:

Back 355

increased

=> more NH4 as well as more HCO3

Front 356

most of our K+ is:

Back 356

intracellular

Front 357

extracellular K+ *needs* to be maintained at:

Back 357

3.5 to 5 mM

Front 358

even though our diet is high in K+, we can maintain the low extracellular concentration by a:

(2)

Back 358

1. short-term solution

and a

2. long-term solution

Front 359

short-term solution to increased extracellular K+:

Back 359

**skeletal muscle stores it**

- takes K+ out of extracellular concentration

- releases it over time

Front 360

long-term solution to increased exracellular K+:

Back 360

**kidney changes excretion of K+ depending on the need**

Front 361

which parts of the nephrons secrete K+?

Back 361

principal cells of the DCT and CD's

Front 362

how are principal cells of the DCT and CD's able to secrete K+?

(2)

Back 362

1. basolateral Na+/K+ ATPases pump K+ in

2. ROMK's secrete K+

Front 363

what stimulates K+ secretion?

(3)

Back 363

1. excess plasma K+

2. aldosterone

3. increased dietary intake

Front 364

acidosis is often associated with:

Back 364

hyperkalemia

Front 365

why is acidosis is often associated with hyperkalemia?

Back 365

due to the H+/K+ antiport

Front 366

incrased plasma H+ => exchange of:

Back 366

intracellular K+ for extracellular H+ => inc. extracellular K+, hyperkalemia

Front 367

more bicarb retained => increased:

Back 367

pH,

due to HH equation

Front 368

water permeability of the ascending loop is NOT altered by:

Back 368

ADH.

Front 369

O2 dissociation curve axes =

Back 369

% over PO2

Front 370

Remember that DCT’s are right next to:

Back 370

glomeruli

Front 371

what do medullary rays do?

Back 371

transport ultrafiltrate from cortex to medulla

Front 372

***Clearance of creatinin is inversely proportional to:***

Back 372

** Plasma** creatinin

Front 373

LOH/interstitium ~~

Back 373

countercurrent multiplication

Front 374

the majority of RBF goes to:

Back 374

the renal cortex

Front 375

Physiological dead space includes:

Back 375

anatomic dead space,

and corresponds to wasted ventilation

Front 376

the ascending LOH has lots of:

Back 376

Na+/K+ on the basolateral surface

Front 377

V/Q of infinity =

Back 377

physiological dead space

Front 378

Remember that while condoms are easier to blow up, they are:

Back 378

much harder to deflate as well

(~ obstructive diseases)