Physio - Kidney Part 2

Front 1

Which nephron has better absorption?

Back 1

cortical nephron

Front 2

Pyelonephritis

Glomerulopathy

Back 2

Acute Renal Failurei
more specifically intrarenal problems
1. ascending urinary tract infection

2. disease of glomerulus

Front 3

3 types of acute renal failure

Back 3

Classified by location of problem area
1. prerenal- decreased blood supply e.g. from low volume or thrombosis of the renal artery

2. intrarenal e.g. Tubular necrosis - due to toxins (e.g. heavy metals, ethylene glycol, insecticides, mushrooms

3. postrenal - Block or partial block of the lower urinary tract

Front 4

Acute Prerenal Failure

oliguria
anuria
edema

Back 4

Decrease in blood flow decreases the GFR and the urine output of water and solutes (normally gets around 25%)

reduced urine production
cessation of urine production

Front 5

What is this, azotemia?

Back 5

High levels of nitrogen-containing compounds, such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds IN BLOOD.
It is largely related to insufficient filtering of blood by kidneys

Front 6

3 types of Azotemia?

Back 6

1.Pre-renal (poor perfusion of kidneys = decreased GFR)
2.Renal azotemia (primary renal disease)
3.Post renal azotemia

Front 7

What type of azotemia is most likely to be reversible: acute pre-renal OR acute postrenal OR chronic renal failure?

Back 7

acute PRErenal (most likely) - give fluids, ensure adequate blood flow to kidneys

>>fyi- as long as blood flow is at least 20% of normal,
renal failure can usually be reversed if cause of ischemia is corrected in time (within hours)

post renal can be reversed also...sometimes

Front 8

As mentioned earlier, severe decrease in blood flow causes ischemia, and Kugler's magic number is 20%. If blood flow to kidney is < 20%, what is prognosis? what's big deal?

Back 8

If blood flow to kidney is < 20%,, basal requirements of kidney tissues cannot be met anymore; hypoxia damages cells (tubular epithelial cells are very sensitive

Front 9

Unilateral obstruction e.g. of ureter or urine outflow tract = decrease of the urine flow...derr. What kind of renal failure is this?
Will we see azotemia (changes in body fluid) with this? Is this reversible?

Give some examples of stuff that can cause obstruction.

Back 9

Acute Post-renal Failure (unilateral)
>>consequently contralateral kidney increases urine production and picks up slack....no major change in the body fluid composition....normal kidney function can be restored if remove obstruction in time
e.g. stones, blood clots, tumor

Front 10

Bilateral obstruction of the urinary tract = decrease of the urine flow...derr. What kind of renal failure is this?
Will we see azotemia (changes in body fluid) with this?

Back 10

Acute Post-renal Failure (bilateral)

both pelvises, both ureters, bladder, urethra
e.g. stones, blood clots, tumor
accumulation of metabolic end products IN BLOOD = azotemia = intoxication

Front 11

Chronic Renal Failure is reversible or not?

Animal will not show clinical signs until ___% of nephrons are gone.

Back 11

Results from irreversible loss of large numbers of nephrons:
animal will not show clinical signs until 70% of nephrons are gone!!

Front 12

Problems associated with CRF include: anuria, polyuria, oliguria, and number of functional nephrons begins to decrease.
Give order in which these chronic kidney problem appear:

Back 12

1. number of functional nephrons decreases
2. polyuria - nephrons reduced by more than 70% !!!!!
- GFR increases: rapid tubular flow causes reduced water resorption
3. oligouria - further decrease of functional nephrons
- metabolic waste products accumulate
4. anuria - no urine produced and only few functional nephrons remain

Front 13

Following Renal Failure what ECF Constituents will appear in most?

What will decrease the most?

Back 13

In ECF?

NPN, followed by K+

HCO3-

Front 14

How does CO2 cross epithelial cell?....like if u wanted to reabsorb it from tubular lumen and eventually back into blood

Back 14

CO2 is very lipid soluble, so diffuses right across cell membrane, binds with H2O, to form HCO3- and H+ inside cell

Front 15

How is HC03- reabsorbed from tubular system (distal and collecting duct)?

Back 15

secretion of H+, form H2CO3, then CO2 and H2O...CO2 diffuses across cell membrane very easily.
..then again form HCO3- in epithelial cell and diffuses into interstitium

Front 16

How does pressure in glomerular caps compare to pressure in other capillaries?

How does hydrostatic pressure in peritubular caps compare to pressure in other capillaries?

Back 16

Slightly higher (~55mmHg)

Lower (7-10mmHg) but varies dep. on resistance in efferent arteriole. Low HP favors reabs.

Front 17

If TF/P = 1.0, what does this tell u about substance?

Back 17

If conc. in tubular fluid is same as in plasma, substance is freely "filtered" like water e.g. such as amino acids, bicarbonate

Front 18

Where in tubular system is osmolarity the greatest?

Back 18

tip of Loop of Henle that extends deep into medulla

the LoH creates the high osmolarity in the medulla interstitium

(can also be found on collecting duct if under maximum pressure from ADH)

Front 19

What is key (direct impact) on changes in osmolarity in renal tubule?

Back 19

H2O reabsorption (from tubule to iinterstitium); whether or it is permeable to H2O

top of ascending limb (leaving LoH) or beginning of distal tubule is not permeable to H2O. At the same time electrolytes are pumped out. Consequently, the osmolarity plummets from 400 to 100 or less.

Front 20

In osmosis, H2O leaves the side of lower osmolarity (less concentrated) across membrane to side of high osmolarity.

Which of these is said have higher osmotic pressure?

Back 20

Its dumb, but diluted side has "high osmotic pressure". The H2O will leave this side to go to more concentrated side.
So this is different from oncotic pressure.

Front 21

1. What stimulates Ca+2 resorption in ascending limb, DT, and collecting ducts?

2. What happens in Ca+2 lvl. in plasma increases?

Back 21

1. PTH; reduces urinary loss of Ca+2

2. secretion of PTH declines, more will be excreted

Note: 1/2 of calcium in plasma is bound by proteins..proteins don't get into glomerular filtrate, so only unbound Ca+2 makes it in. Of the filtered Ca+2 only 1-2% is excreted.

Front 22

Where is ADH produced?

What does it do?

Back 22

neuroendocrine cells of hypothalmus, extending to post.pituatary. Sensory cells in hypoth. monitor osmolarity of ECF and reg. ADH secretion.

Reduced blood volume stimulates its secretion

ADH increases DT and collecting duct's permeability to H2O, allowing it to leave before excreted.

Also increases medullary CD's perm. to urea

Front 23

Weak acid ionizes _____ in solution. Its conjugate base is _____, that is the binding force to H+ is ____.

Back 23

only partly; strong; high

Most of it is bound by strong base, and only if H+ concentration decreases (e.g. by adding OH-: H+ + OH- > H2O) then is H+ released

Front 24

Actual micturition is controlled by a micturition center in the (1)_____ which starts the urine flow. It is interconnected with other centers in the (2)______, ______, and _______, thus getting micturition under (3)______.

Back 24

1. pons
2. upper medulla, the hypthalamus and the cerebrum
3. voluntary control

Front 25

3 Mechanisms of Diuretics

Back 25

1. Osmotically active agents -
2. Transport inhibitors -
3. Carbonic Anhydrase Inhibitors

Front 26

Carbonic Anhydrase Inhibitors

Mode of action? Clinical application? Effect on Na+ and ion reabsorption?Speed? Example?

Back 26

inhibits CA from forming CO2 out of HCO3- (bicarbonate). Therefore can't reabs, so more remains in tubule and gets excreted w/water, thus increasing volume.
Diuresis effect: Very mild, but danger of acidosis (excretion of base HCO3-)
Also Na+ and K+ excretion increases b/c less H+ is available for antiport processes

Main clinical indications: - Reduction of intraocular pressure in glaucoma - Mountain sickness (decrease in [HCO3-]) 
Duration: diuretic effect ceases after 2 – 3 days (low blood levels of bicarbonate)

Front 27

Transport inhibitors: Example?

Back 27

inhibit Na/K pump, NaCl symport, or Na/K/2Cl symport, so everything is excreted in bulk.

e.g. Thiacide Diuretics like Chlorothiazide, Hydrochlorotiazide

e.g.2. K+ Sparing Diuretics
Drugs: Spironolactone, Triamterene, Amiloroide

Front 28

Osmotically active agents -

Mode of action? Clinical application? Speed? Example?

Back 28

Osmotically active agents - attract H2O by increasing osmolarity in tubule.
Treatment or prevention of acute renal failure - accelerated excretion of toxins - contraindication: edema caused by cardiac failure (sudden onset causes hemoconcentration which means risk of thrombosis)
Onset of diuresis: 1 – 3 hours, duration: 3 – 6 hours

e.g. Mannitol, Glycerol
~NaCl excretion increases

Front 29

Where are these found?
1. Osmotic diuretics
2. Carbonic anhydrase inhibitors

Back 29

1. proximal tubule
2. proximal tubule

Front 30

Where are these found?
1. Thiacide diuretics
2. K+ sparing diuretics
3. Loop diuretics

Back 30

1. - early distal tubule
2. cortical collecting duct
3. Thick ascending, Loop or Henle

Front 31

Drug class of: Acetalamide, Dichlorphenamide, Metazolamide, etc.

Duration of effects?

Back 31

Carbonic Anhydrase Inhibitors

Main clinical indications: - Reduction of intraocular pressure in glaucoma - Mountain sickness (decrease in [HCO3-]) 

diuretic effect ceases after 2 – 3 days (low blood levels of bicarbonate)

Front 32

K+ Sparing Diuretics

Example and their mode of action

Back 32

Transport inhibitors:
Spirolactone competitively blocks the Na+ resorption and K+ secretion caused by Aldosterone
Triamterene and Amiloroide block the Na+/K+ pump in the distal tubule and collecting duct

Front 33

Thiacide Diuretics:
Mode of action?
Effect on Na+ and ion reabsorption?
Main clinical indications?
Speed? Example?

Back 33

Transport Diuretic: block Na+/Cl- symport in early distal tubule

Na+ and K+ excretion increases

Main clinical indications: Hypertension, congestive heart failure
Drug classes: Chlorothiazide, Hydrochlorotiazide
Onset of diuresis after 1hour (oral), duration 6 – 48 hours

Front 34

Loop Diuretics

Mode of action?
Effect on Na+ reabsorption?
Main clinical indications?
Example?

Back 34

Transport Diuretic: Substances which block the Na+/ K+/2Cl- symport in the Loop of Henle

Diuresis effect: Very potent, excretion of up to 30% of glomerular filtrate!

“K+ wasting effect”, K+, but also Na+, Cl- and water excretion increases 

Main clinical indications: - Hypertension, congestive heart failure, ascites, acute renal failure, chronic renal failure, acute pulmonary edema

Onset of diuresis after 5 min (iv.) or 20 – 60 min (oral), duration 2 – 8 hours

Front 35

Natraemia, phosphataemia, magnesaemia

Back 35

These disorders of water and electrolyte balance
Abnormally low conc of Na+ in blood. Too little sodium can cause cells to malfunction. Hyponatremia has many causes including medications such as diuretics and antidepressants, hypothyroidism, cortisone deficiency (such as in Addison's disease), dehydration, vomiting or diarrhea, severe burns, kidney or heart failure, and cirrhosis.

Front 36

Where do Na/K pump appear?

Back 36

Proximal tubule, DT, collecting duct,

NOT descending limb

Front 37

Where does secondary active transport occur?

Back 37

apical / luminal side

proximal, ascending LoH