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Renal System
1. Pete A. Gutierrez MD, MMS, PA-C
Miami Dade College Physician Assistant Program
March 2009
2. GFR = UV/P
An Elevated >20:1 Bun/Cr. Ratio indicates
wither pre-renal azotemia
Alkalemia increase in blood calcium level can
lead to diffuse paresthesias/numbness and
muscle spasm.
Formation of carbonic acid and dissociation
into HCO3 and CO2.
3. Anion Gap
◦ Anion Gap normal is 12
◦ Formula is AG = Na –(HCO3+CL)
◦ The anions in blood include
HCO3, Cl, Phosphate, Sulfate, Albumin, and organic
acids.
◦ The Cations include NA, K, Ca, Mg.
◦ Metabolic acidosis occurs with overproduction of
lactic acid or ketoacids.
◦ It can also occur with HCO3 wasting or renal tubular
acidosis or diarrhea.
◦ Underexcretion of acid (renal Failure) and also in
poisonings by agents that are metabolized to acids.
4. Causes of increased anion gap metabolic
acidosis:
◦ Severe CRF decreased acid especially NH4
◦ Ketoacidosis diabetic, alcoholic, starvation
◦ Lactic acidosis drugs, circulatory compromise
◦ Rhabdomyolysis
◦ Poisoning salicylates, methanol, ethylene glycol
5. Causes of normal anion gap acidosis:
◦ Renal tubular acidosis
◦ Diarrhea
◦ Carbonic anhydrase inhibitors
6. Patients who drink methanol produce
formaldehyde and formic acid resulting in a high
anion gap acidosis.
Ethylene glycol (Antifreeze) forms glycolic acid
and oxalic acid resulting in a high anion gap
acidosis and calcium oxalate crystals in the urine.
Patients drinking isopropyl alcohol can have
significant ketosis without acidosis because
isopropyl alcohol breaks down to acetone.
So a patient arriving with stuporous and fruity
smell on his breath and has normal chemistry
except high ketones.
7. These test should be preformed on a patient
who comes in with high anion gap acidosis:
Urine + serum ketones levels
◦
Lactic acid level
◦
And the osmolar gap.
◦
The osmolar gap is the different between measured
◦
and calculated osmolarity. Calculated osmolatity is:
Osm = 2(NA) + BUN/2.8 + glucose/18
Normal osmolar gap is < 10.
If >20 think of intoxication with any one of the
alcohols.
8. Metabolic Alkalosis:
Usually results from volume contraction
caused by diuretics or vomiting which causes
a lost of HCL.
Treatment requires KCL, and NaCl.
10. Normal Osmolality is usually 282+ or – 2
mosm/kg H2O.
If glucose and Bun are normal just use the
(NA) x 2 to see if it is normal
Low Na is the most common electrolyte
abnormality:
◦ Isotonic
◦ Hypertonic
◦ Hypotonic
11. Isotonic hyponatremia occurs when protein or
lipids displace sodium as in multiple myeloma
(MM) and p
hyperlipidemia. There is an increased osmolar
gap. The measured serum osmolality is normal
while the calculated osmolality is low because of
the low NA,
Hypertonic both glucose an mannitol cause an
osmotic shift of water out of cells which dilutes
plasma NA remember that for each 100 mg/dl
increase in glucose, sodium concentrations
decreases by 1.6.
12. Hypotonic:
The hypo tonicity cause intracellular swelling
which may result in neuromuscular
excitability, seizures and coma.
Usually when the NA goes below 120 the
sodium level decreases slowly the cells re-
equilibrate and do not swell enough to cause
these symptoms.
The hypotonic group is further subdivide by
volume status: Low-High-Normal
13. The low-volume is the group of patients that
have lost both water and Na, but more Na
than water this is normally caused by the use
of diuretics, GI loses (Vomiting and Diarrhea)
and adrenal insufficiency. In adrenal
insufficiency, low aldosterone caused
decreased active NA reapsortion which results
in NA and water wasting, with high K and a
mild metabolic acidosis.
14. Hypotonic High:
These people usually have low output CHF or
hypoalbuminemia (From Cirrhosis) they retain
water and NA but usually more water than NA
so they have normal or even elevated total
body NA.
Often these patients have edema and JVD.
Normal treatment is restriction of water and
NA. (Used loop diuretics).
15. Hypotonic (SIADH):
◦ The normal volume patients usually have
SIADH, but this can also be caused by psychogenic
polydipsia (rare) and even by diuretics, if there is
sufficient water replacement.
◦ The serum uric acid and bun are low but this is
dilusional.
◦ The most serious causes of SIADH are CNS
disorders to include meningitis, lung disorders, and
cancer especially small cell carcinoma.
◦ Also cancer of the duodenum and thymus and some
drugs like cyclophosphamide, clofibrate, and
vincristine.
16. Treatment of Hyponatremia:
◦ If the patient is hypovolemic give 1-2 liters of
normal saline.
◦ If the symptoms are severe to include seizures give
3% saline, along with loop diuretics.
◦ Give the 3% saline over 8-12 hours, to increase the
sodium by 10meg/lt.
◦ The meq is calculated by multiplying the total body
water (60% of body weight eg 60 L in a 100 kg
patient) by 10 which would equals 600 meq.
◦ Each liter of 3% saline has 512 meq of NA so about
1 liter could be given over 12 hours.
17. NEVER, Never, Never give hypertonic saline
rapidly.
The correction should not exceed 1-2
mmol/hr.
If the patient has SIADH treat with fluid
restriction and give Demeclocycline 900
mg/day.
Osmotic demyelination syndrome, central
pontine myelinolysis so it is very important
not to replenish the NA too quickly.
18. Hypernatremia:
◦ This is fairly rare and only due to the patient not
been able to get to water or the thirst mechanism is
defective.
◦ Unlike hyponatremia patients these patients are
always hyperosmolar.
◦ The amount of water needed to treat a
hypernatremic patient is calculated by multiplying
the total body water (60% of weight in Kg), by the
fractional difference between the patient NA and
normal NA.
19. Diuretics:
◦ Proximal convoluted tubule (PCT) 90% of the HCO3 is
reabsorbed here by means of several chemical changes.
The reabsortion process is driven by H being secreted.
◦ A carbonic anhydrase inhibitor (acetazolamide (Diamox)
causes diuresis with bicarbonate wasting resulting in a
metabolic acidosis).
◦ Calcium is also absorbed in the proximal tubule.
◦ When treating severe hyperclacemia normal saline is
infused at a high rate along with loop diuretics.
◦ The saline expands the volume and causes increased
flow in the proximal tubules that prevents calcium
reabsorption and the greatly increase calcium load then
delivered to the distal tubule overwhelms the distal
tubules ability to adsorb calcium and its ability is also
block by the loop diuretics
20. Loop of Henle:
◦ As the tubular fluid progresses down the loop of Henle
free H2O is sucked out of the fluid following the osmotic
gradient (The renal medulla is very hypertonic).
◦ At the base of the loop, the tubular fluid is maximally
concentrated.
◦ In the ascending limb 25% of the filtered NaCl is actively
reabsorbed .
◦ This increases the hyper tonicity of the medulla and
causes H2O from the descending limb to effectively
follow the NA out of the ascending limb.
◦ Blockage of this absorption of NA with loop diuretics
results in diuresis.
21.
22. The Distal Tubule:
◦ This is where NA is actively reabsorbed and either H
in the form of salts (NH4 or phosphate salts) or K
are then excreted.
◦ They flow back down the electrical gradient caused
by the reasorption of NA.
◦ This used to be called the NA-K pump but actually
it is the NA pump—K/H electrical excretion
gradient.
◦ Aldosterone facilitate this transport and an K
sparing diuretic like triamterene our
spironolactone.
23. Collecting Duct:
◦ Is where ADH has its effect.
◦ In the normal kidney the urine is very dilute by the
time is reaches the collecting duct.
◦ ADH increases the permeability of the collecting
duct to water, allowing the free water to reabsorbed
into the hypertonic renal medulla.
◦ There there is no ADH a very dilute urine is
produced.
24. Minerals:
◦K
◦ Even slight hyperkalemia stimulates the release of
aldosterone which causes a normally function
kidney to increased absorption of NA distally and
there for increase excretion of K.
◦ Hyperkalemia is caused by decreased excretion
(Drugs, renal failure, hypoaldosteronism such as
Addison disease) increased production
(trauma, tumor lysis) volume contraction in hospital
more common.
◦ Drugs are probably the most common cause of
increase K like ACE inhibitors and beta blockers.
25. The cardiac effects of hyperkalemia are due
to the large difference between intracellular
and extracellular K levels.
Treatment can be done with glucose +
Insulin.
Can also give the patient IV calcium in the
form of Calcium Chloride 1 amp.
Calcium Gluconate.
26. Calcium regulation:
◦ Regulation of calcium PTH and vitamin D
metabolites cause changes in the way the
kidney, GI, and bone handle calcium.
◦ Calcium circulates in an inactive form bound form
(usually albumin) and an active form, called also
ionized/unbound form.
◦ With hypoalbuminemia only the bound form
decreases.
◦ For each decrease in albumin of 1, the total calcium
will decrease by .7
27. Magnesium:
◦ Hypomagnesaemia is rare and occurs from the use
of Mg-containing laxatives or antacids in renal
failure patients and MgSO4.
◦ Symptoms begin with levels of >4-6 meq/l.
◦ Symptoms level are sedation, muscle weakness, and
a loss of deep tendon reflexes and can progress to
paralysis.
28. Hyperphosphatemia:
◦ Acute increase is from acute tubular necrosis, IV
solutions, and tumor lysis after chemotherapy.
◦ Chronic increase in parathyroidism.
◦ Hypophosphatemia:
Think Alcohol if severe PO4< 1mg/dl it may cause
rhabdomyolisis as also can low K.
30. HTN:
◦ Primary Hypertension: 95% of all hypertension is
primary (1.e. essential idiopathic.) The systolic and
diastolic blood pressure (DBP) define the stages of
HTN:
Stage I SBP 140-159 or DBP 90-99
Stage II SBP 160-179 or DBP 100-109
Stage III SBP>180 or DBP>110
33. The breakdown of proteins produces amino
acids and the subsequent metabolism of
amino acids produces nitrogenous wastes like
ammonia.
The Ammonia is converted in the liver into
less harmful Urea.
The body accumulates excess ions of
sodium, chloride, potassium, hydrogen
ions, sulfate and phosphate.
34. The role of the Urinary system is to maintain
a balance of these products and to remove
the excesses from the blood.
The urine consists of the metabolic waste of
urea, excess water, excess ions, and toxic
wasted that may have been consumed with
food.
35. Function’s of the Urinary System:
Excretion/Reabsortion
◦
Maintain blood volume and concentration
◦
pH regulation
◦
Blood Pressure-Renin which helps adjust filtration
◦
pressure.
◦ Erythropoietin-A hormone that stimulates red blood
cell production
◦ Vitamin D Production convert vitamin D to its active
form Calciferol.
36. The kidneys are paired organs that are
reddish in color and resemble kidney beans
in shape. They are the size of a closed fist.
They are located between the parietal
peritoneum and the posterior wall of the
abdomen also known as the retroperitoneal
space.
The right kidney is slighly lower that the left.
The average kidney measures about 11.25cm
long and 5.0 to 7.5 cm wide.
37. Near the center of the kidney is a notch called the
Hilum through which the ureter leaves the
kidney, and blood vessels, nerves, and lymph
vessels also enter and exit the kidney’s.
Three layers of tissue surround each kidney:
◦ The innermost is the renal capsule (serves as barrier
against infection)
◦ The second layer is the adipose capsule (Protects the
kidney’s from blows, and hold the kidney’s in place).
◦ The outermost layer is the renal fascia which is
connective tissue that anchors the kidney’s to their
surroundings.
38. The Internal Anatomy of the Kidney’s:
◦ A frontal section will reveal the outer area called the
cortex , and an inter area called the medulla.
◦ Within the medulla there are 8-18
striated, triangular structures called the renal
pyramids.
◦ The Nephrons are the functional units of the
kidney’s. They regulate the composition and
volume of blood and form the urine.
39. The Minor calyxes surrounds the tip of each
renal pyramid and joint to form the Major
calyxes which them joint together to form the
renal pelvis.
The functional unit of the kidney’s are the
nephrons, which is a microscopic renal tubule
which functions as a filter.
As we age the kidney’s decrease in size. At
age twenty they weigh approximately 260
grams and by age 80 they weigh is
approximately 200 grams.
40. The nephron begins as a double-walled globe
known as the Bowman’s Glomerular Capsule.
This is located in the cortex of the kidney’s
The right and left renal arteries transport one
quarter of the total cardiac output directly to
the kidney’s.
About 1200 ml of blood passes through the
kidney’s every minute
42. Physiology of the nephrons:
◦ In glomerular filtration, the glomerulus filters water
and certain dissolved substances from the plasma
of blood. (Positive charge ions of
sodium, potassium, calcium and magnesium.
◦ Both kidney’s filter about 45 gallons of blood
plasma per day.
◦ Most fluid gets reabsorbed in the renal tubules and
reenters the plasma.
43. Tubular reabsorption:
◦ The majority of the reabsorption occurs in the
proximal tubule. Active transport reabsorbs amino
acids, glucose, creatinine, lactic acid, Uric
acid, Citric acid, and Ascorbic acid.
◦ Osmosis reabsorbs water
◦ Chloride ions and other negatively charge ions are
reabsorbed by electrochemical attraction.
44. Tubular Secretion:
◦ The proximal convoluted tubule actively secretes
penicillin, creatinine and histamine into the tubular
fluid.
◦ It also secretes Hydrogen Ions (H+) thus helping in
the regulation of body pH.
◦ Urine consist of water and solutes that the kidneys
either eliminate or retain in the body in order to
maintain homeostasis.
45. Renal Test:
◦ There should be no RBC’s in the urine, but if the
urine Dip is positive thinks always of
Hemoglobinuria or Myoglobinuria.
◦ One common cause of Hemoglobinuria is red blood
cells lysis.
◦ If you see RBC casts or crenated dysmorphic red
blood cells indicate a renal origin and probable
glomerulonephritis.
◦ If you see eosinophiluria think of drug induce
interstitial nephritis.
46. There should very little proteins found in the
urine less than <150mg.
◦ Proteinuria is the best indicator of underlying renal
pathology.
◦ More than 2.5-3.5 gm (or 40-50mg/kg/d) means
significant glomerular pathology.
◦ A pathology called Myeloma often results in Bence-
Jones proteinuria. The Bence Jones proteins are
light chains which are not picked up on a urine
dipstick.
47. Transient Proteinuria is common in people
during a febrile illness, also after strenuous
exercise, and in patients with CHF and COPD.
You should always check the urine when the
situation as passed.
Benign orthostatic proteinuria is a condition
in which the proteinuria reverts back to
normal when the patient is supine.
48. Microalbuminuria is an indication of early
diabetic nephropathy this is not picked up on
the urine dipstick.
Later in the disease the condition turns into
nephrotic syndrome.
Causes of false positive urine albumin on the
dipstick include a very alkaline urine with a
pH >8, and a very concentrated urine.
49. GFR-Glomerular Filtration Rate, Urine to
plasma creatinine concentration X urine flow
rate.
Medicines that increase GFR are
cimetide, probenecid and trimethroprim sulfa
TMP/SMX.
Acetone and cefoxitin interfere with the test
for creatinine and may give falsely elevated
results.
50. Creatinine is produce by muscle mass and the
breakdown of muscle tissue.
Renal biopsy is used to diagnose causes of
acute renal failure, nephrotic syndrome, and
glomerulonephritis.
51. Fluid and Electrolytes:
◦ Normal Osmolatity is usually 282+or – 2 mosm/kg
H2O.
◦ Osm = 2(Na) +Glucose/18+Bun/2.8
53. Disorders of the Urinary System:
◦ Kidneys stones known as calculi are composed of
the precipitates of uric acid, magnesium or calcium
phosphate, or calcium oxalate.
◦ Cystitis an inflammation of the urinary bladder
◦ Gout is a condition caused by high concentrations
of uric acid in the plasma. Uric acid crystals.
◦ Glomerulonephritis is an inflammation of the
kidneys where the filtration membrane within the
renal capsule is infected with bacteria. (Following
streptococcal sore throat infection).
◦ Renal failure
◦ Hematuria, oliguria or polyuria.
