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Human Pathophysiology: Final > Renal System I > Flashcards

Renal System I Flashcards

1
Q

What are the normal plasma osmolarity levels?

A

285-295 mOsm/L

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2
Q

What values would constitute concentrated vs. dilute urine?

A

concentrated: >1000 mOsm/L
dilute:

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3
Q

What organ is the main regulator of osmolarity?

A

the kidneys

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4
Q

What is the equation for Posm?

A

Posm = 2 x [Na+(mEq/L)]p + [glucose (mg/dl)]/18 + [BUN (mg/dl)]/2.8

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5
Q

What are the main components of the calculated blood osmolarity?

A

Na+, BUN, glucose

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6
Q

How does Ethylene Glycol Poisoning cause an osmolarity gap?

A

It causes an osmolar gap is greater than 10 mOsm/L (the usual osmolarity of K+, phosphate, and other things in the plasma, but not normally considered in the calculation of plasma osmolarity), which signals the presence of an unmeasured osmole (in this case ethylene glycol)

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7
Q

What is an osmolarity gap?

A

the difference between measured serum osmolality and calculated serum osmolality

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8
Q

What are the body’s responses to hypoosmolarity?

A
  • thirst (decreased in response to hypoosmolarity)

- ADH release (decreased in response to hypoosmolarity)

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9
Q

What can cause hypoosmolarity?

A
  • problems with the ability to sense osmolarity or changes in set point for osmolarity
  • alterations in thirst mechanism
  • problems with ADH release
  • problems with the renal response to ADH
  • drinking too much water before or during exercise
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10
Q

What is one simple way to measure urine osmolarity?

A

Measure its specific gravity. A urine osmolarity of 300 mOsm/L (which should occur if one has a normal plasma osmolarity ) is equivalent to a specific gravity of 1.008.

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11
Q

What is one day to determine the mechanism of plasma osmolarity?

A

measure urine osmolarity (body will suppress ADH and urine osmolarity should decrease)

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12
Q

How does pregnancy lower the set point for osmolarity?

A

During pregnancy, ADH release and increased thirst starts to occur at a lower than normal plasma osmolarity. ADH acts on the collecting ducts to make them
permeable, water flows out along its concentration gradient. More water is retained and plasma osmolarity increases.

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13
Q

Definition: when patients have a compulsion to drink large amounts of water; drink excessively (up to 20 L/day) and produce large volumes of very dilute urine

A

psychogenic polydipsia

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14
Q

What occurs during psychogenic polydipsia?

A

ADH decreases –> urine volume rises –> and the urine becomes very dilute (patients can often maintain normal plasma volume and osmolarity unless they have compromised renal function for some reason)

IF kidneys cannot compensate… decreased osmolarity –> hyponaturemia –> water enters cells via osmosis –> fluid in neurons causes neuronal death

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15
Q

What can cause changes in plasma volume and trigger ADH release?

A
  • excessive diarrhea
  • sweating
  • vomiting
  • blood loss
  • ascites/edema
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16
Q

What provides most of the oncotic pressure in vessels?

A

proteins produced by the liver such as albumin

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17
Q

How does cirrhosis cause ascites?

A

Alcohol poisoning has caused permanent damage to liver cells with scarring and loss of function. The liver produces abnormally low amounts of albumin and consequently, Ponc falls. This increases the fluid flux out of the capillaries (causing edema to accumulate in abdomen).

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18
Q

How does resistance to blood flow through the liver contribute to ascites?

A

Scarring of the liver increases the resistance to blood flow through this organ. The liver receives the entire blood supply to the intestines, stomach, spleen, etc., through the portal vein. Portal pressure rises, as do hydrostatic pressures in all the capillary beds upstream of the liver. This further increases fluid flux out of capillaries.

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19
Q

How does injury to the liver affect the epithelium of vessels and oncotic pressure?

A

injury and inflammation in the liver result in release of mediators with the ability to make the capillary endothelium leaky to proteins, effectively reducing oncotic pressure

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20
Q

What does ascites result in and how does the body compensate?

A
  • results in huge build up of fluid in the abdomen and a reduction in blood volume.
  • stimulates ADH release –> water retention in the collecting ducts and distal tubules.
  • effects on blood pressure that will stimulate renin, aldosterone, and angiotensin.
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21
Q

What will increasing aldosterone do?

A

increase sodium retention and decrease sodium concentration in the urine

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22
Q

What is Syndrome of Inappropriate Secretion of ADH release (SIADH)?

A
  • excessive ADH secretion due to carcinomas, brain trauma or other neurologic problems, and certain pneumonias
  • the person retains abnormally high amounts of water and plasma osmolarity falls
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23
Q

Which drugs promote ADH release and can cause SIADH?

A
  • antidepressants
  • nicotine
  • morphine
  • some chemotherapeutic agents like vincristine and cyclophosphamide
  • ecstasy
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24
Q

What are the symptoms of hyperosmolarity?

A
  • muscle weakness
  • lethargy
  • twitching
  • seizures
  • coma
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25
Q

What can cause hyperosmolarity?

A

-administration of sodium salts (such as sodium bicarb to treat acidosis)
-failure to consume sufficient water under otherwise normal circumstances
-excessive vomiting, diarrhea, or sweating (these fluids are often hypoosmolar with
respect to plasma)
-extrarenal water loss
-excessive renal water loss (due to inability to secrete ADH or to respond to it)

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26
Q

Definition: a rare form of diabetes caused by a deficiency of the pituitary hormone vasopressin, which regulates kidney function

A

diabetes insipidus

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27
Q

How can diabetes insipidus cause hyperosmolarity?

A

lack of ADH –> inability to reabsorb water across the distal tubules and collecting ducts –> water that enters these ducts from the ascending loop of Henle is excreted in the urine –> urine cannot be concentrated –> loss of large volumes of hypotonic urine

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28
Q

What are some things that can cause an inability to secrete ADH (diabetes insipidus)?

A
  • central nervous system disorders like tumors, infections, cerebral aneurysms
  • damage to certain parts of the brain
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29
Q

When does hyperosmolarity from diabetes insipidus actually develop?

A

the development of hyperosmolarity depends on whether or not one is able to drink water to replace the fluid losses (infants, the elderly, patients who are unconcious or
immobilized may not have sufficient water intake)

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30
Q

What is nephrogenic diabetes insipidus?

A
  • diabetes insipidus resulting from certain drugs or from renal problems that change the renal architecture resulting in an inability to generate an osmotic gradient in the renal medulla
  • inability to respond to ADH results in loss of large volumes of hypotonic urine
31
Q

Where is potassium reabsorbed in the kidneys?

A
  • proximal tubule (55%).
  • loop of Henle (30%)
  • medullary collecting ducts.
  • depending on diet, either reabsorbed or secreted at the distal convoluted tubule and cortical collecting duct
32
Q

What is the main site of potassium secretion in the body?

A

cortical collecting duct

33
Q

How does Na+/K+/ATPase enzyme in the cortical collecting duct regulate potassium?

A

High potassium increases basolateral uptake through this enzyme, increasing the K+ concentration inside the principal cells (cells that line the cortical collecting duct). This increases the passive movement of K+ into the lumen of the tubule. A low K+ diet, or conditions that lead to K+ loss decreases K+ uptake by the principal cells, slowing secretion.

34
Q

How does aldosterone regulate potassium levels?

A

high extracellular K+ –> stimulates aldosterone secretion from adrenal cortex –> increases K+ uptake by the principal cells (via the Na+/K+/ATPase) –> stimulates K+ secretion by the cortical collecting duct –> elimination of excess K+ from the body.

Aldosterone also increases the permeability of the luminal membrane to potassium, facilitating secretion.

35
Q

How does rate of fluid delivery to the cortical collecting duct affect rate of K+ excretion?

A

potassium moves passively across the cell into the lumen so conditions that are associated with a high rate of urine production are often associated with potassium depletion

36
Q

Definition: high potassium levels

A

hyperkalemia

37
Q

Why do diabetics tend to have hyperkalemia?

A

-Insulin tends to cause potassium to move into cells. When insulin levels are low, K+
stays in the plasma.
-Acidosis (high plasma acidity), which is common in diabetics due to the production of ketoacids, as well as high plasma osmolarity (due to glucose in the blood) tend to cause potassium to move out of cells. Despite being hyperkalemic, diabetes patients tend to be K+ deficient because K+ excretion is flow dependent (increase urine output in diabetics).

38
Q

What is the difference between Type I and Type II diabetes?

A

Type 1 diabetics fail to produce insulin, and Type 2 diabetic are unresponsive to it. Glucose
remains in the plasma in both.

39
Q

What effect on plasma osmolarity and composition does diabetes have?

A
  • excess glucose causes an increase in plasma osmolarity.
  • dilutional hyponatremia: presence of the additional solute –> osmolarity of the extracellular fluid rises –> creates an osmotic gradient across the plasma membrane of all of the cells –> water moves down its concentration gradient.
  • shift in water helps to correct the hyperosmolarity but it dilutes the sodium content of the extracellular fluid – osmolarity may be normal, but the extracellular sodium concentration will be lower than normal
40
Q

What effect does diabetes have on the renal system?

A

high glucose in their plasma (and tubular fluid) –> the capacity of the tubule (transport maximum or Tm) to reabsorb it is exceeded –> excess glucose remains in the tubular fluid –> high osmolarity of the tubular fluid (due to the presence of glucose) inhibits the normal reabsorption of water in the tubule –> loss of large quantities of water in the urine

41
Q

Why do plasma levels of H+ have to stay low/constant?

A

H+ has a high affinity for proteins (including enzymes and receptors) which changes the net charge, shape and function of these proteins

42
Q

How do alterations in plasma H+ concentration influence potassium balance?

A
  • acidosis (excessive H+) causes K+ to move out of cells

- alkalosis (insufficient H+) causes K+ to move into cells

43
Q

How is H+ produced in our bodies?

A

through diet and as the result of metabolism

44
Q

How is H+ removed from the body?

A
  • lost by the expiration of CO2

- excretion in the urine

45
Q

How is H+ ion balance maintained in the short and long term?

A
  • short term: through buffers

- long-term: alterations in excretion of H+

46
Q

What is the most important physiologic buffer and what is it’s normal concentration?

A

HCO3- (bicarbonate): 24 mmol/L

47
Q

Aside from bicarbonate, what are some other buffers for H+?

A

proteins
phosphate
NH4+

48
Q

What does an anion gap indicate?

A

the presence of an unmeasured cation (positive ion), which consumes bicarbonate, lowering bicarbonate level

49
Q

How can you asses acid-base status?

A
  • measure blood pH and concentration of bicarbonate

- measure anion gap

50
Q

What is a normal anion gap?

A

Na+ - Cl- - HCO3-

51
Q

What causes metabolic acidosis?

A
  • excessive lactic acid production (resulting from prolonged periods of anaerobic metabolism)
  • prolonged diarrhea (which leads to loss of an alkaline fluid, and may also involve production of organic acids by infectious bacteria)
52
Q

What causes respiratory acidosis?

A

hypoventilation (can occur when an injury causes respiration to be painful [i.e., a broken rib] or as a result of lung disease)

53
Q

In what ways does the body compensate for acidosis?

A
  • increased ventilation
  • increased renal excretion of H+, w
  • increased glutamine metabolism, leading to NH4+
54
Q

How does increased ventilation help acidosis?

A

blows off extra CO2, shifts the following equation to the left:
CO2 + H2O –> H2CO 3 –> HCO3- + H+

55
Q

How does increased renal excretion of H+ help acidosis?

A

It adds more bicarbonate. This requires a filtered phosphate group (HPO4
2-), in the renal tubule, which binds
to an H+, to make H2PO4-. The H2PO4- goes out in the urine. However, phosphate is in limited supply!

56
Q

How does increased glutamine metabolism help acidosis?

A

Glutamine is broken down in the proximal tubular cells, yielding Na+ and NH4+, both of which are excreted into the lumen, and bicarbonate, which is reabsorbed into the blood stream.

57
Q

What causes metabolic alkalosis?

A

prolonged vomiting, which causes the loss of an acid-containing fluid, or from the ingestion of alkali fluid (common in people with bulimia)

58
Q

What causes respiratory alkalosis?

A

hyperventilation (as is seen in response to the low PO2 of inspired air at high altitude – it can also occur in people with extreme anxiety, or over-ventilation while anesthetized
during surgery)

59
Q

How does the body compensate for alkalosis?

A
  • decreased ventilation sometimes but only a small response
  • increased renal excretion of bicarbonate (shifts the equation to the right, helping to increase plasma H+ concentration)
  • NH4+ production and excretion are inhibited
60
Q

What are the major causes of kidney disease?

A
  • diabetes
  • hypertension
  • glomerulonephritis
  • cystic kidney
  • urologic disease
61
Q

What does the filtrate of the kidney contain?

A
  • filtrate is cell-free and essentially protein-free; -contains most inorganic ions and low molecular weight organic solutes
  • water, urea, amino acids, glucose, and sucrose are freely filtered
62
Q

Why are a molecule with a negative
charge is filtered to a lesser extent, and positively charged particles to a greater extent, than a neutral particle in kidneys?

A

The cells that make up the glomerular barrier have a negative charge on the surface of their membranes.

63
Q

Why is Glomerular Filtration Rate (GFR) important?

A

its a good indicator of renal function (a significant fall in GFR causes substances that are normally eliminated by the kidneys to remain in the blood = renal failure)

64
Q

What is the equation for GFR?

A

GFR = Kf x net filtration pressure

Kf = filtration coefficient

65
Q

What factors affect the filtration coefficient?

A 
Lp = capillary permeability
S = surface area
66
Q

What is net filtration pressure determined by?

A

balance of forces that affect all capillaries (aka “Starling forces”):

  • capillary hydrostatic pressure
  • interstitial hydrostatic pressure
  • capillary oncotic pressure
  • interstitial oncotic pressur
67
Q

What determinants can affect the filtration coefficient?

A
  • diabetes – deposition of extracellular matrix material decreases Kf.
  • obstruction of kidney tubule (due to inflammation or scarring) will increase PBS, which will decrease GFR.
  • autoimmune diseases such as lupus (SLE) involves production of immune complexes that can damage the glomerulus, ultimately decreasing the Kf
68
Q

How is GRF regulated?

A

By changing the net filtration pressure via

  • changes in MAP, which changes renal blood flow
  • changes in contraction of renal arterioles, which can shift the GFR (either increase or decrease)
69
Q

What does ADH do?

A
  • increases the permeability of the distal tubules and collecting ducts to water – causes aquaporin pores to be inserted into the cell membrane, increasing permeability to water
  • acts on the hypothalamus to trigger thirst
70
Q

What triggers ADH?

A
  • increase in plasma osmolarity (as little as a 2% change)
  • decrease in blood volume (need about 10% change to trigger release)
  • Angiotensin II
71
Q

What inhibits ADH?

A
  • decrease in plasma osmolarity
  • increase in blood volume
  • certain drugs (eg: ethanol)
72
Q

What happens during ethylene glycol poisoning in pets?

A

Ethylene glyol is sweet, attracting animals. Animals that have consumed ethylene glycol act disoriented – almost like they’re drunk. An elevated osmolar gap is an early indicator. Ethylene glycol is metabolized to glycolic acid, and then to oxalic acid. Their presence causes metabolic acidosis beginning a few hours after ingestion. Renal toxicity due to calcium oxalate crystals, which precipitate in the renal tubules is the most serious consequence.

73
Q

How does methanol poisoning cause acidosis?

A
  • initially, methanol increases the osmolar gap – it is an abnormal solute present in the plasma
  • methanol is converted to formaldehyde, and then formic acid –> acidosis –> increase in the anion gap (osmolar gap returns to normal)
  • leads to depressed respiration, slow heart rate, coma, irreversible blindness
  • buildup of CO2, leading to increase in plasma H+
74
Q

How is methanol poisoning treated?

A
  • resuscitation, respiratory and circulatory support
  • removal of methanol by hemodialysis.
  • blockage of metabolism by Antizol, which competes with alcohol dehydrogenase

Human Pathophysiology: Final (6 decks)

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