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RENAL > 14 – Diuretics and Renal Diseases > Flashcards

14 – Diuretics and Renal Diseases Flashcards

1
Q

Diuretic substance:

A

-increases urine output
>most work by interfering with reabsorption of Na
>with reduced water reabsorption is a second effect
>can also affect excretion of K, Cl, Mg, Ca

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2
Q

What is the clinical relevance of diuretics?

A

-given to reduce volume of ECF
Ex. edema and hypertension
*work quite quickly (mins to hours)
*can increase urine volume up to 20-fold

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3
Q

Within a few days of having diuretics what happens?

A

-kidneys use compensatory mechanisms to overcome the effects

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4
Q

What are the types of diuretics?

A
  1. Osmotic diuretics
  2. Loop diuretics
  3. Thiazide diuretics
  4. Carbonic anhydrase inhibitors
  5. Competitive inhibitors of aldosterone
  6. Sodium channel blockers
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5
Q

Osmotic diuretics:

A

-enhance osmotic pressure within tubule (keep water inside tubule)
Ex. urea, mannitol and sucrose

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6
Q

Loop diuretics:

A

-reduce Na/Cl/K reabsorption by blocking Na/2Cl/K transporters
-site of action=thick ascending segment of loop of Henle
-very potent: can cause excretion of up to 30% of GFR

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7
Q

Mechanism of loop diuretics:

A
  1. Increased solutes in the tubule interferes with water reabsorption.
  2. Interfere with countercurrent multiplier system
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8
Q

Loop diuretics interfere with countercurrent multiplier system:

A

-reduces osmolarity of renal medullary interstitium
>capacity for concentrating urine is REDUCED

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9
Q

Thiazide diuretics:

A

-reduce Na/Cl reabsorption
-site of action=distal tubule
-can lead to excretion of up to 10% GFR

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10
Q

Carbonic anhydrase inhibitors:

A

-reduce Na/HCO3- reabsorption
-site of action=proximal tubule
-reduced HCO3- reabsorption, reduces Na reabsorption via Na/H counter-transporter
*need to consider acid-base balance will be affected

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11
Q

Competitive inhibitors of aldosterone:

A

-reduce Na reabsorption and K secretion
-site of action=cortical collecting tubule
-antagonists of mineralocorticoid receptors
-K+ sparing diuretics

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12
Q

Na channel blockers:

A

-block Na channels
-site of action=cortical collecting tubule
-K+ sparing diuretics
-reduced Na within cell leads to decreased activity of Na/K pumps (less K enters the cell and less K is secreted)

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13
Q

K+ sparing diuretics:

A

-most other diuretics: increases/maintains K concentration gradient better due to faster urine flow rate=more K is excreted
*when use these=Na reabsorption is minimized and K concentration gradient is smaller=less K excreted

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14
Q

Acute renal failure:

A

-major sudden interruption in renal function which can be REVERSED
-3 categories
*affects K and H secretion
>may lead to K retention and metabolic acidosis

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15
Q

What are the 3 categories of acute renal failure?

A
  1. Prerenal acute renal failure
  2. Intrarenal acute renal failure
  3. Postrenal acute renal failure
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16
Q

Prerenal acute renal failure main problem is:

A

-OUTSIDE the kidneys
*important in patients with severe injuries

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17
Q

What is the main cause of prerenal acute renal failure?

A

-REDUCED blood flow to kidneys
Ex. heart failure, reduced blood pressure/volume, hemorrhage

18
Q

Severe reduction in renal blood flow leads to:

A

-reduced GFR
-reduced urine output

19
Q

Oliguria:

A

-reduced urine output below intake of water and solutes

20
Q

What are the problems that occur with prerenal acute renal failure?

A
  1. With reduced GFR normal function of kidneys for removing waste products, adjusting electrolytes and acid-base, is ADVERSELY AFFECTED
  2. Severe and prolong interruption damages renal cells due to lack of O2 and nutrients
    >Leads to intrarenal failure
21
Q

Intrarenal acute renal failure main problem is:

A

-WITHIN the kidneys

22
Q

What are the different areas of damage in intrarenal acute renal failure?

A
  1. Glomerular capillaries
  2. Tubules (epithelial cells)
  3. Renal interstitium
23
Q

Acute glomerulonephritis:

A

-mainly due to abnormal immune reaction
>usually primary infection in another area of the body
-due to increased Ab production in response to infection=more Ab-antigen complex

24
Q

More Ab-antigen complexes with acute glomerulonephritis leads to:

A
  1. Being trapped in glomerulus=attraction of immune cells and formation of inflammatory response in glomeruli
  2. Followed by disruption of renal function and leakage of proteins and blood into filtrate
25
Q

Tubular necrosis happens due to:

A

-ischemia and lack of O2/nutrients delivered to the epithelial cells
-some positions, toxins and drugs can damage epithelial cells of renal tubules

26
Q

What are some examples of positions, toxins and drugs that can damage epithelial cells of renal tubules?

A

-heavy metals (mercury and lead)
-ethylene glycol (antifreeze)
-insecticides
-tetracyclines (antibiotics)
-cis-platinum (cancer therapy)

27
Q

What happens in tubular necrosis due to damaged epithelial cells?

A

-interrupted tubular functions
-damage and dead cells slough off=plug tubules
*if basement membrane remains intact, then new epithelial cells will cover it in 2-3 weeks

28
Q

Interstitial nephritis:

A

-happens due to damage to glomeruli and tubules
>some poisons and drugs
>bacterial infection

29
Q

Bacterial infection is commonly due to:

A

-fecal contamination of urinary tract
*infection of medulla interferes with concentrating urine

30
Q

Postrenal acute renal failure main problem is:

A

-in the URINARY collecting system

31
Q

Postrenal acute renal failure:

A

-mostly due to obstructions of urinary collecting system
>obstructions lasting days or weeks can IRREVERSIBLY damage the kidney
-if only one kidney affected=other one compensates

32
Q

What are the 3 main causes/forms of postrenal acute renal failure?

A
  1. Ureter obstruction
  2. Bladder obstruction
  3. Urethra obstruction
33
Q

Chronic renal failure:

A

-IRREVERSIBLE decrease in number of nephrons and renal function
-loss of ~70% of nephrons results in serious clinical symptoms
*progressive decline in renal function eventually requires dialysis or kidney transplantation (end-stage renal disease)

34
Q

Primary cause of chronic renal failure can be related to:

A

-blood vessels
-glomeruli
-tubules
-ministerium
-lower urinary tract

35
Q

What happens when there is loss of some nephrons (chronic renal failure)?

A

-hypertrophy of remaining nephrons
-reduced vascular resistance
-functional changes: increase filtration and reduce tubular reabsorption

36
Q

What are some additional injuries with chronic renal failure?

A

-chronic pressure and stretch lead to sclerosis
>accumulation of connective tissue
*leads to end-stage renal disease (ERSD)

37
Q

Why is glomerular filtration increased and reabsorption reduced in the remaining nephrons?

A

-edema
-acidosis
-accumulation of non-protein nitrogen

38
Q

What are the tope 3 common causes of ESRD?

A
  1. Diabetes mellitus (obesity)
  2. Hypertension (obesity)
  3. Glomerulonephritis
39
Q

What are the areas of damage with chronic renal failure?

A
  1. Injury to renal vasculature (ischemia, death of renal cells)
  2. Glomerulonephritis: longer inflammatory reactions and formation of fibrous tissue in the glomeruli)
  3. Injury to renal tubules
  4. Injury to renal interstitium
40
Q

Dialysis:

A

-blood is passed through channels that contain a thin membrane
-dialyzing fluid is located on opposite side of membrane=unwanted substances are diffused from blood to dialyzing fluid

41
Q

Dialysis steps:

A
  1. Blood moves through tubes surrounded by a porous membrane within the dialyzer
  2. Outside porous membrane, dialyzing fluid flows
  3. Substances are diffused from blood into dialyzing fluid based on concentration gradient
42
Q

What does the rate of movement in dialysis depend on?

A

-concentration gradient
-permeability of membrane
-SA
-duration of time for passage of blood through dialyzer

RENAL (15 decks)

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