Diuretics and Renal Diseases Flashcards

1
Q

Diuretics

A

-increases urine output
-they work by interfering with reabsorption of Na, with reduced water reabsorption being a secondary effect (Na inside the tubule increases osmolarity of the filtrate). Since Na reabsorption is associated with excretion of other ions (K, Cl, Mg, Ca), diuretics will affect their excretion as well
Clinical relevance of diuretics
-they are given to reduce the volume of extracellular fluid (eg. Edema, and hypertension)

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2
Q

Diuretics speed

A

-work within minutes to hours
>increase urine volume up to 20-fold
-after a few days, kidneys use compensatory mechanisms to overcome the effects of diuretics (eg. through enhanced renin-angiotensin II system)

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3
Q

Types of diuretics

A

1.Osmotic diuretics
2. loop diuretics
3. Thiazide diuretics
4. Carbonic anhydrases inhibitors
5.Competitive inhibitors of aldosterone
6. Na channel blockers

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4
Q

Osmotic diuretics

A

-they enhance osmotic pressure within tubules (keep water inside the tubule)
-ex. urea, mannitol, sucrose

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5
Q

Loop diuretics

A

-they reduce Na/Cl/K reabsorption by blocking Na/2Cl/K transporters at the thick ascending segment of the loop of Henle
-very potent drugs, which can cause excretion of up to 30% GFR

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6
Q

Loop diuretics effects

A

1.increased solutes in the tubule interferes with water reabsorption
2. interferes with countercurrent multiplier system and this reduces the osmolarity of renal medullary interstitium, so the capacity for concentrating urine is reduced

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7
Q

Thiazide diuretics

A

-they reduce Na/Cl reabsorption at the distal tubule
-can lead to excretion of up to 10% GFR

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8
Q

Carbonic anhydrase inhibitors

A

-Reduce the Na/HCO3- reabsorption at the proximal tubule
-the reduced HCO3- reabsorption reduces the Na reabsorption via the Na/H counter transporter

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9
Q

Competitive inhibitors of aldosterone

A

-Reduce Na reabsorption and K secretion at the cortical collecting tubules
>antagonists of mineralocorticoid receptors
>K+ sparing diuretics
Na channel blockers

-Block Na channels at the cortical collecting tubules
>K+ sparing diuretics

-Reduced Na within the cell leads to a decreased activity of Na/K pumps at basolateral membrane so less K enter the cell and less K+ is secreted

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10
Q

Acute renal failure

A

-a major sudden interruption in renal failure which can be reversed
>affects K+ and H+ secretion and may lead to K+ retention and metabolic acidosis

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11
Q

Categories of Renal failure

A

1.Prerenal acute renal failure- main problem is outside the kidneys
2. Intrarenal acute renal failure- main problem is within the kidneys
3. Postrenal acute renal failure- main problem is in the urinary collecting system

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12
Q

Prerenal acute renal failure cause

A

-main cause is reduced blood flow to the kidney which leads to reduced GFR and reduced urine output
Eg. heart failure, reduced blood pressure/volume, hemorrhage
**normal renal blood flow rate is ~20% cardiac output
-can lead to intrarenal failure due to damage to kidney

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13
Q

Oliguria

A

-reduced urine output below intake of water and solutes

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14
Q

Prerenal acute renal failure problems

A

1.Results in reduced GFR which effects the kidneys ability to remove waste products and adjust electrolytes, acid-base
2. Results in reduced blood flow to kidney which when prolonged can result in renal blood flow damaging the renal cells due to a lack of oxygen and nutrients

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15
Q

Intrarenal acute renal failure areas of damage

A

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

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16
Q

Acute glomerulonephritis cause

A

-happens mainly due to abnormal immune reaction
>usually a primary infection in another area of the body. Body will increase antibody production in response to this infection and antibody-antigen complexes accumulate. These complexes get trapped in glomerulus= attracts immune cells and inflammatory response which affects function. Also results in leakage of proteins and blood into the filtrate

17
Q

Tubular necrosis

A

-damage to the epithelial cells interrupt tubular functions
>the damaged and dead cells may slough off and plug the tubules
**if basement membrane remains intact, then the new epithelial cells will cover it in 2-3 weeks

18
Q

Tubular necrosis cause

A

-happens due to ischemia and lack of oxygen/nutrients delivered to the epithelial cells, OR through poisons, toxins and drugs which damage the epithelial cells of renal tubules
Ex. heavy metals (mercury and lead), ethylene glycol (antifreeze), insecticides, tetracyclines (antibiotics), cis-platinum (cancer therapy)

19
Q

Interstitial nephritis cause

A

-happens due to damage to glomeruli and tubules
>by some poisons and drugs OR by bacterial infection (fecal contamination of urinary tract)
-infection of medulla interferes with concentrating urine

20
Q

Postrenal acute renal failure cause

A

-mostly due to obstruction of the urinary collecting system
>if only one kidney is affected, then the other will compensate
> obstructions lasting for days can cause irreversible damage to kidney

21
Q

3 main causes/forms of postrenal acute renal failure

A

1.ureter obstruction
2.bladder obstruction
3.urethra obstruction

22
Q

Chronic renal failure

A

-irreversible decrease in number of nephrons and renal function
>loss of around 70% of nephrons will result in serious clinical symptoms

23
Q

Primary cause of chronic renal failure

A

-related to blood vessels, glomeruli, tubules, interstitium or lower urinary tract
>diabetes, obesity, infections, obstructions, disorders etc.

24
Q

Progressive decline in renal function

A

-requires dialysis or kidney transplantation (end stage renal disease ESRD)

25
Q

Chronic renal failure mechanism

A

1.primary problem
2. progressive loss of function/damage
3.loss of nephrons
4. Nephrons will undergo hypertrophy, reduce vascular resistance, and increase filtration and reduce tubular absorption
5.Leads to chronic pressure and stretch in renal vessels leading to sclerosis (accumulation of CT)
6. End stage renal disease (ESRD)

26
Q

Top 3 causes of ESRD

A

1.Diabetes mellitus
2.Hypertension
3. Glomerulonephritis

27
Q

Areas of damage for 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 the renal tubules
4.Injury to the renal interstitium

28
Q

Dialysis

A

-blood is passed through channels that contain a thin membrane, dialyzing fluid is located on the opposite side of the membrane therefore unwanted substances are diffused form the blood to the dialyzing fluid

29
Q

Dialysis steps

A

1.blood moves through tubes surrounded by porous membrane within the dialyzer
2. outside of porous membrane dialyzing fluid flows
3.substances are diffused from blood into the dialyzing fluid based in their concentration gradient

30
Q

What does rate of movement during dialysis depend on?

A

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