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Human Pathophysiology: Final > Renal System II > Flashcards

Renal System II Flashcards

1
Q

When/why do kidney stones from?

A

when the urine contains a high concentration of certain substances

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2
Q

What are the most important factor(s) in kidney stone formation?

A

Dehydration is the most important risk factor. In addition, a diet high in meats and refined carbohydrates increases risk of stones. Healthy diets like theDASH diet reduce risk of kidney stones.

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3
Q

What do kidney stones do?

A

Cause blockage of a ureter

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4
Q

What is the most common type of kidney stones and what causes it?

A

Calcium stones - calcium often combines with oxalate, which is found in certain foods, such as berries, beets, spinach, nuts, chocolate and strong tea.
(NOTE: dietary calcium does not increase the risk of calcium stones but calcium supplements might)

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5
Q

What are oxalate stones? How do they form and why?

A

-common in people with Crohn’s disease
-result of fat malabsorption: fat remains in the GI tract where it binds up calcium (ordinarily be bound to oxalate, facilitating their elimination through the GI tract)
-with the calcium bound to fat, the oxalate is free to cross the intestinal wall. It eventually binds to calcium in the body, and then gets
deposited in the kidneys

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6
Q

What is Crohn’s disease?

A

chronic inflammatory condition of the GI tract

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7
Q

What are cysteine stones and why do they form?

A

They form in people who have a genetic defect that interferes with renal processing of this amino acid (3% of kidney stones)

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8
Q

What are struvite stones and why do they form?

A

Struvite stones (ammonium magnesium phosphate) typically form in women who have a urinary tract infection. Bacteria convert urea to ammonium, which raises the pH of the urine. This causes struvite crystals to form.

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9
Q

What patients are susceptible to uric acid crystals?

A

Form in people with gout, also after chemotherapy.

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10
Q

What are symptoms of kidney stones?

A
  • sharp, excruciating pain, either in abdomen or along the back
  • groin pain
  • testicular pain
  • blood in urine
  • fever and chills
  • nausea and vomiting
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11
Q

What are some treatments for kidney stones?

A
  • drinking lots of water and pain medication (help pass stone on its own)
  • Extracorporeal shock-wave lithotripsy - ultrasound waves to break up the stones
  • endoscopy surgery to retrieve the stones
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12
Q

Definition: urine refluxes up towards the kidney

A

congenital vesicoureteral reflux

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13
Q

What causes congenital vesicoureteral reflux?

A
  • immaturity of the junction between the ureter and the bladder (ureter is too short)
  • strong genetic component
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14
Q

What are some of the complications of congenital vesicoureteral reflux?

A
  • increases risk of infection (child usually presents with urinary tract infection)
  • when severe, can put pressure on the kidney itself, causing damage
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15
Q

How is congenital vesicoureteral reflux treated?

A

-as long as the urinary tract can be kept free of infection, this condition usually resolves itself by age 6
-patients are kept on prophylactic doses of antibiotic until the condition
resolves itself
-surgery is indicated if UTIs cannot be controlled with antibiotics, or if reflux is severe

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16
Q

How can congenital vesicoureteral reflux hard the kidney?

A

infection of the kidney, –> scarring –> hypertension –> renal failure

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17
Q

What are some signs of acute renal failure?

A

increases in serum creatinine and urea, reflecting decreased GFR.

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18
Q

Why do creatine and urea indicate decreased GFR?

A
  • creatinine: product of muscle metabolism, its filtered but not reabsorbed. An increase in plasma creatinine is indicative of decreased urinary creatinine excretion which indicates a decrease in GFR.
  • urea: a product of amino acid metabolism. Urea reabsorption in the tubules is passive. If the concentration of urea is increasing, it means that it is not being filtered as effectively.
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19
Q

What happens during prerenal failure?

A

the kidneys are fine, but the blood flow/pressure supplied to them is reduced resulting in a reduced GFR

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20
Q

What causes prerenal failure?

A
  • decreased blood volume (volume losses due to hemorrage/excessive sweating/vomiting/diarrhea)
  • congestive heart failure
  • certain edema forming states (cirrhosis, nephrotic syndrome)
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21
Q

What is intrarenal failure?

A

typically as a result of acute tubular necrosis (usually caused either by ischemia or by toxins/drugs); leads to backleak of filtrate through damaged regions

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22
Q

What are some causes of intrarenal failure?

A

-plugging of tubules with dead/sloughed epithelial cells/detritis
-renal ischemia - loss of blood flow results in loss of
O2/nutrients to cells and resulting cell death
-drugs/toxins which have no renal transport processes and so become concentrated in the kidneys (Ex. some antibiotics/certain heavy metals used for chemotherapy, a radiocontrast media used for some procedures that require imaging of blood vessels)

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23
Q

What is postrenal failure?

A

any kind of obstruction of the urinary tracts, such as renal stones, anatomic defects of urinary tract, prostatic hypertrophy and cancers

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24
Q

How is acute renal failure treated?

A
  • identifying and treating causes

- supporting renal function

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25
Q

What are the epidmeilogic stats for chronic kidney disease?

A
  • 1 in 9 adults suffer from CKD

- 5-fold increase in the last 30 years

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26
Q

What is ESRD and what treatments are required?

A

End-Stage Renal Disease: chronic renal failure. It requires dialysis or renal transplant.

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27
Q

What are the risk factors for CKD?

A
  • hypertension
  • diabetes
  • autoimmune diseases
  • low birthweight
  • exposure to certain drugs
  • family history
  • older age
  • AA, native american. or hispanic ethnicity
  • low income/eduction
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28
Q

What causes ESRD?

A
  • Irreversible, progressive injury to kidney

- Normal architecture is replaced by scar tissue

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29
Q

What are the signs of ESRD?

A

-increased plasma creatinine and urea characteristic of decreased GFR
-loss of hormonal and other functions of the kidney such as loss of production of erythropoetin and the active form of Vitamin D, and the slowing of the
clearance of drugs and toxins

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30
Q

What is uremic syndrome?

A

when the GFR is reduced down to about 10ml/min (normal is 120 ml/min)

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31
Q

What are symptoms of kidney disease?

A
  • uremic syndrome

- problems with excretion of large salt or water loads

32
Q

How does hypertension cause CKD?

A

The high pressure in the renal vessels causes damage. The progression of renal disease worsens the hypertension.

33
Q

What is Polycystic Kidney Disease?

A

a common genetic disease that causes CKD; caused by inheritance of an autosomal dominant gene for the disease; about 10-20% of cases are due to a spontaneous mutation; 50% are in end stage renal disease by age 60

34
Q

What happens during Polycystic Kidney Disease?

A

-cysts form from outpouches along the nephron (affects 2% of nephrons)
-cysts eventually detach from the nephron, forming a fluid-filled cyst that enlarges over time
-cysts take up room and eventually interfere with renal function
-can also become
infected, which can cause further damage to the kidney
-cysts can also form elsewhere in the body, particularly the liver, but generally do not lead to liver failure

35
Q

What are the symptoms of Polycystic Kidney Disease?

A
  • abdominal pain
  • hematuria
  • UTIs
  • hypertension
  • eventually renal insufficiency and renal failure
36
Q

Definition: blood in urine

A

hematuria

37
Q

What are the treatments for Polycystic Kidney Disease?

A

renal transplant

38
Q

What is Systemic lupus erythematosus (SLE)?

A

Autoimmune disease: patient makes autoantibodies against many cellular components, including DNA, and other molecules in the nucleus and cytoplasm of cells; severity is variable, depending on which autoantibodies are present; often starts with symptoms in just one system of the body, then progresses to affect multiple systems

39
Q

Who does SLE affect the most?

A
  • 90% of cases are women of childbearing age

- more common in AA

40
Q

How does SLE cause chronic kidney failure?

A

Damage results largely from deposition of immune complexes in the glomeruli. Leads to the appearance of protein in the urine, and can cause acute renal failure.

41
Q

How does diabetic nephropathy occur?

A

increased pressure of GFR –> abnormal thickening of the mesangial matrix, the material that surrounds and supports the glomerular capillaries to prevent damage –> decreased filtration surface area –> decrease in GFR (after +10 years of diabetes) –> proteinuria

42
Q

Definition: protein in the urine; indication of globular barrier malfunction

A

proteinuria

43
Q

What is common in diabetics that can decrease the renal blood flow?

A

atherosclerosis; further lowers GFR

44
Q

What are some of the few proteins that are found in urine?

A
  • plasma proteins filtered in the glomerulus (usually small ones: microglobulin and lysozyme)
  • Tamm-Horsfall protein (a mucous protein secreted by the thick ascending loops of Henle)
  • proteins from the bladder, ureters, genital tract
  • immunoglobulins
45
Q

What are 3 things that prevent most proteins from filtering through the kidney?

A
  • endothelial cells (contain holes, but most proteins can’t go through these)
  • basement membrane (constitute much of the sieve function in terms of size restrictions)
  • glomerular epithelial cells/podocytes (constitute some of the sieve function and most of the charge restriction)
46
Q

Protein in urine should be less than __ mg/100ml. Total protein excreted per day should be less than ___ mg. Protein/creatine rations should be less than ___.

A

10
150
0.2

47
Q

Definition: loss of charge function of the barrier and/or loss of the size barrier in the glomerular filter

A

Glomerular Proteinurea

48
Q

What causes loss of charge function of the barrier in Glomerular Proteinuria?

A

typically results from damage to glomerular cells that produces anionic proteins such as heparin sulfate –> causes albumin/transferrin to be able to cross –> results in massive loss of protein in the urine (>3g/day)

*associated with immunologic dysfunction

49
Q

What happens when there is a loss of the size barrier in Glomerular Proteinuria?

A

causes albumin, transferrin, and IgG to be able to cross to tubule –> results in massive loss of protein in the urine (>3g/day)

50
Q

What causes loss of the size barrier in Glomerular Proteinuria?

A

an inflammatory reaction occurring in the glomerulus
and damage resulting from products released from inflammatory cells; often caused advanced diabetes mellitus and immune complexes lodging in the capillaries as in lupus

51
Q

Definition: inability to reabsorb the small amounts of protein that are normally
filtered at the glomerulus

A

tubular proteinurea

52
Q

What are common causes of tubular proteinurea?

A

toxins, immune processes, some infections

53
Q

Definition: plasma concentrations of small proteins that are filtered increases, capacity of tubular cells to reabsorb protein is overwhelmed, protein ends up in the
urine

A

overload proteinuria

54
Q

What are some causes of overload proteinuria?

A

-cancers of plasma cells (immune cells that make immunoglobulins -
light chains of the immunoglobin are produced in large excess)
-hemolysis - results in hemoglobin in urine
-muscle tissue breakdown

55
Q

How does muscle tissue breakdown contribute to overload proteinuria?

A

muscle tissue breakdown –> myoglobin
to be released –> myoglobinuria.

*high levels or myoglobin are nephrotoxic

56
Q

Definition: acute muscle breakdown

A

rhabdomyolysis

57
Q

How is overload proteinuria due to rhabdomyolysis treated?

A
  • giving sufficient fluid to maintain a high level of diuresis (urine output) until urine is negative for myoglobin
  • urine is alkalinized to prevent the dissociation of myoglobin into its nephrotoxic metabolites, particularly ferrihemate
58
Q

Definition: appearance of substantial protein in urine; protein in urine greater than 3g/day (usually as a result of damage to
glomerular barrier)

A

Nephrotic syndrome

59
Q

What are some symptoms of nephrotic syndrome?

A
  • decreased protein concentrations in the plasma
  • frothy urine
  • edema (in children, often in eyes)
  • excess lipids in the plasma (a liver response to the low proteins - increases the risk of cardiovascular disease if nephrotic syndrome persists)
  • loss of immunoglobulins may increase the risk of infection
  • loss of protein inhibitors of clotting in the urine increases the risk of clot formation
60
Q

Summarize what happens with SLE and diabetic neuropathy.

A

damage to glomerulus –> lost of protein in urine –> decreased plasma oncotic pressure –> decrease blood volume/bp –> stimulation of carotid /aortic baroreceptors and release of ADH due to stimulation of atrial/venous volume receptors –> sympathetic activation –> increase renin –> increased angiotensin –> increased salt and water retention –> more edema

61
Q

How does kidney failure affect Na+ and water balance?

A

Na+: GFR is reduced and salt intake is high, the kidney’s cannot
excrete enough salt and salt is retained. Alternatively, if the salt intake is very low, the diminished capacity of the tubule to reabsorb sodium can lead to excessive sodium loss and hyponatremia.

Water: ability of the kidney to generate the osmolar gradient that allows for excretion of concentrated or dilute urine is compromised. Problems of osmolarity (hypo or hypernatremia) occur if the patients drink too much or too little water.

62
Q

How does kidney failure affect hypertension?

A

In patients with high salt intake, inability to excrete the sodium results in water retention. Plasma volume increases, as does blood pressure

63
Q

How does kidney failure lead to edema?

A

Increased blood pressure results in increased efflux of fluid into the vascular space. This is further enhanced by retention of water along with salt.

64
Q

What is a consequence of Uric Acid retention?

A

may result in gout or arthritis, also causes itchiness and rash

65
Q

How does kidney disease affect potassium levels?

A

K+ excretion increases with GFR. Big reductions in GFR result in inability to excrete K+, and increased plasma potassium results. This can result in cardiac arrthymias.

66
Q

How does kidney disease affect acid-base levels?

A

Normal metabolism results in the formation of acid, which is normally excreted in the urine. When the GFR gets low enough, acids cannot be excreted and plasma pH drops (i.e. the concentration of H+ ions increases).

67
Q

How does kidney disease affect drug/toxin clearance?

A

Patients with reduced kidney function have a reduced ability to excrete these and they may build up in the blood.

68
Q

How does kidney disease affect calcium metabolism?

A

The kidney is the site of activation of Vitamin D. When this function is lost, insufficient calcium is absorbed in the gut and plasma calcium falls. This results in PTH release by the posterior pituitary and results in osteoclast breakdown of calcium phosphate salts in bone (results in bone demineralization). When the GFR falls, the kidney is unable to excrete phosphate. The increased phosphate results in the formation of calcium phosphate salts which precipitate in soft tissues. This removes more calcium from the plasma

69
Q

How does kidney disease affect hormones?

A
  • The kidneys help clear the body of insulin, so patient with renal failure often have hyperinsulinemia.
  • Sex steroid levels are low, often causing amenorrhea in women and impotence in men.
70
Q

How does kidney disease contribute to anemia?

A

The kidney is the site of production of erythropoetin, a hormone necessary to the formation of red blood cells.

71
Q

How does kidney disease affect the nervous system?

A

Build up of toxins can cause seizures, and other neurologic problems

72
Q

How does kidney disease affect the GI tract?

A

Nausea and vomiting resulting from electrolyte disturbances

73
Q

How is chronic renal failure treated?

A
  • dialysis

- transplantation

74
Q

Definition: dialysis in which one must go to the clinic about 3 times a week for 4 h.

A

hemodialysis

75
Q

Definition: dialysis that is more frequent, but can be done at home

A

peritoneal dialysis

76
Q

What are the normal values for BUN, creatine, and Na+?

A

BUN: 8-25 mg/dL
Creatine: 1 mg/dL
Na+: 135-145 mEg/L

Human Pathophysiology: Final (6 decks)

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