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Renal Pathophysiology Flashcards

1
Q

Kidney structure

A
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1
Q

Physiological Function of Kidneys

A

-endocrine functions
-excretion
-control solutes/fluids
-control BP
-acid/base balance

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2
Q

Glomular Filtration depends on

A

-GFR
-size of drug
-extent of plasma protein binding (only unbound is unfiltered)

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3
Q

Renal drug excretion

A

-slide 8 structure
-major route of elimination for 25-30% of drugs

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4
Q

renal anatomy

A

-Bowman’s capsule
-Proximal Tubule
-Loop of Henle
-Distal Tubule
-Collecting Tubule

-most H20 and solutes reabsorbed
-concentrate waste

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5
Q

Bowman’s capsule

A

-100% filtrate produced

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6
Q

Proximal Tubule

A

-80% reabsorbed
-active and passive absorption
-secretion and reabsorption of organic acids and bases (**uric acid and most diuretics)

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7
Q

Loop of Henle

A

-6% reabsorbed
-H2O (descending) and salt conservation (ascending)
-active reabsorption of Na, K, Cl
-2’ reabsorption of Ca and Mg

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8
Q

Distal tubule

A

-9% reabsorbed
-variable reabsorption
-active secretion
-parathyroid hormone control

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9
Q

Collecting Tubule

A

-4% reabsorbed
-variable salt and H20 reabsorption
-water reabsorption under vasopressin

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10
Q

Key physiolofical flow values??

A

??

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11
Q

Anatomical Solute and Water Flux in nephron

A
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12
Q

Measures of Kidney Function

A

-Serum Creatinine
-Blood Urea Nitrogen (BUN)
-Creatinine Clearance
-GFR

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13
Q

Serum Creatinine

A

-mostly removed by filtration
-increase is bad

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14
Q

Blood Urea Nitrogen (BUN)

A

-measure of waste from liver breakdown of AAs
-increase is bad

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15
Q

Creatinine Clearance

A

-predicts secretion and drug clearance

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16
Q

Markers of Kidney Damage

A

-urinary abnormalities (protein, RBC suggestive of membrane malfunctions)
-imaging abnormalities (MRI/CT scans)

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17
Q

Aging Kidney

A

-decline in kidney mass = decline in function
-prob gotta lower the dose slide 14

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18
Q

Compensatory response to renal injury

A
  1. injury
  2. decrease of nephrons
  3. compensatory inc in size and function of remaining nephrons
  4. glomerular/tubular lesions
  5. Loss of nephrons greater than compensatory capacity
  6. progressive decrease in GFR
  7. Azotemia
  8. Uremic Syndrome
    9.Death
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19
Q

Sources of kidney injury/failure

A

-HTN and Diabetes >60%
-glomerulonephritis
-cystic kidney
-other urologic diseases (stones)

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20
Q

impact of acute kidney failure

A

-300,000 deaths per year in US (more than breast cancer, prostate. cancer, heart failure, and diabetes combined)

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21
Q

Pathophysiology of Acute Kidney Failure

A

-inc in SCr 0.3mg/dL or more within 48hours
OR
-50% inc in SCr within the last 7 days
OR
-reduction in urine output

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22
Q

Classification of Major causes of acture kidney injury

A

-prerenal
-intrinsic
-postrenal

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23
Q

Prerenal causes of AKI

A

-hypovolemia
-dec cardiac output
-dec circulation
-impaired renal autoregulation (NSAIDs, ACE-I/ARB, cyclosporine)

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24
Intrinsic sources of AKI
-acute glomerulonephritis -ischemia, sepsis/infection, nephrotoxins in tubules -vasculitis, HTN, TTP-HUS (vascular)
25
Postrenal sources of AKI
-bladder outlet obstruction -bilateral pelvoreteral obstruction
26
Normal perfusion pressure
-normal glomerular capillary pressure is maintained by afferent vasodilation and efferent vasoconstriction
27
Decreased perfusion rate
-inc vasodilatory prostaglandins -inc angiotensin II -maintain normal glomerular capillary pressure
28
Reduced perfusion pressure in the presence of NSAIDs
-dec vasodilatory prostaglandins -inc angiotensin II =inc afferent resistance =GCP and GFR dec
29
Decreased Perfusion pressure w ACE-I or ARB (angiotensin inhibitor)
-slight inc vasodilatory prostaglandins -dec angiotensin II =dec efferent resistance =GCP and GFR drop
30
Kidney and ureter obstructions
-stones -clots -external compression -tumor -fibrosis
31
Bladder obstruction
-prostate enlargement -blood clots -cancer
32
Urethra obstruction
-strictures -obstructed Foley catheter
33
Pathophysiology of CKD (key elements)
-inc GCP -proteinuria -glomerulosclerosis
34
CKD-MBD
35
CKD-MBD causes
-impaired phosphate excretion -dec vit D3 production
36
Kidneys and Vit D metabolism
-managing CKD requires dealing with Ca homeostasis -mineral bone disorder maybe
37
Uremia
-accumulation of waste usually cleared by kidneys
38
Symptoms of Uremia
-fatigue -neuropathy -seizures -nausea -ammenorrhea -bone disease -insulin -itching -anemia
39
Specific Nephropathies
-NephrItic Syndrome -NephrOtic Syndrome -cycstic disease -nephrolithiasis -contrast-induced nephropathy
40
NephrItic Syndrome
-Inflammation disrupting glom membrane -hematuria (dark urine) -RBC casts
41
NephrOtic syndromes
-pOdcyte damage that disrupts charge-barrier of glom -massive prOteinuria -more edema -low serum albumin
42
Glomerulonephritis
-inflammation of glomeruli -acute or chronic -proteinuria or hematuria
43
Glomerulonephritis causes
1': inheritable (Alport Syndrome) 2': infections, drugs, auto-immune disorders (vasculitis, Lupus)
44
Pathogenesis of Glom disease
-Immune 1. Antibody-associated injury 2. Cell-mediated immune 3. Other mechs of injury
45
Pyelonephritis
-inflammation of kidney tissue -acute or chronic -flank pain -painful pissing -bacteria from blood or urinary tract -WBC in urine -could lead to sepsis
46
UTI patho
-colonize urethral area and acesnds -fimbria allow bacteria to attach and penetrate -replicate and may form biofilms
47
Interstitial Nephritis
-primary injury to renal tubules -indetected until sig dec in renal function
48
Causes of interstitial nephritis
-drugs (75%) mostly antibiotics -infection -autoimmune
49
Drugs associated w AIN
-PENICILLINS -abx (cephalosporins, sulfa) -diuretics (thiazide, furosemide) -NSAIDs -anticonvulsants (phenytoin, carbamazepine, phenobarbital) -allopurinol, cimetidine
50
Cystic Diseases of the Kidney
-simple cysts -autosomal dominant polycystic kidney disease (adulthood) -autosomal recessive polycystic kidney disease (childhood)
51
Simple Cysts
-most common cystic renal disease -NOT tumor
52
Autosomal Dominant Polycystic Kidney Disease (APKD)
-expanding cysts that destroy the intervening parenchyma -adulthood
53
APKD
-inherited mutation of PKD1 or 2 in renal tubular cells -abnormal cysts form -destroy intervening parenchyma -intermittent gross hematuria (blood in urine) -HTN and UTI end up being fatal -need renal transplant
54
Autosomal Recessive polycystic kidney disease
-autosomal recessive inheritance -mutation in PKHD1 (fibrocystin) -present at birth -infants die fast from pulmonary/renal failure -if survive, develop liver cirrhosis (congenital hepatic fibrosis)
55
Nephrolithiasis
-kidney stones -10% of men 5% of women -arises from supersaturation of solutes -esp calcium
56
Renal Calculi (kidney stones)
-males over 40 esp -N/V -flank pain, sharp and sudden -hematuria
57
Promoters of kidney stones
-sodium intake -calcium intake -high acid intake
58
Inhibitors of kidney stones
-Citrate -Magnesium
59
Non-infection kidney stones
-calcium -uric acid
60
Infection stones
-Struvite -alkalized urine from UTI
61
Genetic Stones
-Cystine -defective transporter -tx w alkaline citrates
62
Primary treatment of kidney stones
-analgesics -hydration -lithotripsy -surgery
63
Prevention of kidney stones
-diet (eliminate Ca) -hydration -diuretics
64
Contrast-Associated Nephropathy
-25% inc in SCr within 72 hours of contrast media admin -CIN causes 1/3 of hospital acquired AKI -1-2% US -hydrate and avoid nephrotoxins
65
Contrast-Associated Nephropathy patho
-contrast media =cytotoxicity or inc viscocity =dec perfusion =medullary ischaemia or dec GFR
66
When may NSAIDs be appropriate in patients with acute heart failure and chronic kidney disease?
-Never
67
Risk of NSAIDs in heart failure and CKD
-sodium retention -fluid overload -acute kidney injury -hyperkalemia

Therapeutics II (55 decks)

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