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Therapeutics II > Renal Pathophysiology > Flashcards

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
Q

Intrinsic sources of AKI

A

-acute glomerulonephritis
-ischemia, sepsis/infection, nephrotoxins in tubules
-vasculitis, HTN, TTP-HUS (vascular)

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25
Q

Postrenal sources of AKI

A

-bladder outlet obstruction
-bilateral pelvoreteral obstruction

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26
Q

Normal perfusion pressure

A

-normal glomerular capillary pressure is maintained by afferent vasodilation and efferent vasoconstriction

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27
Q

Decreased perfusion rate

A

-inc vasodilatory prostaglandins
-inc angiotensin II
-maintain normal glomerular capillary pressure

28
Q

Reduced perfusion pressure in the presence of NSAIDs

A

-dec vasodilatory prostaglandins
-inc angiotensin II
=inc afferent resistance
=GCP and GFR dec

29
Q

Decreased Perfusion pressure w ACE-I or ARB (angiotensin inhibitor)

A

-slight inc vasodilatory prostaglandins
-dec angiotensin II
=dec efferent resistance
=GCP and GFR drop

30
Q

Kidney and ureter obstructions

A

-stones
-clots
-external compression
-tumor
-fibrosis

31
Q

Bladder obstruction

A

-prostate enlargement
-blood clots
-cancer

32
Q

Urethra obstruction

A

-strictures
-obstructed Foley catheter

33
Q

Pathophysiology of CKD (key elements)

A

-inc GCP
-proteinuria
-glomerulosclerosis

34
Q

CKD-MBD

A
35
Q

CKD-MBD causes

A

-impaired phosphate excretion
-dec vit D3 production

36
Q

Kidneys and Vit D metabolism

A

-managing CKD requires dealing with Ca homeostasis
-mineral bone disorder maybe

37
Q

Uremia

A

-accumulation of waste usually cleared by kidneys

38
Q

Symptoms of Uremia

A

-fatigue
-neuropathy
-seizures
-nausea
-ammenorrhea
-bone disease
-insulin
-itching
-anemia

39
Q

Specific Nephropathies

A

-NephrItic Syndrome
-NephrOtic Syndrome
-cycstic disease
-nephrolithiasis
-contrast-induced nephropathy

40
Q

NephrItic Syndrome

A

-Inflammation disrupting glom membrane
-hematuria (dark urine)
-RBC casts

41
Q

NephrOtic syndromes

A

-pOdcyte damage that disrupts charge-barrier of glom
-massive prOteinuria
-more edema
-low serum albumin

42
Q

Glomerulonephritis

A

-inflammation of glomeruli
-acute or chronic
-proteinuria or hematuria

43
Q

Glomerulonephritis causes

A

1’: inheritable (Alport Syndrome)
2’: infections, drugs, auto-immune disorders (vasculitis, Lupus)

44
Q

Pathogenesis of Glom disease

A

-Immune
1. Antibody-associated injury
2. Cell-mediated immune
3. Other mechs of injury

45
Q

Pyelonephritis

A

-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
Q

UTI patho

A

-colonize urethral area and acesnds
-fimbria allow bacteria to attach and penetrate
-replicate and may form biofilms

47
Q

Interstitial Nephritis

A

-primary injury to renal tubules
-indetected until sig dec in renal function

48
Q

Causes of interstitial nephritis

A

-drugs (75%) mostly antibiotics
-infection
-autoimmune

49
Q

Drugs associated w AIN

A

-PENICILLINS
-abx (cephalosporins, sulfa)
-diuretics (thiazide, furosemide)
-NSAIDs
-anticonvulsants (phenytoin, carbamazepine, phenobarbital)
-allopurinol, cimetidine

50
Q

Cystic Diseases of the Kidney

A

-simple cysts
-autosomal dominant polycystic kidney disease (adulthood)
-autosomal recessive polycystic kidney disease (childhood)

51
Q

Simple Cysts

A

-most common cystic renal disease
-NOT tumor

52
Q

Autosomal Dominant Polycystic Kidney Disease (APKD)

A

-expanding cysts that destroy the intervening parenchyma
-adulthood

53
Q

APKD

A

-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
Q

Autosomal Recessive polycystic kidney disease

A

-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
Q

Nephrolithiasis

A

-kidney stones
-10% of men 5% of women
-arises from supersaturation of solutes
-esp calcium

56
Q

Renal Calculi (kidney stones)

A

-males over 40 esp
-N/V
-flank pain, sharp and sudden
-hematuria

57
Q

Promoters of kidney stones

A

-sodium intake
-calcium intake
-high acid intake

58
Q

Inhibitors of kidney stones

A

-Citrate
-Magnesium

59
Q

Non-infection kidney stones

A

-calcium
-uric acid

60
Q

Infection stones

A

-Struvite
-alkalized urine from UTI

61
Q

Genetic Stones

A

-Cystine
-defective transporter
-tx w alkaline citrates

62
Q

Primary treatment of kidney stones

A

-analgesics
-hydration
-lithotripsy
-surgery

63
Q

Prevention of kidney stones

A

-diet (eliminate Ca)
-hydration
-diuretics

64
Q

Contrast-Associated Nephropathy

A

-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
Q

Contrast-Associated Nephropathy patho

A

-contrast media
=cytotoxicity or inc viscocity
=dec perfusion
=medullary ischaemia
or dec GFR

66
Q

When may NSAIDs be appropriate in patients with acute heart failure and chronic kidney disease?

A

-Never

67
Q

Risk of NSAIDs in heart failure and CKD

A

-sodium retention
-fluid overload
-acute kidney injury
-hyperkalemia

Therapeutics II (55 decks)

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