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Therapeutics > L5-6: Renal > Flashcards

L5-6: Renal Flashcards

1
Q

Physiological functions of the kidneys

A

Endocrine functions
Control of solutes and fluids
BP control
Acid/Base balance
ADME
Metabolic waste excretion

When something goes wrong with the kidney - BIG problem - not easy to manage

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2
Q

Main function of the kidney

A

Filtration
Continuously working - if damaged - management difficult

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3
Q

Avg kidney has how many nephrons

A

1 million - decreases with age

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4
Q

Bowman’s Capsule

A

Osmatic pressure filtering (BP makes a big deal)
How much pressure is present DIRECTLY AFFECTS how much filtering happens in Bowman’s capsule

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5
Q

All parts are surrounding the _ and therefore do heavy function around it

A

Glomerulus

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6
Q

Glomerular Filtration depends on

A

GFR
Size of drug
Extent of plasma protein binding: only unbound is filtered
Renal excretion of unchanged drug is a major route of elimination for 25-30% of drugs

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7
Q

Main site of drug secretion and drug reabsorption

A

Secretion: Proximal tubule
Reabsorption: Distal Tubule

ONLY two places drug can go in and out

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8
Q

Review of Renal Anatomy and Reabsorption

A

Bowman’s Capsule: 100% filtrate produced

Proximal Tubule: 80% filtrate reabsorbed Active and Passive absorption

Loop of Henle 6% filtrate reabsorbed H2O and salt conservation

Distal Tubule 9% Filtrate reabsorbed Variable reabsorption active secretion

Collecting Tubule 4% Filtrate reabsorbed Variable salt and H2O reabsorption

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9
Q

What % of filtrate (including water) is reabsorbed in proximal tubule

A

80% most H2O and solutes reabsorbed
Concentrate waste

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10
Q

What is the percent of filtrate produced volume?

A

1%
Filtrate is VERY strong
Water ALWAYS follows sodium

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11
Q

Cardiac output

A

6,000mL/min

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12
Q

Renal blood flow rate (18%CO)

A

1,100mL/min

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13
Q

Renal Plasma flow rate (60% RBF)

A

660mL/min

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14
Q

Effective renal plasma Flow rate (90% RPF)

A

600ml/min

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15
Q

Filtration fraction (18% ERPF)

A

110mL/min

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16
Q

Urine output

A

1mL/min

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17
Q

Reabsorbed Filtrate (FF-UO)

A

109mL/min

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18
Q

Cardiac output cont

A

6,000mL/min
10% (600) is plasma
-Very small
Less than half is our urine output
Normal urine frequency: 2-4 hours
More frequent if diuretics used = less patient adherence

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19
Q

Anatomical Solute and water flux in nephron

A

ALL organic things are reabsorbed from proximal
Blood in urine = something wrong with proximal = reabsorption impaired

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20
Q

Bicarbonate role

A

Goes with proton (acid/base)
All water transportation is controlled

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21
Q

Potassium goes (with/against) sodium

A

Against

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22
Q

Collecting duct

A

Urea and Water excreted
K, H, NH3 reuptake

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23
Q

Glomerulus

A

Function: Formation of glomerular filtrate

Water permeability: Extremely high

Primary Transporters and drug targets at apical membrane: None

Diuretic with major action: None

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24
Q

Proximal convoluted tubule (PCT)

A

Function: Reabsorption of 65% of filtered Na+/K+/Ca+ and Mg2+; 85% of NaHCO3, and nearly 100% of glucose and amino acids, isosmotic reabsorption of water

Water permeability: very high

Primary Transporters and drug targets at apical membrane: Na/H1, carbonic anhydrase, Na/glucose cotransporter 2(SGLT2)

Diuretic with major action:
Carbonic anhydrase inhibitors; adenosine antagonists (under investigation)

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25
Q

Proximal Tubule, straight segments

A

Function: secretion and reabsorption of organic acids and bases, including uric acid and most diuretics

Water permeability: very high

Primary Transporters and drug targets at apical membrane: Acid (eg. uric acid) and base transporters)

Diuretic with major action:
None

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26
Q

Thin descending limb of Henle’s loop

A

Function: Passive reabsorption of water

Water permeability: high

Primary Transporters and drug targets at apical membrane: Aquaporins

Diuretic with major action:
None

27
Q

Thick ascending limb of Henle’s loop (TAL)

A

Function:
Active reabsorption of 15-25% of filtered Na+/K+/Cl-; secondary reabsorption of Ca2+ and Mg2+

Water permeability: Very low

Primary Transporters and drug targets at apical membrane: Na/K/2Cl (NKCC2)

Diuretic with major action:
Loop diuretics

28
Q

Distal Convoluted tubule (DCT)

A

Function: Active reabsorption of 4-8% of filtered Na+ and Cl-; Ca2+ reabsorption under PTH control

Water permeability: Very low

Primary Transporters and drug targets at apical membrane:
Na/Cl (NCC)

Diuretic with major action:
Thiazides

29
Q

Medullary Collecting duct

A

Function: Water reabsorption under vasopressin control

Water permeability: variable

Primary Transporters and drug targets at apical membrane:
Aquaporins

Diuretic with major action:
Vasopressin antagonists

30
Q

Cortical Collecting Tubule (CCT)

A

Function:
Na+ reabsorption (2-5%) coupled to K+ and H+ secretion
Water permeability: variable

Primary Transporters and drug targets at apical membrane: Na channels (ENaC), K channels, H+ transporter, aquaporins

Diuretic with major action:
K+ sparing diuretics: Adenosine antagonists

31
Q

Measures of Function

A

Serum Creatinine
-Predominantly removed by filtration
-Increase = bad

BUN
-Measure of waste from liver breakdown of AAs
-Increase = BAD

CrCl
-Useful for predicting secretion and drug clearance

GFR
-measure of nephron function

32
Q

Markers of damage

A

Urine abnormalities
(Protein, RBC suggestive of membrane malfunctions)

Imaging abnormalities (MRI/CT scans)

33
Q

Kidney function declines with age due to

A

Decline in nephrons
Decreased by HALF
Higher pressure - ones that are there will not last as long

34
Q

Compensatory Response to Renal Injury

A

Renal injury

Decrease in number of nephrons

Compensatory increase in size and function of remaining nephrons

Glomerular and tubular lesions

Loss of nephrons greater than compensatory capacity

Progressive decrease in GFR

Azotemia

Uremic Syndrome

DEATH

35
Q

Sources of Kidney Injury/Failure

A

HTN and Diabetes account for >60% of renal failure cases in the US!!

Pts often realize too late

Glomerulonephritis
-Kidney injury/disease

Cystic Kidney

36
Q

AKI Death rate

A

300,00 people US annually
-Death rate more than breast cancer, prostate cancer, heart failure AND diabetes combined

37
Q

Pathophysiology of Acute Kidney Failure

A

An increase in Scr >0.3mg/dL *26.5mmol/L) within 48 hr

OR

Increase in SCr >50% (>1.5 times baseline) which is known or presumed to have occurred in last 7 days

OR

A reduction in urine output (oliguria of <0.5 mL/kg/h for 6 hours)

38
Q

Major causes of AKI: Prerenal

A

Hypovolemia

Decreased Cardiac Output

Decreased effective circulating volume
-Congestive Heart failure
-Liver failure

Impaired renal autoregulation
-NSAIDs
-ACE-I/ARB
-Cyclosporine

39
Q

Major causes of AKI: Intrinsic (Intrarenal)

A

Glomerular
-Acute glomerulonephritis

Tubules and interstitium
-Ischemia
-Sepsis/infection
Nephrotoxins

Vascular
-Vasculitis
-Malignant HTN
-TTP-HUS

40
Q

Major causes of AKI: Postrenal

A

Bladder outlet obstruction
-Bilateral pelvoureteral obstruction (uinlateral obstruction of a solitary functioning kidney)

41
Q

Intrarenal mechanisms for autoregulation of GFR under decreased perfusion pressure and reduction of GFR by drugs

A

Normal Glomerular capillary pressure is maintained by afferent vasodilation, and efferent vasoconstriction

Reduced perfusion pressure with an NSAID - Loss of vasodilatory = prostaglandins increases afferent resistance

Drops pressure, causes GFR to decrease

**reduced perfusion pressure with an angiotensin-converting enzyme inhibitor (ACE-I) or an angiotensin receptor blocker (ARB)

Loss of Angiotensin II action reduces efferent resistance, this causes the glomerular capillary pressure to drop below normal values and the GFR to decrease

42
Q

Primary causes of AKI

A

Sepsis
Ischemia
Nephrotoxins

43
Q

Obstruction sites causing AKI

A

Kidney
-Stones, blood clots, external compression, tumor, retroperitoneal fibrosis

Bladder
-Prostatic enlargement, blood clots, cancer

Urethra
-Strictures
-Obstructed Foley Catheter

44
Q

Pathophysiology of CHRONIC kidney disease

A

THREE MAIN CAUSES
-Increased glomerular capillary pressure
-Causes damage

Proteinuria
-Filtration damage = kidney damage

Glomerulosclerosis

45
Q

Key abnormalities that give rise to CKD-Mineral Bone disorder

A

Potassium (Impaired phosphate excretion)

Vitamin D conversion
(1,25-Dihydroxyvitamin D3)

46
Q

Vitamin D metabolism

A

Production of active Vitamin D requires conversion of 7-dehydrocholesterol to cholecalciferol (Vitamin D3) by sunlight, followed by the first hydroxylation step in the liver to form 25-hydroxyvitamin D3, or 25(OH)D3, and the final conversion step in the kidney to form 1,25-dihydroxyvitamin D3 or Calcitriol.

Managing CDK patients requires dealing with Ca homeostasis

ONLY the liver and Kidney carry calcitriol - without proper function = cannot have Vitamin D

47
Q

Uremia

A

Uremic illness is due largely to the accumulation of organic waste products, not all identified as yet, that are normally cleared by the kidneys

Uremic solutes
-Signs and symptoms
-Can be termina l

-Neuro, muscular, endocrine, metabolic

48
Q

Specific Nephropathies

A

Nephritic Syndromes

Nephrotic Syndrome

Cystic Disease of the Kidney

Nephrolithiasis

Contrast-induced Nephropathy

49
Q

Nephritic vs Nephrotic

A

Nephritic
I = inflammation
Blood in urea

Nephrotic
o = pOdOcyte damage
Once structure/barrier damaged - protein can easily get through

50
Q

Typical Features of Nephrotic syndrome

A

Insidious Onset
LARGE edema - proteins LEAKING
Normal BP
Normal jugular venous pressure
**LARGE proteinuria **
Hematuria may/may not occur
RBC casts - absent
Serum Albumin - LOW

51
Q

Typical features of nephritic syndrome

A

Abrupt onset
Some Edema
BP raised
Jugular venous pressure raised
Proteinuria - present
Hematuria - SIGNIFICANT
RBC casts - PRESENT
Serum albumin - normal/slightly reduced (wasted)

52
Q

Glomerulonephritis

A

Inflammation of Glomeruli

acute and chronic forms

Presents with proteinuria and or hematuria

Primary causes include inheritable trait (Alport Syndrome)

Secondary causes: infections DRUGS, and autoimmune disorders (vasculitis, Lupus

53
Q

Pathogenesis of Glomerular Diseases (Pathogenesis = Immune reaction)

A
  1. Antibody associated injury
  2. Cell mediated immune
  3. Other mechanisms of Glomerular Injury
54
Q

Pyelonephritis

A

Inflammation of kidney tissue
-Usually bacterial infection
-ANNA

Acute and chronic forms

Presents flank pain with painful urination

Causes are bacteria from blood or urinary tract

White cells in urine

May lead to sepsis

55
Q

Interstitial Nephritis

A

Primary injury to renal tubules and interstitium

Undetected until causes significant decrease in renal function

Causes:

DRUGS 70-75% - mostly antibiotics

Infection 4-10%

Autoimmune (10-20%) SLE, sarcoidosis

56
Q

Drugs associated with interstitial nephritis

A

Antibiotics
Penicillin
Cephalosporins
Sulfonamides

Diuretics
-Thiazides
-Furosemide

Anticonvulsants
-Phenytoin
-Carbamazepine
-Phenobarbital

Analgesics
-NSAIDs

Other
-Allopurinol
-Cimetidine

57
Q

Cystic Diseases of the Kidney: Simple Cysts

A

Simple cysts
-Most common form of cystic renal disease
-Should be distinguished from kidney tumors

58
Q

Cystic Diseases of the Kidney - Autosomal Dominant (Polycystic Kidney Disease (Adult) (APKD)

A

Definition: multiple expanding cyts of both kidneys that ultimately destroy the intervening parenchyma

Pathogenesis of Autosomal adult PKD
-Inherited mutation of PKD1 or pKD2
Abnormal cysts formation in both kidneys
Ultimately destroy the intervening parenchyma
HTN and UTI - ultimately fatal - renal transplant necessary

59
Q

Cystic Diseases of the Kidney Autosomal Recessive (childhood) PKD

A

Pathogenesis:
-Autosomal recessive inheritance
-Mutation in PKHD1 - fibrocystin (polyductin)

Clinical features
-Serious manifestations are usually present at birth
-Young infants die quick
-Patients who survive infancy develop cirrhosis

60
Q

Nephrolithiasis - Kidney Stones

A

Lifetime prevalence - 10% men, 5% women
Arises from a supersaturation of solutes (Calcium)

61
Q

Hematuria

A
62
Q

Nephrolithiasis (Kidney stones) composition and treatment

A

70-80% from calcium
-Majority of kidney stones - cannot do anything, has to pass

Change diet
-Hydration
Main cause: acute dehydration - precipitation

Surgery/procedure - rare

Primary treatment
-Analgesis
Hydration
-Lithotripsy
-Surgical Removal

Prevention
-Diet (hydration; eliminate Ca supplements)
Diuretics

63
Q

Contrast-Associated Nephropathy

A

25% increase in SCr within 72 of contrast media admin

CIN causes 1/3 hospital acquired AKI

Affects 1-2% of the US population

Hydration for prevention

Avoid concurrent nephrotoxins

Recent work suggests frequency may be overestimated and most methods to reduce incidence have proven to be ineffective

Therapeutics (61 decks)

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