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Therapeutics > L5-6: Renal > Flashcards

L5-6: Renal Flashcards

(63 cards)

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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
**Proximal Tubule, straight segments**
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
26
Thin descending limb of Henle's loop
Function: Passive reabsorption of water Water permeability: high Primary Transporters and drug targets at apical membrane: Aquaporins Diuretic with major action: None
27
**Thick ascending limb of Henle's loop (TAL)**
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
Distal Convoluted tubule (DCT)
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
Medullary Collecting duct
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
Cortical Collecting Tubule (CCT)
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
Measures of Function
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
Markers of damage
Urine abnormalities (Protein, RBC suggestive of membrane malfunctions) Imaging abnormalities (MRI/CT scans)
33
Kidney function declines with age due to
Decline in nephrons Decreased by HALF Higher pressure - ones that are there will not last as long
34
Compensatory Response to Renal Injury
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
Sources of Kidney Injury/Failure
**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
AKI Death rate
300,00 people US annually -Death rate more than breast cancer, prostate cancer, heart failure AND diabetes combined
37
Pathophysiology of Acute Kidney Failure
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
Major causes of AKI: Prerenal
Hypovolemia Decreased Cardiac Output Decreased effective circulating volume -Congestive Heart failure -Liver failure **Impaired renal autoregulation** -NSAIDs -ACE-I/ARB -Cyclosporine
39
Major causes of AKI: Intrinsic (Intrarenal)
Glomerular -Acute glomerulonephritis Tubules and interstitium -Ischemia -Sepsis/infection **Nephrotoxins** Vascular -Vasculitis -Malignant HTN -TTP-HUS
40
Major causes of AKI: Postrenal
Bladder outlet obstruction -Bilateral pelvoureteral obstruction (uinlateral obstruction of a solitary functioning kidney)
41
Intrarenal mechanisms for autoregulation of GFR under decreased perfusion pressure and reduction of GFR by drugs
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
Primary causes of AKI
**Sepsis** **Ischemia** **Nephrotoxins**
43
Obstruction sites causing AKI
Kidney -Stones, blood clots, external compression, tumor, retroperitoneal fibrosis Bladder -Prostatic enlargement, blood clots, cancer Urethra -Strictures -Obstructed Foley Catheter
44
Pathophysiology of CHRONIC kidney disease
**THREE MAIN CAUSES** -Increased glomerular capillary pressure -Causes damage Proteinuria -Filtration damage = kidney damage Glomerulosclerosis
45
Key abnormalities that give rise to CKD-Mineral Bone disorder
Potassium (Impaired phosphate excretion) Vitamin D conversion (1,25-Dihydroxyvitamin D3)
46
Vitamin D metabolism
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
Uremia
**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
Specific Nephropathies
Nephritic Syndromes Nephrotic Syndrome Cystic Disease of the Kidney Nephrolithiasis Contrast-induced Nephropathy
49
Nephritic vs Nephrotic
Nephritic I = inflammation Blood in urea Nephrotic o = pOdOcyte damage Once structure/barrier damaged - protein can easily get through
50
Typical Features of Nephrotic syndrome
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
Typical features of nephritic syndrome
Abrupt onset Some Edema BP raised Jugular venous pressure raised Proteinuria - present **Hematuria - SIGNIFICANT** **RBC casts - PRESENT** Serum albumin - normal/slightly reduced (wasted)
52
Glomerulonephritis
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
Pathogenesis of Glomerular Diseases (Pathogenesis = Immune reaction)
1. Antibody associated injury 2. Cell mediated immune 3. Other mechanisms of Glomerular Injury
54
Pyelonephritis
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
Interstitial Nephritis
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
Drugs associated with interstitial nephritis
Antibiotics **Penicillin** Cephalosporins Sulfonamides Diuretics -Thiazides -Furosemide Anticonvulsants -Phenytoin -Carbamazepine -Phenobarbital Analgesics -NSAIDs Other -Allopurinol -Cimetidine
57
Cystic Diseases of the Kidney: Simple Cysts
Simple cysts -Most common form of cystic renal disease -Should be distinguished from kidney tumors
58
Cystic Diseases of the Kidney - Autosomal Dominant (Polycystic Kidney Disease (Adult) (APKD)
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
Cystic Diseases of the Kidney Autosomal Recessive (childhood) PKD
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
Nephrolithiasis - Kidney Stones
Lifetime prevalence - 10% men, 5% women Arises from a supersaturation of solutes (Calcium)
61
Hematuria
62
Nephrolithiasis (Kidney stones) composition and treatment
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
Contrast-Associated Nephropathy
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 (63 decks)

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