Exam 2: Renal and Urinary Tract Disease Flashcards

(121 cards)

1
Q

Overview

Kidney disease is classified by __

A

Cause

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2
Q

Causes of Kidney Disease

Pre-renal

A

Volume depletion (including sweat loss and hemorrhage)
Hypotension
Heart failure
stenosis
cirrhosis
NSAIDs

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3
Q

Causes of kidney disease

Intrarenal

A

Vascular (sclerosis, vasculitis)
Glomerular (membrane damage)
Tubular (cancer, toxic injury, altered ionic homeostasis

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4
Q

Causes of kidney disease

Postrenal

A

Obstruction
Stones
Prostatic disease

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5
Q

Pre-Renal Kidney Disease

Renal Artery Stenosis

A

Narrowing of at least one artery that supplies the kidneys

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6
Q

Pre-Renal Kidney Disease

What does Renal Artery Stenosis do to the kidneys?

A

Reduces blood flow and pressure into the kidneys
Activates renin-angiotensin system
cannot raise pressure within the kidney

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7
Q

Pre-Renal Kidney Disease

What causes the thickened tunica media in Renal Artery Stenosis?

A

Excess smooth muscle
fibrosis

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8
Q

Pre-Renal Kidney Disease

How is blood pressure regulated in the kidney?

A

Juxtaglomerular apparatus at vascular pole
Specialized JG cells produce renin
Macula densa cells detect ions

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9
Q

Pre-Renal Kidney Disease

What causes elevated arteriole pressure?

A

Higher glomerular filtration rate aters ionic concentration
Release of vasoactive compounds constricts arteriole, which decreases GFR
Lower NA+, Cl- concentration stops release

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10
Q

Pre-Renal Kidney Disease

How does a higher glomerular filtration rate alter ionic concentration in the kidney? How is it detected?

A

Less sodium and chloride can be recovered
Detected by cells in macula densa

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11
Q

Pre-Renal Kidney Disease

What does decreased arteriole pressure do in the kidneys?

A

Stimulates juxtaglomerular cells and release of renin

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12
Q

Pre-Renal Kidney Disease

Renin-Angiotensin System

A

JG cells release Renin from kidney
cleaves angiotensinogen into angiotensin I
Angiotensin-converting enzyme converts angiotensin I to angiotensin II
Angiotensin II causes vasoconstriction (decreased vascular space) in cardiovascular system and salt/water retention in kidneys (increases blood volume) - together increase BP

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13
Q

Pre-Renal Kidney Disease

What is the rate limiting step in the Renin-Angiotensin system?

A

Serum renin concentrations
System is controlled by JG cells in kidneys

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14
Q

Pre-Renal Kidney Disease

Where is angiotensin converting enxyme (ACE) found? How much Angiotensin II is converted in the kidneys?

A

Lung capillaries (also kidneys and other organs) express the enzyme
20% is converted

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15
Q

Pre-Renal Kidney Disease

Angiotensin II

A

Potent vasoconstrictor that directly increases blood pressure

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16
Q

Pre-Renal Kidney Disease

How does angiotensin II increase blood pressure? What does it do?

A

Stimulates adrenal glands to release aldosterone - promotes Na+ and water absorption in kidneys - increases blood volume - increases BP - increases BP shuts off renin release

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17
Q

Pre-Renal Kidney Disease: Renal Artery Stenosis

What are the symptoms of Renal Artery Stenosis?

A

High Blood Pressure (Renal HTN) (hyper tension in kidney, hypotension outside kidney)
Symptoms of Kidney Injury

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18
Q

Pre-Renal Kidney Disease: Renal Artery Stenosis

What are the causes of Renal Artery Stenosis?

A

Most common: athersclerosis
Less common: fibromuscular dysplasia
Decrease lumen - stenosis

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19
Q

Pre-Renal Kidney Disease: Renal Artery Stenosis

What are the treatments for Renal Artery Stenosis?

A

ACE inhibitors
Stent in renal artery/vessel

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20
Q

Intrarenal: Nephrosclerosis

Nephrosclerosis

A

Sclerosis of arterioles and small arteries within the kidneys

AKA Patchy atrophic ischemia

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21
Q

Intrarenal: Nephrosclerosis

What is the cause of Nephrosclerosis? What does it cause?

A

Caused by, and cause of, hypertension
Hylainization of vessel walls
genetics, age, general HTN

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22
Q

Intrarenal: Nephrosclerosis

What are the glomerular changes in Nephrosclerosis?

A

Partial to total sclerosis
GBM damage, collagen in Bowman’s space
Fibrosis around capsule

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23
Q

Intrarenal: Nephrosclerosis

What are the tubular changes in Nephrosclerosis?

A

Loss of tubules

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24
Q

Intrarenal: Nephrosclerosis

What is the result of vessel wall hyalinization in Nephrosclerosis?

A

Fibrin leaks through endothelium into vessel walls
Form smooths appearing eosinophilic membrane

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25
# Intrarenal: Nephrosclerosis What are the clinical symptoms of Nephrosclerosis?
Unresolved HTM, diabetes increase risk of renal failure
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# Intrarenal: Nephrosclerosis Does nephrosclerosis present with symptoms of clinical renal failure?
If nephrosclerosis is the only disease present, rare to present with symptoms of clinical renal failure
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# Intrarenal: Nephrosclerosis Malignant HTN (unresolved HTN)
Endothelial damage results in protein leakage and development of clots leads to renal ischemia (fibrinoid necrosis, hyperplastic arteriolitis) | Also frequent cause of renal failure in patients with sytemic sclerosis
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# Intrarenal: Nephrosclerosis What effect does involvement of afferent arterioles have on unresolved HTN?
Leads to renin elevation
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# Intrarenal: Glomerular Damage What are the causes of Glomerular Damage?
Secondary effects of systemic diseases Circulating antigen:antibody complexes deposit in filtration membrane Antibodies reacting against components of the filtration membrane
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# Intrarenal: Glomerular Damage Primary glomerular disease starts in the...
Kidney
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# Intrarenal: Glomerular Damage Where do immune complexes deposit?
1. Podocyte effacement (between podocyte and their BM) 2. Subepithelial deposits (In BM, but exterior to Lamina densa under podocytes) 3. Subendothelial deposits (between endothelial cells and lamina densa) 4. Mesangial deposits (mesangial membrane)
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# Intrarenal: Glomerular Damage What disease is podocte effacement associated with?
Minimal change disease
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# Intrarenal: Glomerular Damage What disease are subepithelial deposits associated with?
Membranous nephropathy
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# Intrarenal: Glomerular Damage What disease are subendothelial deposits associated with?
Membranoproliferative glomerulonephritis
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# Intrarenal: Glomerular Damage What disease are mesangial deposits associated with?
IgA nephropathy
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# Intrarenal: Glomerular Damage What are the clinical consequences of glomerular damage?
Nephritic or Nephrotic Syndrome
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# Intrarenal: Glomerular Damage Nephritic Syndrome
Glomerular inflammation proliferative changes and leukocyte infiltration Proteinuria and edema are less severe than nephrotic syndrome
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# Intrarenal: Glomerular Damage Nephrotic Syndrome
Podocyte Injury Immune or non-immune causes Structural and/or physiochemical alterations Damage to glomerular membrane - protein leakage
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# Intrarenal: Glomerular Damage Compare and contrats Nephritic and Nephrotic Syndrome
Nephrotic: No hematuria, oliguria, hypertension Both have proteinuria (lower level in nephritic)
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# Intrarenal: Glomerular Damage What is the clinical presentation of Nephritic Syndrome?
Hematuria Oliguria with azotemia Proteinuria Hypertension
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# Intrarenal: Glomerular Damage What are the most common causes of Nephritic Syndrome?
Immunologically-mediated glomerular injury Acute postinfectious glomerulonephritis Rapidly progressive glomerulonephritis (RPGN) which often leads to crescentic lesions
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# Intrarenal: Glomerular Damage What is the clinical presentation of Nephrotic Syndrome?
Massive proteinuria - depletes serum albumin Hypoalbuminemia - low albumin reduces osmotic pressure of blood Generalized edema due to reduced osmotic pressure and compensatory aldosterone secretion (hypovolemia) Hyperlipidemia and lipiduria
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# Intrarenal: Glomerular Damage What are the causes of Nephrotic Syndrome?
Minimal-change disease Membranous Nephropathy
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# Intrarenal: Glomerular Damage: Nephrotic Syndrome Minimal-change disease
Due to glomerular damage, leakage across filtraion membrane Lipoproteins accumulate in proximal convoluted tubules (visible lipid droplets and protein accumulations) somep odocyte effacement - causes nephrotic syndrome
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# Intrarenal: Glomerular Damage: Nephrotic Syndrome Minimal-change disease is most common in...
children
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# Intrarenal: Glomerular Damage: Nephrotic Syndrome Membranous Nephropathy
Diffuse thickening of capillary walls (Ig deposits or self-antibodies) Ig activates complement Attack on podocytes allows protein leakage Sudden onset
47
# Intrarenal: Glomerular Damage: Nephritic Syndrome What are the causes of Nephritic Syndrome?
Post-Streptococcal Glomerulonephritis Goodpasture Syndrome Crescentic Glomerulonephritis
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# Intrarenal: Glomerular Damage: Nephritic Syndrome Post-Streptococcal Glomerulonephritis
Antibodies to steptococcal proteins will recognize glomerular proteins activation of complement causes infiltration of neutrophils and other leukocytes Immune response will also induce proliferation of cells in glomerulus (increased cellularity of glomerulus, deposits in subendothelial space, membrane, subepithelial space)
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# Intrarenal: Glomerular Damage: Nephritic Syndrome Goodpasture syndrome
Renal failure with pulmonary hemorrhage Parietal epithelial cells can transdifferentiate to produce replacement podocytes (immune response causes necrosis in glomerulus)
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# Intrarenal: Glomerular Damage: Nephritic Syndrome What causes Goodpasture Syndrome?
Antbodies against basement membrane components (Anti-GBM in kidney, which may recognize alveolar bm) | Anti-GBM antigen is in collagen IV; source of pulmonary hemorrhage
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# Intrarenal: Glomerular Damage: Nephritic Syndrome What is the clinical presentation of Goodpasture Syndrome?
Hemoptysis Hematuria Nephritic (and possibly nephrotic) syndrome
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# Intrarenal: Glomerular Damage: Nephritic Syndrome What is the treatment for Goodpasture Syndrome?
Plasmaphereis to remove antibodies immunosuppression
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# Intrarenal: Glomerular Damage: Nephritic Syndrome Crescentic Glomerulonephritis | Rapidly progressive glomerulonephritis (RPGN)
Crescents form due to proliferation of parietal cells of Bowman's membrane (induced my macrophages, monocyte chemotaxis)
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# Intrarenal: Glomerular Damage: Nephritic Syndrome Why is Crescentic Glomerulonephitis also known as rapidly progresisve glomerulonephritis?
Clinical syndrom - rapid loss of renal function
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# Intrarenal: Glomerular Damage: Nephritic Syndrome What are the 3 types of Crescentic Glomerulonephritis based on? What are they?
Immunological mechanisms 1. Anti-GBM antibody mediated disease (Goodpasture Syndrome) 2. Immune complex deposition (lupus) 3. Anti-neutrophil cytoplasmic antibodies (ANCAs) (idiopathic, systemic vasculitis)
55
# Intrarenal: Tubular Damage Tubulointerstitial nephritis
Inflammation(nephritis) of interstitium (interstitial) and tubules(tubulo)
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# Intrarenal: Tubular Damage: Pathways of Renal infection Acute Pyelonephritis
Bacterial infection due to UTI
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# Intrarenal: Tubular Damage: Pathways of Renal infection Chronic Pyelonephritis
History of UTI Fibrosis of pelvis and calyx
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# Intrarenal: Tubular Damage: Pathways of Renal infection Drug-induced inflammation
Edema and mononuclear infiltrate into interstitium Penicillin derivatives, other antibiotics, NSAIDs, others
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# Intrarenal: Tubular Damage Ionic Homeostasis
Balance between cations and anions
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# Intrarenal: Tubular Damage What is the purpose of Ionic Homeostasis?
maintain pH around 7.4 Concentrationsof ions maintain osmolarity Ions necessary for function maintained at correct concentration
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# Intrarenal: Tubular Damage Exretion must be _ by intake to maintain balannce
matched
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# Intrarenal: Tubular Damage How much of your body weight is body water? What is it comprised of?
60% of body weight breaks down to: * 20% bw is ECF * 40% bw is ICF
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# Intrarenal: Tubular Damage What is the ECF? What are the major cations and anions?
Plasma + interstitial (filtrate of plasma; no cells or large proteins) (Extracellular fluid) Cation: Na+ Aniona: Cl- and HCO3-
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# Intrarenal: Tubular Damage What is the ICF? What are the major cationd and anions?
Intracellular fluid Cations: K+ and Mg2+ Anions: proteins and organic phosphates (ATP, ADP, AMP)
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# Intrarenal: Tubular Damage Water Intoxication | Water poisoning/Fatal hyponatremia
Drink so much water it becomes toxic - kidney cant remove fluid fast enough Urine excretion can be increased to 16 mL/min (usually 1 ml/min) when large quantities of hypotonic fluid are ingested If ingestion exceeds this, or continues for too long, cells will swell due to water uptake to cope with Hypotonic ECF
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# Intrarenal: Tubular Damage What are the symptoms of water intoxication?
Swelling of CNS neurons Convulsions, coma (can kill)
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# Kidney Injury What is the most common cause of acute renal failure? Why?
Acute Kidney Injury Rapid reduction of renal function, including output <400 ml/day (oliguria to anuria) 50% of acute renal failure occurs in hospital patients
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# Kidney Injury What evidence could you find of tubular injury?
glomerular, interstitial, vascular injury
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# Kidney Injury What are the causes of Acute Kidney Injury?
Ischemia Direct Toxic Injury Inflammation Urinary Obstruction
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# Kidney Injury What causes ischemia in AKI?
Malfunction of intrarenal blood vessels Thomboses Decreased blood volume
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# Kidney Injury What causes urinary obstruction in AKI?
Tumors, prostatic hypertrophy, blood clots
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# Kidney Injury Pathogenesis of AKI
Tubule Cell injury (Toxic/Ischemic Injury) Distrubed Blood flow
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# Kidney Injury Tubule Cell Injury: Toxic Injury
Cells are more sensitive due to higher metabolic requirements, high absorption rates, and concentration capacity
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# Kidney Injury Tubule Cell Injury: Ischemic Injury
Tubules cells are more sensitive to lack of nutrients ischemia causes vasoconstriction
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# Kidney Injury Disturbed Blood Flow
Hemodynamic alterations affect GFR
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# Kidney Injury What is the treatment for AKI?
Prevent further damage (address cause) Antibiotics - prevent secondary infections Diuretics - flush out the kidneys Dialysis
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# Kidney Injury How is the damage distributed in AKI?
Proteins, lipids, blood cells acculate on the inner aspect of the tube Form casts that can be passed into the urine Necrosis occurs in areas most impacted by damage
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# Kidney Injury How do you differentiate the connvoluted tubules?
DCT: Less esosinophilic PCT: Visible brush border Both: Cuboidal Cells
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# Chronic Kidney DIsease What is the difference between Chronic Kidney Disease and AKI?
Chronic Kidney Disease: Irreversible loss of tubular cells AKI: can resolve through regeneration
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# Chronic Kidney DIsease What is the cause of chronic kidney disease?
Most common cause is diabetes mellitus Other common causes include hypertension and glomerulonephritis | endpoint of all chronic renal parenchymal diseases
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# Chronic Kidney DIsease What are the markers of kidney damage?
Alterations in blood urine composition
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# Chronic Kidney DIsease What is the treatment for Chronic Kidney Disease?
Address underlying cause Changes in diet, lifestyle to prevent damage Serious: Dialysis, transplant
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# Chronic Kidney DIsease Chronic Kidney Disease
Irreversible loss of tubular cells Significntly decreased GFR and/or albuminuria for 3 months
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# Chronic Kidney DIsease What are the clinical manifestations of kidney damage?
altered kidney functions that affect: * Sodium and potassium homeostasis * Water balance * Acid-base balance * Urea excretion
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# Chronic Kidney DIsease How does kisney damage affect sodium potassium homeostasis?
Excess Na+ expands intravascular volume Hypertension and congestive heart failure
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# Chronic Kidney DIsease How does kidney damage affect urea excretion?
Reduced excretion increases BUN and serum creatinine, produces uremia | BUN = blood urea nitrogen
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# Chronic Kidney DIsease What are clinical symptoms of kidney damage?
Dehydration, edema, hyperkalemia Hyperphosphatemia, hypocalcemia, bone/parathyroid effects anemia Hypertension, congestive heart failure, cardiomyopathy, pulmonary edema, uremic pericarditis Nausea and vomiting, GI bleeds, inflammation of the esophagus, stomach, colon Skin: sallow, pruritic, dermatitis
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# Kidney Damage Uremia
Increases levels of urea in the blood
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# Kidney Damage What are the symptoms of Uremia?
Decreased appetite Fatigue Neurological symptoms (confusion, coma) Skin excretion (uremic frost)
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# Kidney Damage What causes uremia?
Accumulation of nitrogenous waste products due to kidney failure Hypotension dehydration trauma (increased protein catabolism)
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# Kidney Damage What are other consequences of Uremia?
Kidneys no longer activate vitamin D Necessary for calcium/phosphate absorpion
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# Renal Osteodystrophy Renal Osteodystrophy
Lack of vitamin D reduces intestinal Ca2+ absorption
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# Renal Osteodystrophy What is the mechanism of Renal Osteodystrophy?
Low plasma Ca2+ causes parathyroid hyperplasia PTH increases oteoclast activity Secondary hyperparathyroidism causes bone calcium depletion
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# Obstructive Uropathy What are the most common sites of Kidney Stones?
Collecting system Renal pelvis and calcyes
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# Obstructive Uropathy What are the causes of kidney stones?
Genetics Dehydration Dietary Intake Hormonal imbalance (parathyroid tumor)
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# Obstructive Uropathy What are the 4 types of kidney stones?
Calcium (75%) Uric Acid (<10%) Cystine (1%) Infection (15%)
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# Obstructive Uropathy Kidney Stones: Calcium
75% of kidney stones are calcium oxalate and/or phosphate salts
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# Obstructive Uropathy Kidney stones: Uric Acid
<10% of kidney stones 25% of gout/hyperuricemia patients most are idiopathic
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# Obstructive Uropathy Kidney Stones: Cystine
1% of kidney stones Children with hereditary cystinuria
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# Obstructive Uropathy Kidney Stones: Infection
15% of kidney stones Bacteria cleave urea * Proteus or providencia species * produces ammonia - caused urine to become alkaline - favors salt deposition - Struvite NH4MgPO4.6H2O - apatite Ca5(PO4)3(OH)2
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# Obstructive Uropathy What are the consequences of the obstruction of kidney stones?
Damage typically seen in tubules Causes increased intrarenal pressure (will damage tissue, infection or abscess can occur behind stone) Hypertension due to renin production
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# Obstructive Uropathy What causes pain from kidney stones?
Due to distension of renal capsule, renal pelvis or ureters Damage to these structures can cause ureters
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# Obstructive Uropathy Hydronephrosis
Expansion of pelvis and calcyes due to obstruction in ureters or further out | Urine backs up into kidneys
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# Obstructive Uropathy What causes hydronephrosis?
Calculus can block ureters Will compress parenchyma and damage it (tubules first, then glomeruli; atrophy and fibrosis)
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# Obstructive Uropathy Hydronephrosis: Unilateral Blockage
Blockage in ureter
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# Obstructive Uropathy Hydronephrosis: Bilateral blockage
Blockage in bladder or urethra
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# Obstructive Uropathy How do you treat kidney stones?
Pain magement Prevent dehydration (water and other fluids) Use shock waves to break up the stone Stent in ureter to maintain patency Prevent new stones from forming (depends on type of stone)
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# Obstructive Uropathy How can allopurinol be used to treat kidney stones?
Inhibits purine catabolism to reduce uric acid production
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# Postrenal Actue cystitis
Neutrophil infiltrate Inflammation of bladder
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# Postrenal Chronic Cystitis
Mononuclear infiltrate (macrophages and T cells) Inflammation of bladder
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# Postrenal Types of cystitis (bladder inflammation)
Bacterial infection (or viral) Hemorrhagic Interstitial Malakoplakia Polypoid
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# Postrenal Hemorrhagic cystitis
Side-effect of cytotoxic chemotherapeutics can be due to adenovirus infection
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# Postrenal Interstitial Cystitis
Pain when bladder fills Other symptoms: Urgency, hematuria, dysuria
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# Postrenal Malakoplakia Cystitis
Defects in phagocytic cells (undigested bacterial components accumulate)
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# Postrenal Polypoid Cystitis
May look like papillomatous cancer but due to submucosal edema
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# Postrenal What are the most common species to cause Cystitis?
E. coli (most common), Proteus, Klebsiella, Enterobacter
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# Postrenal What are the predisposing factors of cystitis?
Bladder stones Obstruction Diabetes mellitus Immune defificency
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# Postrenal What are the triad of symptoms of cystitis?
1. Frequency (up to every 15-20 minutes) 2. Lower abdominal pain 3. Dysuria (pain/burning upon urination)