Conditions Effecting the Urinary System and Pharmacotherapy Flashcards
Exam 1: Just kill yourself already you idiot.
Glomerulonephritis
inflammation of glomeruli and of the small blood vessels in the kidney
Causes of inflammation of the glomeruli
Primary glomerular injury- isolated to the kidney
Secondary glomerular injury- systemic disease (drugs, DM, HTN)
What are the main components of inflammation of glomeruli/
Immune mechanisms are the main component
Immune mechanisms are the main component of inflammation of glomeruli, what are the examples:
Antigen-antibody complexes, activated inflammatory response
* Complement activation, WBC recruitment, activated platelets, cytokine release injury
to GBM
* Increased glomerular mem permeability proteins & RBCs escape into urine
* Swelling & cell proliferation in Bowman’s space
Risk factors leading to inflammation of glomeruli?
- Streptococcal infection, typically precedes (most common)
- It affects children between the ages of 3 to 7 years, especially boys
- Staphylococcus, Pneumococcus, varicella
- Immunodeficiency
- Inflammatory DX ~ SLE
- Meds (eg NSAIDs)
Complications of inflammation of glomeruli?
CKD, renal failure are the leading cause
How long does it take for clinical manifestations of glomerulonephritis?
Sudden or gradual
What can occur before symptoms appear for glomerulonephritis?
Significant nephron function loss can occur before symptoms
How is symptoms presentation of glomerulonephritis?
Symptom presentation may be silent, mild, moderate or severe
What kind of disease is glomerulonephritis considered?
Severe or progressive disease oliguria, htn, renal failure
What are two major signs and symptoms of severe glomerulonephritis?
Hematuria with red blood cell casts & Proteinuria (foamy urine) exceeding 3 to 5 g/day with albumin (macroalbuminuria) as the major protein
What is used to evaluate glomerulonephritis?`
Urinalysis
Renal biopsy
Reduced GFR
Urinalysis for glomerulonephritis should include:
proteinuria, rbcs, wbcs, casts
Renal biopsy for glomerulonephritis should find out:
Type of lesion, extent of renal injury
Reduced GFR: slide I don’t understand
Elevated plasma urea
* Cystatin C in blood
* Biomarker of kidney function
* Elevated creatinine concentration &
reduced CrC
Treatment of glomerulonephritis includes:
Treating Edema
High calorie, low protein diet
Antibiotics
Corticosteriods
Cytotoxic agents
ANticoagulants
BP management
To treat edema related to glomerulonephritis what should be done?
diuretics, dialysis, restrict Na & H2O
intake, I &O, daily weight
What should antibiotics be used for in glomerulonephritis?
mgmt of underlying infection causing
antigen-antibody response
What are corticosteroids used for in glomerulonephritis?
suppress the inflammatory
response, decrease Ab synthesis
What are cytotoxic agents used for in glomerulonephritis?
(cyclophosphamide) – suppress immune response
What are Anticoagulants used for in glomerulonephritis?
– fibrin crescent formation
Tetrad of manifestations of Nephrotic syndrome
- Proteinuria
- Hyperlipidemia (Dyslipidemia)
- Hypoalbuminemia
- Peripheral edema
What is the pathophysiology of nephrotic syndrome:
- Inflammation/damage of the glomerulus
- Proteins are able to pass to tubule (more permeable)
- Protein travels through tubule and becomes part of urine
- Protein loss is proteinuria w/wo hematuria
What types of proteins are lost in urine in nephrotic syndrome?
immunoglobulins
albumins
lipiduria
What would loss of protein lead to in nephrotic syndrome?
Edema-
Susceptibility to infection
Liver produces more cholesterol= hypercholesterolemia
Why would edema occur in nephrotic syndrome?
Hypoproteinemia would lead to reduced oncotic pressure. Water and electrolytes move to interstitial space. There are no solutes to hold the water and electrolytes in the vascular compartment.
What is nephritic syndrome?
Nephritic syndrome is hematuria and red blood cell casts in the urine.
What does nephritic syndrome usually occur with?
It occurs primarily with infection-related glomerulonephritis and rapidly progressive crescentic glomerulonephritis.
What is nephritic syndrome caused by:
It is caused by increased permeability of the glomerular filtration membrane with pore sizes large enough to allow the passage of red blood cells and protein.
Renal insufficiency
Decline in renal fxn to ≈25% of normal, GFR <30 ml/min, & mildly elevated serum creatinine (SCr) and urea
Kidney failure
Kidney failure refers to significant loss of renal function.
End Stage Kidney Disease
When less than 10% of kidney function remains, this is termed end-stage kidney disease (ESKD).
Uremia (uremic syndrome)
is a syndrome of renal failure and includes elevated blood urea and creatinine levels accompanied by fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes.
Uremia represents numerous consequences related to kidney failure, including:
retention of toxic wastes, deficiency states, electrolyte disorders, and immune activation promoting a proinflammatory state.
Azotemia
is characterized by increased blood urea nitrogen (BUN) levels (normal is 8 to 20 mg/dl) and frequently increased serum creatinine levels (normal is 0.7 to 1.4 mg/dl).
What do both azotemia and uremia indicate?
Both azotemia and uremia indicate an accumulation of nitrogenous waste products in the blood
Acute kidney injury (AKI)
is a sudden decline in kidney function with a decrease in glomerular filtration and urine output with accumulation of nitrogenous waste products in the blood
AKI can be classified as what?
- Prerenal
- Intrarenal
- Postrenal
What is the most common reason for AKI?
Prerenal acute kidney injury is the most common reason for AKI and is caused by inadequate kidney perfusion.
Prerenal acute renal failure
a condition that occurs when the blood supply to the kidneys is reduced or compromised
Prerenal acute kidney injury causes include:
Hypovolemia
Renal Hypoperfusion/Renal Vasoconstriction
Systemic Vasodilation
Decreased arterial blood volume (decreased cardiac output)
Poor perfusion of kidneys can occur because of:
Poor perfusion can result from hypotension, hypovolemia associated with hemorrhage or fluid loss (e.g., burns), sepsis, inadequate cardiac output (e.g., myocardial infarct [heart attack]), or renal vasoconstriction (e.g., caused by NSAIDs or radiocontrast agents) or renal artery stenosis.
The GFR declines in Prerenal acute kidney injury why?
The GFR declines because of the decrease in glomerular filtration pressure.
Failure to restore blood volume in prerenal acute kidney injury includes:
Failure to restore blood volume or blood pressure and oxygen delivery can cause ischemic cell injury and acute tubular necrosis or acute interstitial necrosis, a more severe form of AKI.
Intrarenal acute kidney injury:
(disorders involving renal parenchymal or interstitial tissue)
a type of AKI that occurs when the kidney’s structure is damaged.
Intrarenal acute kidney injury:
Acute tubular necrosis (postischemic or nephrotoxic)
Glomerulopathies
Acute interstitial necrosis (tumors or toxins)
Vascular damage
Malignant hypertension, vasculitis
Coagulation defects
Renal artery/vein occlusion
Bilateral acute pyelonephritis
Post acute renal failure (ARF)
occurs when waste builds up in the kidneys due to an obstruction in the lower urinary tract
Examples of obstructive uropathies that cause post renal AKI?
BPH
Renal calculi
Bladder/prostate cancer
Blood clots
Tumors
What are characteristic findings of Post renal AKI?
Characteristic finding: flank pain & anuria followed by polyuria
Post renal AKI: Prolonged mechanical obstruction leads to what?
Prolonged mechanical obstruction leads to tubular atrophy and irreversible kidney fibrosis
Treatment of Post renal AKI?
Perform urinary catheterization
Prevent UTI.
Relieve obstruction
Treat reversible causes
Four phases of AKI:
- Onset
- Oliguric
- Diuretic phase
- Recovery phase
Onset phase of AKI
Onset phase: Kidney injury occurs.
Oliguric (anuric) phase of AKI
- Oliguric (anuric) phase: Urine output decreases from renal tubule damage.
Diuretic phase of AKI
- Diuretic phase: The kidneys try to heal and urine output increases, but tubule scarring and damage occur. The kidneys recover their ability to excrete waste but cannot concentrate the urine.
Recovery phase of AKI
Tubular edema resolves and renal function improves.
Chronic Kidney Disease (CKD)
Progressive loss of renal function, affects nearly all organ systems
What are some qualities of Chronic Kidney Disease
Slow, progressive, and irreversible loss of kidney function & GF based on eGFR
What do people with Chronic Kidney Disease require?
Requires dialysis or kidney transplantation to maintain life.
AKI can progress to what?
AKI can progress to CKD or AKI on CKD
Normal gfr values
Normal GFR 120 to 140 mL/min
Stages of chronic kidney disease
- Normal kidney function (GFR > 90 mL/min)
- Mild CKD (GFR 60-89 mL/min)*
- Moderate (GFR 30-59 mL/min)
- Severe (GFR 15-29 mL/min)
- End stage (GFR less than 15)
What occurs during stage 1- Normal kidney function (GFR > 90 mL/min)
Mild damage, reduced renal reserve
What happens to the kidneys during stage 1- Normal kidney function (GFR > 90 mL/min)
Unaffected nephrons overwork to compensate for diseased nephrons
What kind of symptoms are common in stage 1 of ckd?
Htn common, proteinuria, high Cr or no sx at all
What is the kidney function in stage 1 of ckd?
Kidney function 90-100%
What happens to nephrons in stage 2 of ckd?
Kidney nephron damage has occurred
What happens to metabolic waste in stage 2 of ckd?
Slight elevation of metabolic waste in BUN/Cr
What symptoms occur during stage 2 of ckd?
Inability to concentrate urine, polyuria and nocturia
Htn
How is stage 3 of ckd divided?
split into two substages based on eGFR (3a & 3b):
What happens to nephrons in the third stage of CKD?
Nephron damage continues with decreased nephrons
What may be needed in stage 3 of ckd?
Restriction of fluids, proteins, electrolytes, including phosphorus, may be needed
What occurs in stage 4 of CKD?
Erythropoietin deficiency, anemia, HyperPhos/K, Increased triglycerides, Met acidosis, Na+/H2O retention
WHat occurs during stage 5 of ckd?
Oliguria occurs
Uremia (“urea in blood”) is the result and is fatal; classic marker
What happens to BUN and Cr levels in CKD?
Excessive urea (BUN) and Cr builds up in the blood
What is a classic marker of stage 5 - end stage ckd?
Uremia (“urea in blood”) is the result and is fatal; classic marker
What are two factors known to advance renal disease?
proteinuria and angiotensin II activity
How does proteinuria contribute to injury?
Proteinuria contributes to tubulointerstitial injury by accumulating in the interstitial space of the nephron tubules.
Angiotensin II (from activation of the renin-angiotensin-aldosterone system [RAAS]) causes efferent arteriolar vasoconstriction and promotes glomerular hypertension and hyperfiltration. Hyperfiltration is also associated with hyperglycemia and diabetic nephropathy. The chronically high intraglomerular pressure increases glomerular capillary permeability, contributing to proteinuria. Angiotensin II also may promote systemic hypertension and the activity of inflammatory cells and growth factors that participate in tubulointerstitial fibrosis and scarring.
Parathyroid acts on the kidneys to do what?
PTH acts on the kidneys to increase calcium reabsorption and decrease phosphate reabsorption
Vitamin D works with PTH to do what?
Vitamin D, particularly its active form calcitriol, works with PTH to maintain calcium and phosphorus homeostasis by facilitating intestinal absorption of calcium and phosphate.
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Skeletal presentation of CKD?
Results are pathological fxs, bone pain, deformities of long bones
What is the treatment of skeletal issues with CKD?
Activated Vitamin D
Phosphate binders work to bind phosphate in gut & excrete in stool
Phosphate-restricted diet
Activated Vit D replacement
Possible parathyroidectomy
Cardiovascular presentation of CKD?
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Neuro clinical presentation of CKD?
Uremic encephalopathy from toxins in CSF
Spectrum of cognitive & consciousness changes
What is the treatment of neuro problems with CKD?
Tx: dialysis/kidney transplant
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