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Renal System Flashcards

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1
Q

How might a child with strep throat end up with glomerulonephritis?

A

the strep infection can linger and lead to an inflammatory response that results in injury, proliferation of cells obstructs capillary flow, pulling little crystals through blood vessels leads to damage

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2
Q

What accounts for cola-colored urine?

A

hematuria, red blood cells in the pee

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3
Q

What is AKI?

A

acute kidney injury

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4
Q

What causes prerenal AKI?

A

renal hyperfusion is MAIN cause, hypotension, hypovolemia/hemorrhage, sepsis, poor cardiac output, shock, renal artery vasoconstriction or clots

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5
Q

What are the clinical manifestations of prerenal AKI?

A

decreased filtration pressure and GFR, increased creatinine and BUN, oliguria

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6
Q

What causes intrarenal AKI?

A

tissue disorder and ATN causes by ischemia are MAJOR causes, acute glomerulonephritis, allograft rejection, infection and tumor

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7
Q

What are the clinical manifestations of intrarenal AKI?

A

loss of renal function, decreased GFR, increased creatinine and oliguria

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8
Q

What causes postrenal AKI?

A

disorders associated with acute urinary tract obstruction are MAIN cause, urethral obstruction, decreases GFR, increases creatinine and BUN, oliguria/anuria

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9
Q

What are the clinical manifestations of postrenal AKI?

A

bowman hydrostatic pressure > glomerular, decreased GFR, increased creatinine and BUN, oliguria and anuria

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10
Q

What accounts for the development of anemia in chronic kidney disease (CDK)?

A

the kidneys can’t produce enough erythropoietin (stimulates bone marrow to produce RBCs)

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11
Q

Which electrolyte imbalance is likely to trigger initiation of dialysis?

A

potassium imbalance, especially hyperkalemia as it can cause heart arrhythmias

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12
Q

How do renal system obstructions effect GFR?

A

decreases it

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13
Q

How do renal system obstructions effect creatinine and BUN?

A

they increase levels of both

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14
Q

How do renal system obstructions effect urine output?

A

it decreases

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15
Q

How do kidney stones develop?

A

crystals and mineral salts collect and form in the bladder, ureters, or kidneys

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16
Q

How does increasing fluid intake help prevent or treat kidney stones?

A

it dilutes the solutes in the fluid so they aren’t as likely to clump up

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17
Q

How are UTIs categorized?

A

by location and complicating factors

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18
Q

Where are cystitis UTIs located?

A

UTI in bladder, most common

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19
Q

Where are pyelonephritis UTIs located?

A

UTI affecting the kidneys

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20
Q

What is an uncomplicated UTI?

A

run of the mill, no complications, “easy”, happens in healthy, non-pregnant females

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21
Q

What is a complicated UTI?

A

effects older populations, catheter associated, can occur during pregnancy and in males

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22
Q

What are symptoms of cystitis?

A

inflammation of bladder, frequency and urgency of urination, dysuria, suprapubic and back pain, foul-smelling urine, polyuria, and hematuria

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23
Q

What are symptoms of pyelonephritis?

A

inflammation of kidneys, renal obstruction, edema, scar tissue, fibrosis, fever, chills, flank pain, nausea, vomiting, dysuria, pyuria, and WBC casts

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24
Q

What are the signs and symptoms of uremia?

A

hypertension, edema, hyperkalemia, fatigue, anorexia, nausea/vomiting/diarrhea/constipation, malnutrition, weight loss, neurologic changes, anemia, metabolic acidosis

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25
How does uremia differ from azotemia?
both have decreased GFR and increased creatinine and BUN, but azotemia has no/mild symptoms
26
In which stage of CKD does uremia typically develop?
stage 4, with severe loss of function (25% of function remaining)
27
What are the systematic effects of CKD?
azotemia leads to uremia, diabetes mellitus, lupus erythematosus, and chronic hypertension
28
What is acute tubular necrosis (ATN)?
necrosis of living epithelial cells lining renal tubules
29
What causes ATN?
post-ischemia (hypotension, septic shock, loss of blood, dehydration, heart failure, eclusion in renal artery) nephrotoxic things (alcohol, medications, contrast in medical conditions)
30
What are the tests of renal function?
GFR, renal clearance, plasma creatinine, blood urea nitrogen, and urinalysis
31
What is a glomerular filtration rate test? When is it used?
rate of blood filtration at glomeruli per unit of time, best estimate of renal tissue; determined by capillary hydrostatic pressure, oncotic pressure, and. bowman hydrostatic pressure
32
What is a renal clearance test?
how much substance is removed from blood by kidneys at a time (usually creatinine removed)
33
What is a plasma creatinine test?
it calculates GFR by using plasma creatinine, age, gender, and race
34
What is a blood urea nitrogen test?
related to altered protein intake/metabolism or dehydration
35
What is a urinalysis test?
proteins and sediments should not be in pee
36
What are characteristics of nephrOtic syndrome?
hypoalbuminemia, edema, hyperlipidemia (loss of transport proteins and immunoglobulin)
37
What are manifestations of nephrOtic syndrome?
foamy urine, edema/ascites, water retention, weight gain, hypertension, lipiduria, vitamin D deficiency and hypothyroidism
38
What are characteristics of nephrItic syndrome?
hematuria and RBC casts
39
What are manifestations of nephrItic syndrome?
cola-colored urine, oliguria, edema, and hypertension
40
How does hyperlipidemia develop from nephrOtic syndrome?
hypoalbuminemia leads to increased hepatic synthesis of lipoproteins which then leads to hyperlipidemia
41
How does vitamin D deficiency develop from nephrOtic syndrome?
loss of transporter proteins = we can't transport vitamin D
42
How does weight gain develop from nephrOtic syndrome?
glomerular permeability increases which lets water leak out, leading to decreased intravascular volume. The body attempts to correct this by increasing ADH and aldosterone in order to retain water. Because it can leak out so easily, this worsens edema which results in weight gain
43
How do RBC casts develop from nephrItic syndrome?
blood cells leak out and aggregate to form RBC casts after passing through kidney tubules
44
How does cola-colored urine develop from nephrItic syndrome?
glomerular inflammation leads to increases permeability which lets blood leak into urine resulting in cola-colored urine
45
What are hypersensitivity reactions?
there is an over zealous immune system where circulating immune complexes deposit in glomeruli, or antibodies react against planted antigens or glomeruli antigens (autoimmune)
46
What are inflammation reactions?
activation of cytokines and complement lead to chemotaxis, glomerular injury due to free radicals occurs which leads to increased glomerular permeability and loss of negative charge, then proteins and RBCs can leak out causing the area to junk up
47
What are functions of the kidneys?
fluid and electrolytes regulation, hormone secretion, acid-base balance, and excretion of toxins like urea
48
What test do we use for renal function?
glomerular filtration rate (GFR), renal clearance, creatinine, cleared creatinine and GFR, plasma creatinine and GFR, blood urea nitrogen (BUN), and urinalysis
49
What does GFR test? Whats the normal range?
the rate of blood filtration at glomeruli per unit of time, best estimate of renal tissue; normal range = 90-120 ml.min
50
What does renal clearance test?
how much of a substance is removed from the blood by kidneys per unit of time, creatinine often used as substance
51
What is creatinine? What's it's normal range?
creatinine is a nitrogenous waste product produced by the muscles that is released into the bloodstream, it freely filters at glomerulus and is not reabsorbed; normal plasma volume = 0.7-1.2 mg/dl
52
How are GFR and plasma creatinine related?
INVERSELY
53
What is BUN? How do we calculate it?
a byproduct of protein metabolism, it's filtered at glomerulus and capable of being reabsorbed; normal plasma value = 10-20 mg/dl
54
What is urinalysis?
a non-invasive and inexpensive way to evalute color/clarity, pH (normal = 5-6.5), specific gravity (solute con.), protein, sediment (RBCs, WBCs, casts)
55
What are casts?
accumulations of cellular precipitates that form in renal tubules, some are benign and some indicate disease
56
What is acute glomerulonephritis?
inflammation/injury to the glomerulus (endothelium, basement membrane, podocytes)
57
What causes acute glomerular injury?
non-immune mechanisms such as ischemia/free radicals, vasculitis, drugs and toxins immune mechanisms such as inflammatory damage to glomeruli, hypersensitivity reactions, and inflammatory response
58
What are the clinical manifestations of glomerulonephritis?
decreased GFR, increased creatinine and BUN, nephrotic/nephritic syndrome, oliguria, systematic effects such as hypertension, edema and renal failure
59
How do we treat glomerulonephritis?
treat the primary cause first, then minimize immune response (corticosteroids, plasmapheresis), after this manage symptoms (hypertension, edema, dialysis)
60
What is chronic glomerulonephritis?
glomerular disease with progressive course leading to CKD
61
What causes chronic glomerular injury?
diabetic nephropathy and lupus nephritis
62
What is diabetic nephropathy?
glomerular damage resulting from chronic hyperglycemia due to podocyte injury, thickening and fibrosis of basement membrane, and glomerulosclerosis
63
What is lupus nephritis?
glomerular damage caused by systemic lupus erythematosus from formation of autoantibodies with glomerular deposition, and immune response
64
What are clinical manifestations of chronic glomerular injury?
progressive decline in GFR and increase of BUN and creatinine, nephrotic/nephritic syndrome, renal insufficiency after 10-20 years, oliguria/anuria, uremia, and end stage kidney disease
65

Pathophysiology (8 decks)

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