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CV487 > Class 7: Renal > Flashcards

Class 7: Renal Flashcards

1
Q

Concentration & dilution of urine

A

-Water, sodium, chloride, urea & catecholamines
-Renal hormones

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2
Q

Renal hormones

A

ADH, aldosterone, natriuretic peptides, vitamin D, erythropoietin & renin-angiotensin

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3
Q

Renal assessment (males)

A

-Frequency, urgency, nocturia, dysuria, hesitancy & straining
-Urine color, GU history
-Penis: Pain, lesion, discharge
-Scrotum: Self-care behaviors, lumps
-Sexual activity and contraceptive use & STI contact

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4
Q

Renal assessment (female)

A

-Menstrual & obstetrical hx
-Menopause, self-care behaviors, urinary symptoms, discharge
-Sexual activity, contraceptive use & STI contact and risk reduction

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5
Q

Renal objective assessment

A

-Fluid balance
-Lab values: Electrolytes, creatinine and BUN

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6
Q

Renal obstruction

A

-May be anatomical or functional
-Flow is impeded; dilation of the urinary system; increased risk for infection; compromises the renal system

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7
Q

Etiology of upper urinary tract obstructions

A

-Stricture, kidney stones, malignancy
-Congenital compression of a calyx, ureteropelvic or ureterovesical junction
-Compression from an aberrant vessel, tumor or abdominal inflammation and scarring

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8
Q

Pathophysiology of upper urinary tract obstructions

A

-Obstruction causes dilation of the ureter, renal pelvis, calyces and renal parenchyma proximal to the site of the blockage
-Dilation is an early response to the obstruction
-Increased pressure decreases filtration

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9
Q

Response to relief of upper urinary tract obstructions

A

-Post-obstructive diuresis
-Restoration of fluid and electrolyte imbalance
-May be further complicated by severe post obstructive diuresis

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10
Q

Kidney stones

A

-Calculi or urinary stones are masses of crystals, protein or other substances
-Most common stone type is calcium oxalate or phosphate, struvite and uric acid

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11
Q

Pathophysiology of kidney stones

A

-Super-saturation of one or more salts in urine
-Precipitation of salts from liquid to a solid state
-Crystallization or agglomeration
-Presence or absence of stone inhibitors

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12
Q

Kidney stone influencing factors

A

-Age, gender, race, genetic predisposition
-Seasonal factors
-Fluid intake, diet, occupation, previous UTI
-HTN, obesity

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13
Q

Kidney stone clinical manifestations

A

-Moderate to severe pain:
-Located in the flank and radiating to the groin
-Lateral flank or lower abdomen pain
-Urinary urgency, frequency, UI hematuria & N/V

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14
Q

Evaluation & diagnosis of kidney stones

A

-Functional study of renal pelvic and urethral pressures
-Urinalysis (including pH)
-X-Rays, CT scan or ultrasound

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15
Q

Lower urinary tract obstruction

A

Related to how urine is stored in the bladder or how urine is emptied from the bladder

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16
Q

Etiology of lower urinary tract obstruction

A

-Neurogenic, anatomic alterations
-Both Neurogenic and Anatomic
-Primary symptom is incontinence*

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17
Q

Neurogenic bladder is caused by

A

Spinal cord or brain disruption

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18
Q

Neurogenic bladder: Lesion above C2 or the pontine micturition center resulting in detrusor hyperrefelxia that causes

A

Loss of coordinated neuromuscular contraction and overactive or hyper-reflexive bladder function

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19
Q

Neurogenic bladder: Lesion located on the upper motor neurons between C2 & S1 resulting in detrusor hyperreflexia with vesical shincter dyssynergia

A

Loss of bladder muscle contraction and overactive bladder

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20
Q

Neurogenic bladder lesions can occur…

A

-In the sacral area of the spinal cord or peripheral nerves below S1 resulting in detrusor areflexia causing an underactive, hypotonic or flaccid bladder function with loss of sensation

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21
Q

Lower urinary tract obstruction: Overactive bladder syndrome

A

-Syndrome of detrusor over-activity
-May be spontaneous or provoked
-Affects men, women and children

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22
Q

Characterization of overactive bladder syndrome

A

Characterized by urgency with involuntary detrusor contractions during the bladder filling

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23
Q

Diagnosis of overactive bladder syndrome

A

Diagnosed by symptoms and assessment confirmed by urodynamic studies

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24
Q

Lower urinary tract obstruction: Obstruction to urine flow

A

-Anatomic causes of impedance to urine flow:
-Urethral stricture, prostate enlargement, pelvic organ prolapse, partial obstruction of the bladder outlet or urethra

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25
Diagnosis & tx of obstructed urine flow
Diagnostic tests to identify correct issue & hx
26
UTIs
-Inflammation of the urinary epithelium caused by bacteria from the gut -Can occur anywhere along the urinary tract -Classified by location or complicating factors
27
Classification of UTIs
-Cystitis, pyelonephritis -Uncomplicated & complicated UTI
28
UTIs: Cystitis
-Inflammation of the bladder -Most common site of UTI* -Mild inflammation leads to hyperemic mucosa
29
Etiology of cystitis
Most common infecting microorganism is Esherichia coli (E. Coli)
30
Advanced cystitis
May show hemorrhage, pus formation, or exudate on epithelial surface of the bladder
31
Manifestations of cystitis
Asymptomatic to frequency, urgency, dysuria and suprapubic and lower back pain -Hematuria, cloudy and foul-smelling urine
32
Diagnosis of cystitis
Assessment, symptoms and urinalysis
33
Tx of cystitis
Antibiotics
34
Cystits may lead to...
Urosepsis and septic shock; Emergency Situation!!!
35
Urinary tract infection: Acute pyelonephritis
Infection of one or both upper urinary tracts (ureter, renal pelvis and interstitium)
36
Etiology of acute pyelonephritis
Kidney stones, vesicoureteral reflux, pregnancy, neurogenic bladder, instrumentation and/or female sex trauma
37
Pathophysiology of acute pyelonephritis
Infection spreads, tubules most affected, rarely causes renal failure
38
Acute pyelonephritis manifestations
-Onset is acute, fever, chills, flank or groin pain -Similar to symptoms of UTI including frequency, dysuria and costovertebral tenderness -Older adults have low grade fever and malaise
39
Diagnosis and Treatment of acute pyelonephritis
-Blood cultures and urinary tract imaging -Treated with antibiotic therapy -May require surgical intervention to remove lesions
40
Glomerulonephritis
Inflammation of the glomerulus
41
Etiology of glomerulonephritis
Infection, immunologic abnormalities (most common cause), ischemia, free radicals, drugs, toxins, vascular disorders, systemic disease (ie: diabetes mellitus and lupus)
42
Glomerulonephritis pathophysiology
-Glomerular capillary endothelium is disturbed d/t streptococcal infection -aPermeability -Basement membrane of the epithelium becomes thickened
43
Glomerulonephritis presentation
-Nephrotic syndrome -Nephritic syndrome -Acute or chronic Kidney Failure
44
Glomerulonephritis clinical manifestations
-Insidious or sudden -Occurs 10 to 21 days post infection (Impetigo or pharyngitis) -Hematuria, RBC casts, proteinuria, decreased GFR, elevated Cr and BUN -Oliguria, HTN, edema around the eyes feet & ankles, ascites or pleural effusions
45
Glomerulonephritis tx
No specific treatment and patients resolve without significant loss of function
46
Pertinent labs for the renal system
-CBC -Electrolytes -Kidney function: Creatinine, BUN & GFR
47
Acute kidney injury
-Sudden decline in kidney function with decrease in GFR -Accumulation of nitrogenous waste products in the blood -Elevated Creatinine and BUN
48
Acute kidney injury pathophysiology
-Extracellular volume depletion -Decreased renal blood flow -Toxic/inflammatory injury to the kidney cells that results in alterations of function
49
Causes of acute renal failure: Prerenal
Sudden and drop in BP (shock) or interruption of blood flow to the kidneys from severe injury or illness
50
Causes of acute renal failure: Intrarenal
Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply
51
Causes of acute renal failure: Postrenal
Sudden obstruction of urine flow d/t enlarged prostate, kidney stones, bladder tumor or injury
52
Acute kidney injury classification
-RIFLE -Risk, injury, failure, loss & end-stage kidney disease
53
Progression of acute kidney injury: Initiation phase
-Kidney injury evolving with reduced perfusion or toxicity -Prevent injury possible
54
Progression of acute kidney injury: Maintenance phase
-Renal injury and dysfunction resolved -Urine output is lowest during this phase -Elevated creatinine and BUN
55
Progression of acute kidney injury: Recovery phase
-Injury repaired and normal renal function reestablished -Diuresis common -Decline in creatinine and urea -Increase in CrCl
56
Acute kidney injury clinical manifestations
-Oliguria -Anuria is uncommon in acute tubular necrosis -Increased BUN and creatinine with decreased GFR -Monitor for hyperkalemia and hyperphosphatemia -Fluid retention; CHF in people with CV disease -N/V & fatigue
57
Acute kidney injury clinical manifestations: Oliguria
-3 mechanisms to contribute to oliguria: -Alterations in renal blood flow -Tubular obstruction (ie: necrosis) -Backleak
58
AKI tx
-Prevention of AKI and maintenance of perfusion are major treatment factors -Correct fluid and electrolyte disturbances, manage BP, treat infections, maintain nutrition -Remember drugs or metabolites that are not excreted -Continuous Renal Replacement Therapy (CRRT- short term dialysis)
59
AKI monitoring
-CV arrhythmias by ECG -Ins & outs
60
Pertinent labs for a patient with an AKI
-CBC -Coagulation -Electrolytes -Kidney function: Creatinine, BUN & GFR -Liver function tests -Specialty labs
61
Rhabdomyolysis
-Life-threatening complication of muscle trauma with muscle cell loss -Muscles breakdown and release myoglobin; myoglobinuria -Protein molecule is too large to excrete
62
Rhabdomyolysis etiology
-Immobility & unresponsiveness, malignant hyperthermia, infection, herbal medicines, snakebite, cowfish ingestion -Cocaine, hypernatremia, fire ant bites, & venlafaxine
63
Rhabdomyolysis clinical manifestations
-Urine becomes dark reddish brown color -CK is released in massive quantities (100x normal) -Hyperkalemia, hypophosphatemia & hypocalcemia -Increase in cr & BUN
64
Pertinent labs to monitor in rhabdomyolysis
-CBC -Coagulation -Electrolytes -Kidney function -Specialty labs
65
Reflex urinary incontinence etiologies, where it occurs & what it effects
-Stroke, MS, hydrocephalus, cerebral palsy, TBI, brain tumours, & alzheimers -Influences the detrusor motor area, lesions above C2
66
Detrusor hyperreflexia with vesicosphincter dyssynergia etiologies & where it occurs
-Disk problems, MS, transverse myelitis & Guillain-Barré syndrome -Spinal cord injury/issue between C2-T12
67
Detrusor areflexia, with or without urethral sphincter incompetence etiologies & where it occurs
-Myelodysplasia, peripheral polyneuropathies, MS, tabes dorsalis, cauda equina syndrome, herpes -Spinal injury/issue below S1
68
Mechanism of oliguria in AKI + Prerenal
Decreased renal blood flow (hypoperfusion); reduced GFR, increased proximal tubule reabsorption of Na+ & H2O; increased aldosterone & ADH secretion, increased distal tubule reabsorption of Na+ & H2O... Oliguria
69
Mechanism of oliguria in AKI + intrarenal
Renal vasoconstricition; hypoxia; renal tubular injury; cast formation; increased intratubular obstruction (increases pressure); tubular backleak; reduced GFR... Oliguria
70
Mechanism of oliguria in AKI + postrenal
Obstruction of urine flow; increased intraluminal pressure, inflammatory response & entholial cell injury; renal vasoconstriction; edema; reduced GF pressure... Oliguria
71
Kidney dysfunction often leads to...
Left sided heart complications, HTN, & respiratory compromise if severe enough
72
Obstruction in the renal pelvis or proximal ureter
Pain located in the flank radiating to the groin
73
Obstruction in the mid ureter is characterized by
Pain located in the lateral flank or lower abdomen
74
Calcium oxalate is made up of...
Crystals & struvite (struvite is smoother)
75
Diet that contributes to kidney stone formation
Valentine's day diet
76
Upper urinary tract obstructions range from...
The kidney to the bladder
77
Lower urinary tract obstructions range from...
The bladder to the urethra
78
Blank is more common in pediatrics
Nephrotic
79
Normal urine output & what happens if it decreases
-30mL/hr or 0.5-1mL/kg/hr -If voiding decreases, Cr & BUN will increase
80
Detrimental effects of hypocalcemia
Chvostek's sign, trousseau's sign, prolonged QT & CATS (convulsions, arrhythmia, tetany & stridor)
81
Chvostek's sign
Twitch of the facial muscles that occurs when gently tapping an individual's cheek, in front of the ear
82
Trousseau's sign is...
Considered positive when a carpopedal spasm of the hand and wrist occurs after an individual wears a blood pressure cuff inflated over their systolic blood pressure for 2 to 3 minutes
83
Chvostek & trousseau signs can...
Be used to determine if someone has hypocalcemia

CV487 (15 decks)

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