renal Flashcards

1
Q

concentration and dilution

A
Water, Sodium and Chloride
Urea
Catecholamines
Renal Hormones
Antidiuretic Hormone                                                                               
Natriuretic Peptides
Vitamin D
Erythropoietin
Renin- Angiotensin 
Aldosterone
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2
Q

male assessment (subjective)

A
Frequency, urgency and nocturia
Dysuria
Hesitancy and straining
Urine colour
Past GU history
Penis: pain, lesion, discharge
Scrotum, self-care behaviors, lump
Sexual activity and contraceptive use
STI Contact
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3
Q

female assessment (subjective)

A
Menstrual History
Obstetrical History
Menopause
Self-Care Behaviors
Urinary symptoms
Vaginal discharge
Past history
Sexual activity
Contraceptive use
STI Contact and Risk reduction
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4
Q

renal assessment objective

A

Inspect and report any abnormal findings to the physician
Urine
Continent or Incontinent
Fluid Balance
24 hour fluid balance and how much they are voiding within your shift
Lab Values(Which Lab Values are most Pertinent to Renal?)
Electrolytes
Creatinine and BUN
sodium
potassium

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5
Q

obstruction

A

There is an interference with flow of urine any where along the urinary tract
May be anatomical of functional
Flow is impeded  dilation of the urinary system increase risk for infection compromises the renal system

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6
Q

upper urinary tract obstruction etiology

A

Stricture
Congenital compression of a calyx, ureteropelvic or ureterovesical junction
Compression from an aberrant vessel, tumor or abdominal inflammation and scarring
Ureteral blockage form stones
Malignancy of the renal pelvis or ureter

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7
Q

upper urinary tract obstruction pathophysiology

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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8
Q

response to relief of upper urinary tract obstruction

A

Diuresis (called post-obstructive diuresis)
Restoration of fluid and electrolyte imbalance
May be further complicated by severe post obstructive diuresis

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9
Q

upper urinary tract obstruction 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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10
Q

kidney stone pathophysiology

A

Stone formation requires:
Super-saturation of one or more salts in urine
Precipitation of salts from liquid to a solid state
Growth through crystallization or agglomeration
Presence of absence of stone inhibitors

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11
Q

stone formation is influenced by

A
Age, gender, race
Geographic location seasonal factors
Fluid intake
Diet
Occupation
Genetic predisposition
Previous UTI
HTN
Obesity
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12
Q

clinical manifestations of kidney stones

A

Moderate to severe pain
located in the flank and radiating to the groin
lateral flank or lower abdomen pain
Urinary urgency, frequency and urge incontinency
Nausea and vomiting
Gross or microscopic hematuria

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13
Q

kidney stones evaluation and diagnosis

A
Presenting Symptoms
Patient history
Assessment
Imaging studies
Functional study of renal pelvic and ureteral pressures
Urinalysis (including pH)
Diagnostic Tests
X-Rays, CT scan or ultrasound
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14
Q

lower urinary tract obstructions

A

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

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15
Q

etiology of lower urinary tract obstruction

A

Neurogenic
Anatomic alterations
Or Both Neurogenic and Anatomic

Primary symptom is incontinence*

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16
Q

lower urinary tract obstruction neurogenic bladder

A

Bladder dysfunction caused by neurological disorders

Lesion above C2 or above the pontine micturition center result in detrusor hyperreflexia
Loss of coordinated neuromuscular contraction and overactive or hyperreflexive bladder function

Likely a lesion located in the upper motor neurons of the brain and spinal cord between C2 and S1 results in detrusor hyperreflexia with vesicosphincter dyssynergia
Loss of bladder muscle contraction and overactive bladder

Lesions can also occur in the sacral area of the spinal cord or peripheral nerves below S1 results in detrusor areflexia
Results in an underactive, hypotonic or flaccid bladder function with loss of sensation

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17
Q

lower urinary tract obstruction overactive bladder syndrome

A

Syndrome of detrusor over-activity
Characterized by urgency with involuntary detrusor contractions during the bladder filling
May be spontaneous or provoked
Affects men, women and children
Diagnosed by symptoms and assessment confirmed by urodynamic studies
Treated with antimuscarinics or surgery

18
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
Diagnosis and Treatment
History and physical assessment associated with symptoms
Diagnostic tests to identify correct issue

19
Q

urinary tract infection

A

Inflammation of the urinary epithelium caused by bacteria from the gut
Can occur anywhere along the urinary tract

20
Q

UTI classified by location or complicating factors

A

Cystitis
Pyelonephritis
Uncomplicated UTI
Complicated UTI

21
Q

cystitis

A

Inflammation of the bladder
Most common site of UTI*
Mild inflammation leads to hyperemic mucosa
More advanced may show hemorrhage, pus formation, or exudate on epithelial surface of the bladder
Most common infecting microorganism is Esherichia coli (E. Coli)
Clinical manifestations: asymptomatic to frequency, urgency, dysuria and suprapubic and low back pain, hematuria, cloudy and foul-smelling urine
Diagnosed by assessment, symptoms and urinalysis
Treatment: antibiotics
May lead to urosepsis and septic shock; Emergency Situation!!!

22
Q

acute pyelonephritis

A
Infection of one or both upper urinary tracts (ureter, renal pelvis and interstitium)
Etiology:
Kidney stones
Vesicoureteral reflux
Pregnancy
Neurogenic bladder
Instrumentation 
Female sex trauma
23
Q

acute pyelonephritis pathophysiology

A

Pathophysiology:
Infection spreads
Tubules most affected
Rarely causes renal failure

24
Q

acute pyelonephritis clinical manifestations

A

Onset is acute
Fever
Chills
And flank or groin pain
Similar to symptoms of UTI including frequency, dysuria and costovertebral tenderness
Older adults have low grade fever and malaise

25
Q

acute pyelonephritis diagnosis and treatment

A

Blood cultures and urinary tract imaging
Treated with antibiotic therapy
May require surgical intervention to remove lesions

26
Q

glomerulonephritis etiology

A
Inflammation of the glomerulus
Etiology:
Infection
immunologic abnormalities (most common cause)
Ischemia
Free radicals
Drugs
Toxins
Vascular disorders
Systemic disease (ie: diabetes mellitus and lupus)
27
Q

glomerulonephritis pathophysiology

A

Epithelial layer of the glomerular capillary membrane is disturbed usually due to streptococcal infection
Changes in permeability occur
Basement membrane of the epithelial becomes thickened

28
Q

glomerulonephritis clinical manifestations

A

Nephrotic syndrome
Nephritic syndrome
Acute or chronic Kidney Failure

29
Q

clinical manifestations of glomerulonephritis

A
Clinical Manifestations:
Insidious or sudden
Occur 10 to 21 days post infection Impetigo or pharyngitis)
Hematuria
RBC casts,
Proteinuria
Decreased GFR and elevated Creatinine and BUN
Oliguria
HTN
Edema around the eyes or feed and ankles
Occasional ascites or pleural effusions
Treatment:
No specific treatment and patients resolve without significant loss of function
30
Q

acute kidney injury

A

Sudden decline in kidney function with decrease in glomerular filtration
accumulation of nitrogenous waste products in the blood
Elevated Creatinine and BUN

31
Q

acute kidney injury patho

A

Extracellular volume depletion
Decreased renal blood flow
Toxic/inflammatory injury to the kidney cells that results in alterations of function

32
Q

acute kidney injury classification

A
RIFLE
risk 
injury 
failure
loss 
end-stage kidney disease
33
Q

initiation phase of AKI

A

Kidney injury evolving with reduced perfusion or toxicity

Prevention of injury possible

34
Q

maintenance phase of AKI

A

Established renal injury and dysfunction resolved
Urine output is lowest during this phase
serum creatinine and blood urea nitrogen both increase

35
Q

recovery phase of AKI

A

Injury repaired and normal renal function reestablished
Diuresis common
Decline in serum creatinine and urea
Increase in creatinine clearance

36
Q

clinical manifestations of AKI

A

Oliguria
3 mechanisms to contribute to oliguria:
Alterations in renal blood flow
Tubular obstruction (ie: necrosis)
backleak
may begin within 1 day after hypotensive event and last for 1-3 weeks
Anuria is uncommon in acute tubular necrosis
Increase BUN and Creatinine with decrease GFR
Hyperkalemia and hyperphosphatemia to be monitored
Fluid retention  CHF in people with CV disease
Nausea, vomiting and fatigue

37
Q

AKI treatment

A

Prevention of AKI and maintenance of perfusion are major treatment factors
Correct fluid and electrolyte disturbances
Manage blood pressure
Treat infections
Maintain nutrition
Remember drugs or metabolites that are not excreted
Monitoring CV arrhythmias by ECG
Continuous Renal Replacement Therapy (CRRT- short term dialysis)
Strict monitoring of intake and output

38
Q

rhabdomyolysis

A

Potential life-threatening complication of severe muscle trauma with muscle cell loss
Muscles breakdown and release myoglobin myoglobinuria
Protein that is a big molecule that is too large to excrete

39
Q

etiology of rhabdomyolysis

A
Immobility and unresponsiveness
Malignant hyperthermia
Infection
Herbal medicines
Snakebite
Cowfish ingestion
Cocaine
Hypernatremia
Fire ant bites
Venlafaxine
40
Q

clinical manifestations of rhabdomyolysis

A
Urine becomes dark reddish brown color
Creatine Kinase (CK) is released in massive quantities (100x normal)
Hypokalemia, hypophosphatemia
Increase in creatinine and BUN
Hypocalcemia
41
Q

treatment of rhabdomyolysis

A

Identify cause and treat it
IV Fluids
Dialysis (CRRT)
Correction of electrolyte imbalances