Renal Disorders Flashcards
if left untreated will spiral out of control to ESRD causing dialysis; some reversible if treated appropriately
All renal diseases -
How control BP
Increased fluid volume
Issues when think not getting enough fluid = increase BP and cause more damage
Renin Angiotensin Aldosterone System (RAAS)
GFR/E-GFR greater than 90
GFR - taken from 24-hour urine to see mL/hr urine\ being put through kidney through greater than 90 without proteinurea looks at normal GFR; E-GFR - serum
GFR/E-GFR <90
Renal diet/restrictions
High calories
Normal to increased fluid volume 2-4 liters per day = keep kidneys flushing
May need a dietitian consult
Modification of Diet in Renal Disease (MDRD) equation - changing renal diet depending on scenario for each pt; need have dietician seeing them
Each renal process requires differing dietary additions/subtractions.
GFR/E-GFR greater than 90
Protein spilling
High calories - prevent protein breakdown
Low protein
Low sodium - less fluid
Do not use salt substitute - contain Potassium
Potassium restrictions
Phosphorus restrictions
Magnesium restrictions
Fluid Restrictions
Prepackaged food are high in sodium as a preservitive
Down to level Dialysis requires even greater restrictions
Dietitian consultation is a must!
Lab values and fluid status guide treatment
GFR/E-GFR <90
Genetic disorder characterized by the growth of numerous fluid-filled cysts in the kidneys
Fluid-filled sacs bursting all over it; destroy the nephrons (funx unit of kidney)
Cyst growth- destroy nephrons
Pathophysiology - Polycystic kidney disease (PKD)
Abdominal distention - size of a football
Flank pain
Increased abdominal girth
Hematuria - from rupturing cyst
Constipation - Kidney failure stops lot fluid from going through kidney or reabsorped by the kidney - fluid pumped into SI and allows for stool to flow freely - stool softeners, high fiber diets to get fluid in
Clinical Manifestations - Polycystic kidney disease (PKD)
Genetic testing for family - autosomal dominant genetic disease - see if hx
Personal history - HTN
Labs
Urinalysis - shows proteinurea (glomerular destruction), BUN, creatinine, K, electrolytes, GFR - see where at on scale kidney destruction
Proteinuria
Ultrasound - cheap and easy; size kidneys within abdominal compartment
Diagnostics - Polycystic kidney disease (PKD)
Managing blood pressure
RAAS - not get fluid - not filter; RAAS still push out and raise BP - HTN
Antihypertensive
ACE-I (lisinopril) or ARB (usually only if not tolerate ACE-I)
Managing pain - opioid
Preventing constipation
Slowing progression - not compounding with HTN, hypotension, lack of fluid
Graft or shunt placement - for dialysis; temp dialysis/quinton catheter; AV graft in arm
Renal replacement
Dialysis - hemo or peritoneal
Transplant - do transplant this but no matter what have PKD - slower progressive disease; hoping new kidney with good care will outlast the pt
Med-surg - Polycystic kidney disease (PKD)
Excess Fluid Volume - BIG
Risk for electrolyte imbalance - elevated K, Mg, phosphorous, low Ca - leak from bones causing weak and brittle bones - telemetry - tall peak T waves with hyperkalemia
Health Promotion
Dietary adjustments
Weight maintenance - not overweight because super HTN, super thin - breaking down protein causing more kidney damage
Smoking cessation
Exercise - keep bowels running well
Limitation of alcohol
N. diagnosis - Polycystic kidney disease (PKD)
Weight DAILY; same amt clothing, machine, time - SAME AT HOME; best way quickly assess for gain/loss fluid
Assessment
Fluid overload - pulm edema, reg edema, HTN
Lab values (Cr, BUN, Electrolytes, GFR)
Neurological states - PKD - weaker blood vessels in head and HTN from RAAS sys can have easier stroke or hypertensive encephalopathy
Fluid/Na restrictions
Dietary restrictions
Pain Management
Medication administration - do good job with this is imp
N. interventions - teaching and do within hospital - Polycystic kidney disease (PKD)
Inflammation glomeruli
Common etiology
Post infection
Infection treated
Group A beta-hemolytic streptococcal; Autoimmune disease (SLE)
Diabetic Glomerulosclerosis
Lyses blood cells that lodge in the kidney and cause nephronal and glomeruli breakdown allowing lot diff fluids not be allowed through and other things cannot go through either; stuff cannot be reabsorped either
Acute or chronic
Complications
Hypertensive encephalopathy - loss LOC - extremely HTN and flaming things in head
Heart failure (heart failing due to ischemia or hypertrophic myopathy or heart not able to push that amount of fluid around the body)/pulmonary edema
Patho - Glomerulonephritis
Azotemia
an abnormal concentration of nitrogenous wastes in blood
Elevated BUN,CR
Edema/hypertension
Fluid volume excess - in lungs, hands, feet, HTN
Hematuria - blood cells breaking down and out into glomeruli
Proteinuria (upper limit 3 g)/Decreased serum albumin - peeing out large protein molecules - mainly albumin - swollen up really big
Severe: AKI - treated in ICU; Oliguria
CM - Glomerulonephritis
Urinalysis
Hematuria
Proteinuria
Destructive points in glomeruli
EKG
High potassium
Tall peak T waves
CXR - fluid in lungs
Laboratory values
(BUN, CR, Electrolytes, Protein)
CT/MRI
Sizing of kidneys
Biopsy
Cause
Diagnosis - Glomerulonephritis
Antihypertensive medications - protein spilling: ACE-I (lisinopril)
Immunosuppressant - SLE
Antibiotics
Diuretics - flush and get kidneys moving
EKG
Dialysis - down to certain level
Epogen - stimulate bone marrow to make RBC; to replace EPO
Laboratory values
BUN,CR, electrolytes, protein
Sometimes - E-GFR, GFR - acute process - treating with fluids and diuretics - GFR not correct
Med-surg - Glomerulonephritis
Excess Fluid Volume
Risk for electrolyte imbalance
Risk for confusion - hypertensive encephalopathy, buildup waste in blood, lower/elevated Na
Imbalanced nutrition, less than - calorie destruction - destruction protein
Acute pain
N. diagnosis - Glomerulonephritis
Administer medications
Monitor I&O/labs
Assess fluid status - not fluid overloaded/underloaded - euvolemic (equal)
Daily weight - most IMP; fastest way assess if pt gaining/losing fluid
Fluid/Na restriction
High carb diet- energy prevent catabolism of protein
Assess for pain and treat
Monitor for further complications
N. interventions - Glomerulonephritis
Serious/horrible damage to glomerular capillary membrane
Increased glomerular permeability and loss of protein in urines (big things go through it) - including albumin - urinate out large amounts protein
Due to altered immunity and inflammation
Acute versus chronic
Patho - Nephrotic syndrome
HALLMARK: Proteinuria greater than 3.5 g/day
Hypoalbuminemia - serum - inverse; gone out through renal sys; without albumin little control over oncotic pressure and goes into third space -
Massive edema/periorbital edema/anarsarka - edema upon edema
Hypertension - RAAS - certain amount pressure - left with bunch RBCs - pump sludge around body and get HTN
CM - Nephrotic syndrome
Thromboembolism - sludge - clump together easier and get clots easier
Pulmonary edema - fluids going someplace where no pressure; fluid in lungs
Hyperlipidemia - liver gets overzealous - needs protein and shooting out lot protein - pee it out - not good for kidney but at same time as pulls protein also takes fats (lipids esp) but no place to go so get seriously high lipid levels - statin: ZOCOR
Complications - Nephrotic syndrome
Urinalysis - protein in urine
Protein electrophoresis - separate out proteins by charge
Immunoelectrophoresis
Categorize type proteins and antibiodies
Needle biopsy of the kidney
Confirm diagnosis
Diagnostics - Nephrotic syndrome
Treat underlying cause - inflammatory process: decrease (steroids); immune: suppress - increased risk for infection now - hopefully treated infection before nephrotic syndrome
Slow progression to CKD
Relieve symptoms - pain management
Diuretics- decrease edema
ACEI-reduce protein loss
Antihyperlipidemic - liver
Heparin Therapy - thin blood in vessels so easier to circulate
Med-surg - Nephrotic syndrome
Excess fluid volume (extracellular) - fluid volume not inside vessels but in third space - fluid volume deficit intside vessels
Imbalanced nutrition
Fatigue - lack good O2 carrying capability
Deficient knowledge
Risk for Infection - esp immunosuppression
Activity intolerance
Disturbed Body Image
N. diagnosis - Nephrotic syndrome
Monitor I&O/edema/weight
Monitor for hypertension - reported and treated
Assess fluid/electrolyte balance
Cardiac and neuro status - thromboembolism - could cause stroke/MI/PE; hypertensive encephalopathy
Monitor for vascular dehydration
Pt education
Follow all med/dietary regimens/restrictions
Signs of complications
N. interventions - Nephrotic syndrome