Renal Failure Flashcards

1
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Extracted Text

A

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2
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acute renal failure

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-Sudden loss of kidney function resulting in:
-Lack of Acid-base maintenance
-Abnormal fluid and electrolyte management
-Loss of ability for excrete nitrogenous waste

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3
Q

acute renal failure: signs and symptoms

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-Uremia:
-Nausea
-Vomiting
-Malaise
-Altered mentation*
-Perfusion defects:
-third spacing
-Edema
-Dizziness
-Electrolyte abnormality- Abdominal pain / ileus
-hypo/hyperkalemia -> ileus bc K influences muscle
-silent bowel
-Pericardial effusion- Pericardial Friction Rub
-Electrolyte abnormality- Arrhythmias
-Platelet dysfunction- Bleeding
-buildup of nitrogenous waste -> platelets dysfunction -> capillary bleeds
-Neurologic findings

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4
Q

acute renal failure: pre-renal

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-BUN:creatinine ratio will be > 20:1 due to increased urea reabsorption
-Look at the cause of the failure for other findings
-why isnt blood getting to kidney?
-MC cause (40-80% of ARF cases)
-Due to renal hypo-perfusion:
-Volume depletion
-Dehydration
-GI loss
-Hemorrhage
-Vascular resistance
-Sepsis, anaphylaxis
-Afterload reducing medications (ACE-I and NSAIDS combo (dilation and constriction))* -> glomerulus affected
-Renal artery stenosis- CT angiography
-Low cardiac output
-post MI
-Heart failure, PE, pericardial tamponade
-Ventilator effect from positive end pressure ventilation
-make sure urine output starts up again after surgery

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5
Q

acute renal failure: renal (intrinsic) caused

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-Accountable for 50% of cases
-Referral to:
-Nephrologist : if signs have been present for 1-2 weeks but no acute uremia -> physiological issue
-Urologist : if signs of urinary tract obstruction -> surgical/anatomical issue
-Admit to hospital when: Sudden loss of function with abnormalities that cannot be managed as an outpatient safely

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6
Q

acute renal failure: renal (intrinsic) caused -> dx and tx based on condition

A

-Acute Tubular Necrosis
-Interstitial Nephritis
-Glomerulonephritis

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7
Q

acute renal failure: post renal caused

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-Least common cause (5-10%)
-elderly male
-urologist referral usually- surgical issue usually
-Typically easily reversed
-Caused by:
-Urethra obstruction
-Bladder dysfunction/obstruction
-Ureteral obstruction B/L (or unilateral if single kidney)
-BPH in men

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8
Q

catheters

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-folley catheter-
-kuday catheter- stiffer to get past obstructions

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9
Q

acute renal failure: post renal caused -> findings and tx

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-Anuria or frequent but small volume voids
-Suprapubic pain
-Palpably or percussed distended bladder or enlarged prostate
-High BUN/creatinine ratio (like pre-renal ARF)
-Ultrasound will often find the location of obstruction!!!
-Tx:
-Bladder catheterization to allow for release of urine
-Correction of underlying cause
-Followed by saliuresis (IV saline -> flush out kidneys) and diuresis
-Prompt treatment often leads to complete reverse of injury

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10
Q

acute renal failure: approach to testing

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-When ARF is detected, the cause should always be determined so that treatment is focused accordingly
-Immediate diagnosis is critical, if you suspect:
-Decreased renal perfusion- Test for volume status and urine output
-Glomerulonephritis (intrinsic)- Test for urine sediment, serologic tests
-Urinary tract obstruction- Renal ultrasound will be diagnostic

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11
Q

diff dx of ARF

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-can take a day
-casts

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12
Q

acute renal failure: clinical criteria for staging/prognosis**

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-RIFLE/AKIN criteria
-Risk/Stage 1: 1.5 x increase in serum creatinine from the baseline OR <0.5 for 6-12hrs
-Injury/Stage 2: 2-3 x increase in serum creatinine from the pts baseline OR urine output <0.5 for > 12hr
-Failure/Stage 3- 3+x increase in serum creatinine from pts baseline OR decline of urine output to <0.3mL/kg/hr for 24 hr or anuria for 12 hours
-Correlated with Outcomes:
-Loss
-ESRD risk
-Acute Kidney Injury Network

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13
Q

acute renal failure: stage based management***

A

-stage 1- why is there renal failure…work up pt
-stage 2- start decreasing meds, consider ICU (pts change status very fast)
-stage 3- renal replacement- dialysis

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14
Q

acute renal failure: contrast induced injury

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-Changes in kidney function after administration of intravascular contrast media
-METFORMIN- BAD REACTION -> transition to sliding scale of insulin
-Prevent by prescreening for risk:
-History of prior kidney disease
-Fluid status: dehydration
-Diabetes: is the patient on metformin
-CHF/vascular disease: perfusion ability
-History of gout due to hyperuricemia
-Current use of nephrotoxic medications
-Recent exposure to IV contrast

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15
Q

acute renal failure: contrast induced injury- risk reduction

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-NON-PHARMACOLOGIC
-Use lowest dose of IV contrast possible
-Assure adequate hydration prior to and following administration
-Decrease exposure to nephotoxic medications prior to and following
-PHARMACOLOGIC
-Consider IV volume expansion with isotonic saline or sodium bicarbonate in high risk patients has renal protective effect
-Oral n-acetylcysteine may be protective if given prior -> Be aware that allergic reaction may occur in up to 48% of people (not really used)
-Avoid use of diuretics

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16
Q

acute renal failure: tx with dialysis

A

-Initiate renal replacement therapy if: Life-threatening fluid, electrolyte or acid-base abnormalities exist
-Goals of treatment with dialysis are:
-Maintain homeostasis
-Prevent further injury to kidneys
-Permit renal recovery
-Allow treatment of underlying condition to proceed without complications
-Discontinue when patient is able to maintain by their own ability -> May need to attempt trial of intermittent dialysis (ween pt off) -> need to monitor closely

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17
Q

chronic kidney disease**

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-a gradual, progressive loss of the ability to excrete wastes, concentrate urine, and conserve electrolytes
-memorize the stages

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18
Q

chronic renal failure

A

the continuing irreversible reduction in nephron number (corresponds to CKD Stages 3-5)

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19
Q

pre-renal causes of CKD

A

-Caused by HYPOPERFUSION
-Examples:
-Renal artery stenosis-Fibromuscular Dysplasia
-Extrinsic Compression- tumor, anything compressing on artery
-Decreased Renal Perfusion Pressure- CHF
-Decreased Oncotic Pressure:
-Cirrhosis
-Nephrotic Syndromes (also intra-renal)
-fibromuscular dysplasia- females < 40

20
Q

intra-renal causes of CKD

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-Intrinsic Renal Vascular Disease:
-Renal artery stenosis
-Glomerulosclerosis
-Recurrent thromboembolic disease
-hypoperfusion to kidney
-Glomerular Disease
-Nephritic/nephrotic syndromes
-Tubular and Interstitial Disease
-Nephrocalcinosis due to hypercalcemia or hypercalciuria
-Systemic Lupus Erythematosus
-Polycystic kidney disease (m/c genetic cause)
-Autoimmune

21
Q

post-renal causes of CKD

A

-Caused by Chronic OBSTRUCTION*
-Examples:
-Benign Prostatic Hyperplasia (BPH)
-Neoplasm

22
Q

summary of etiologies for chronic kidney disease

A

-pre-renal disease- CHF/cirrhosis
-post renal disease- BPH, obstructing malignancy
-intrinsic renal glomerular disease- nephritic/nephrotic
-intrinsic tubular and interstitial disease:
-Nephrocalcinosis due to hypercalcemia or hypercalciuria
-Systemic Lupus Erythematosus
-Polycystic kidney disease (m/c genetic cause)
-Autoimmune- Sjögren’s Syndrome and Sarcoidosis
-intrinsic renal vascular disease:
-Renal artery stenosis
-Glomerulosclerosis
-Recurrent thromboembolic disease- from previous renal artery dissection or aneurism
-MC CAUSES* :
-Diabetic glomerular disease
-Hypertensive nephropathy- primary glomerulopathy w/ HTN and vascular and ischemic renal disease
-Chronic glomerulonephritis

23
Q

pathophysiology: mechanisms of damage

A

-Initiating -> Initial loss of nephron mass
-Immune complexes
-Hypertension/Diabetes
-Progressive -> Maladaptive compensatory changes:
-Activation of Renin-Angiotensin-Aldosterone-System (RAAS)
-Hyperfiltration! of remaining viable nephrons
-Release of vasoactive hormones, cytokines, growth factors
-Maladaptative hypertrophy! and sclerosis
-Further reduction in renal mass
-unfunctional flow

24
Q

sodium and water homeostasis

A

-Extra-Cellular Fluid Volume (ECFV) Expansion - Dietary sodium intake > Urinary sodium excretion -> tendency for fluid overload
-decrease GFR -> increase salt/water retention -> increase vascular volume (fluid overload) -> increase hydrostatic pressure -> edema
-increase salt water retention can also lead to HTN and then HF
-increase vascular volume (fluid overload) can lead to HF
-tx-
-Dietary Salt/fluid restriction +/- diuretics (usually loops) -> if HF and edema
-Dialysis if non-responsive to diuretics
-ECFV Depletion
-Extra-renal salt/fluid loss -> impaired salt/water reabsorption -> ECFV depletion
-Common cause of “Acute-on-chronic Renal Failure”
-Excess free water consumption- Free water consumption > Urinary free water excretion -> hyponatremia

25
Q

potassium homeostasis (common issue in CKD)

A

-decrease GFR -> decreased ability to excrete K -> hyperkalemia
-exacerbation of hyperkalemia:
-increased intake
-transcellular shift
-decreased excretion
-effect of hyperkalemia:
-impaired neuromuscular transmission:
-muscle weakness
-life threatening arrythmias
-which ECG finding?
-malaise
-during hyperkalemia- gut starts taking on more excretion
-management:
-limit dietary K
-avoidance of meds that cause hyperkalemia
-dialysis in presence of ECG changes

26
Q

metabolic acidosis (issue in severe CKD- stage 4/5)

A

-CKD -> H+ retention
-effects:
-chronic metabolic acidosis - big belly, skinny limbs
-osteoporosis- via slow release of Ca hydroxyapatite from bone matrix
-protein catabolism
-muscle wasting
-tx- sodium bicarbonate PO daily

27
Q

hematologic effects of CKD: anemia*

A

-normocytic, normochromic
-Primary Cause: Erythropoietin (EPO) deficiency
-Other causes:
-Iron Deficiency
-Anemia of Chronic Disease (impaired iron utilization)
-Bone marrow fibrosis
-Treatment:
-Recombinant EPO (darbopoetin-alpha)
-decreases risk associated with repeat blood transfusions

28
Q

hematologic effects of CKD- impaired platelet function*

A

-Primary Cause: UREMIA
-Decreased activity of platelet factor III
-Abnormal aggregation and adhesiveness
-Prolonged bleeding time

29
Q

hematologic effects of CKD: impaired immune function*

A

-Primary Cause- UREMIA
-impaired WBC function
-Leukocyte suppression/impaired degranulation
-Other factors: acidosis/malnutrition

30
Q

normal calcium/phosphate homeostasis

A

-vitamin D -> 25-OH vit D -> 1-25-(OH)2 vit D -> calcium absorption from the gut -> maintenance of Ca2+ homeostasis
-slide 35, 36?
-chronic kidney disease- 25 OH vit D NORMAL (made in liver)
-1-25 (OH)2 Vit D -> ABNORMAL -> KIDNEY does not converts to active form in disease
-phosphate retention -> hypocalcemia
-hypocalemia
-causes increase PTH -> bone manifestations, uremic manifestations
-bones look cancerous but its not (brown tumors)

31
Q

bone manifestation of CKD/renal osteodystrophy

A

-hypocalcemia:
-impaired osteoid mineralization by osteoblasts
-osteomalacia- accumulation of unmineralized bone matrix
-hyperparathyroidism- increased osteoclast activity/calcium resorption from bone
-osteitis fibrosa cystica:
-abnormal osteoid
-bone marrow fibrosis
-formation of cysts- +/- hemorrhage, brown tumors
-osteomalacia + osteitis fibrosa cystica +/- osteoporosis = renal osteodystrophy
-(barely touched on this)

32
Q

causes of hypocalcemia

A

-Malabsorption
-Vitamin D deficiency
-Chronic kidney disease
-Loop diuretic use
-Hypoparathyroidism
-Pancreatitis
-Septic shock
-Hyperphosphatemia
-(barely touched on this)

33
Q

causes of hypercalcemia

A

-Milk-alkali syndrome
-Vitamin D toxicity
-Hyperparathyroidism
-Pheochromocytoma
-Thyrotoxicosis
-PTH producing tumor
-Multiple myeloma
-Lymphoma
-Thiazide diuretic use
-Lithium use
-(barely touched on this)

34
Q

chronic kidney disease: management goals

A

-Slow and delay progression to complete renal failure (stage 5)
-Treat associated symptoms of renal failure
-Avoid damage to other organ systems
-Limit disability
-usually dont get better but you can stop progression

35
Q

chronic kidney disease: primary prevention

A

-Encourage healthy lifestyles in patients
-Diet
-Exercise
-Avoidance of substance abuse
-Identifying patients at higher initial risk

36
Q

chronic kidney disease: secondary prevention

A

-After risk factors begin- Such as DM or HTN
-Initiate aggressive treatment
-Targeted drug regiments know to prevent progression to renal disease
-ACE-Inhibitors in DM -> any microalbumin in urine -> put them on
-Initiate aggressive screening for renal involvement

37
Q

chronic kidney disease: tertiary prevention/treatment

A

-Diagnosis of chronic renal impairment
-Focus shifts from prevention of disease to treating disease and/or associated effects
-Planning for future complications begins

38
Q

delaying progression of renal disease

A

-Aggressive treatment of underlying cause
-HTN
-Aggressive BP management with goals of SBP < 120 and DBP < 80
-usually requires multiple medications
-Dyslipidemia
-LDL goal of 100 (unless indicated for lower)
-Aggressive treatment of triglycerides
-DM
-Aggressive glycemic control with HbA1c goal of <7%
-*Oral hypoglycemics need to be used with caution in advanced CKD
-Metformin may lead to lactic acidosis
-Thiazolidinediones lead to increased cardiac events
-ACE-Inhibitors are encouraged for diabetics with proteinuria *
-Recent studies have not shown clear renal benefits in very early stages
-Monitor Potassium level
-Avoid ACE-I in advanced CRF (stage 4-5) *
-Avoid with Renal Artery Stenosis
-Avoid medications/treatments that may further damage kidney function
-Commonly used medications/treatments that cause renal dysfunction include:
-IV contrast for CT
-NSAIDs
-Aminoglycosides

39
Q

management of chronic kidney disease

A

-renal replacement therapy:
-preparation of kidney replacement -> stage 4- GFR 15-29
-kidney replacement tx -> stage 5- GFR < 15
-pts should be educated to ds progression and anticipatory care throughout care
-dialysis:
-hemodialysis
-peritoneal dialysis
-renal transplantation:
-best potential for complete recovery
-typically dialysis tx is needed prior to transplant option

40
Q

chronic renal disease morbidity/mortality

A

-Hospitalization and increased morbidity:
-Dialysis patients average 2 hospital admissions/yr
-Patients s/p renal transplant average 1 admission/yr
-5 year survival ESRD = 35%
-Coupled with DM = 25%
-Transplantation increases the survival of patients with stage 5 CKD significantly
-MC cause of death in CKD patients is Cardiovascular Disease**
-MC cause of chronic kidney disease -> DM!!!

41
Q

dialysis

A

-HEMODIALYSIS
-MC form of renal replacement in the US
-Requires vascular access
-Complications:
-Hypotension is most common
-Muscle cramping and anaphylatoid reactions can occur
-PERITONEAL DIALYSIS
-Infusion of a dextrose containing solution into the peritoneal cavity and then allowed to dwell for a period of time
-Access by peritoneal catheter
-Complications:
-Peritonitis
-Metabolic complications

42
Q

hemodialysis

A

-MC form of renal replacement
-Move solutes across a semi-permeable membrane by:
-Diffusive clearance
-Ultra-filtration
-Solvent drag
-access:
-*AV fistula – preferred access form
-AV graft
-Venous catheter(least preferred)

43
Q

renal transplant

A

-Start planning for transplant options when planning for renal replacement with dialysis
-Donor Selection
-Live- Typically family relative with matched HLA
-Deceased- Testing to ensure HIV/Hepatitis negative serology
-Malignancy/failure risk

44
Q

MC opportunistic infection in renal transplant

A

-Peritransplant (<1 month)
-Wound infections
-Herpesvirus
-Oral candidiasis
-Urinary tract infection
-Early (1–6 months)
-Pneumocystis carinii
-Cytomegalovirus
-Legionella
-Listeria
-Hepatitis B
-Hepatitis C
-Late (>6 months)
-Aspergillus
-Nocardia
-BK virus (polyoma)
-Herpes zoster
-Hepatitis B
-Hepatitis C

45
Q

post transplant complications

A

-Malignancy- 5-6% of patient on immunosuppressive therapy will develop cancer
-Hypercalcemia
-Hypertension
-Hepatitis -Immunosuppressive therapy decreases immune control of Hepatitis B and C (test prior to transplant to counsel)

46
Q

outcomes following renal transplant

A

-Improved quality of life and decreased disability when compared to dialysis
-Improved life expectancy
Compare to 5 year survival rate of 34% in dialysis population
-Highest mortality post transplant is in the 1st year