Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
32 Cards in this Set
- Front
- Back
|
• azotemia?
|
- ↑ serum concentration of end products of protein metabolism (usually BUN, Cr)
|
|
|
• urinalysis
o heme – detects free Hb and myoglobin as well as Hb contained within RBCs o protein – more sensitive to albumin than immunoglobulins/other proteins o microscopy – 5 RBC/HPF threshold for abN • hyaline casts – • red cell casts – • white cell casts – • granular casts – • fatty casts – |
hyaline - devoid of contents; seen with dehydration, prerenal failure, after exercise, proteinuria
red cell casts seen in glomerulonephritis, vasculitis white - renal inflammation granular -composed of cellular remnants and debris, seen in ATN fatty - occur with heavy proteinuria in nephrotic syndrome |
|
|
• serum BUN rises with?
|
– rises with renal dysfunction as well as ↑ protein intake, GI bleeding, catabolic effects of fever/trauma/infection, tetracycline and steroid use
|
|
|
• Cr to BUN ratios
|
|
|
|
• urine Na ?
|
indicates integrity of tubular reabsorptive function
|
|
|
Urinaylsis pre renal VS ATN
|
Laboratory Test Prerenal Azotemia ATN
Urinalysis Normal, or hyaline casts Brown granular casts, cellular debris Urine sodium concentration (mEq/L<20 >40 Fractional excretion of sodium (%) <1 >1 Urine/plasma creatinine ratio >40 <20 |
|
|
FENA low vs high
|
UNa <20 mEq/L, FENa <1%
Prerenal azotemia Acute glomerulonephritis Acute obstruction Contrast-induced ATN (some cases) Rhabdomyolysis-associated ATN (some cases) Early sepsis Nonoliguric ATN (10% of cases) UNa >40 mEq/L, FENa >1% ATN (90% of cases) Post renal - Chronic obstruction Diuretic drugs Osmotic diuresis Underlying chronic renal failure ATN, acute tubular necrosis; FENa, fractional excretion of sodium; UNa, urine sodium |
|
|
Hematuira causes
|
• Prerenal
o Coagulopathy o Collagen vasc dz o Sickle cell dz • Renal o Glomerular (dysmorphic rbc.s, rbc casts, proteinuria > 2+) • IgA nephropathy • Glomeruloneprhitis • Lupus neprhtis • Vasculitis: HSP, wegeners, goodpastures, sle • HUS o Non-Glomerular (normal round rbcs, no rbc casts or proteinuria) • Pyelonephritis • Renal cell ca • Polycystic kidney disease • Interstitial neprhitis • Papillary necrosis • Renal infarct or trauma • Post Renal o Ureter: stone o Bladder: Cysitis (infectious or inflammatory) or cancer o Prostate: prostatitis, BPH o Epididmis: epididymitis o Urethra: urethritis, FB, factitious, catheter placement • Factitious o Vaginal bleeding, Rectal bleeding, Automanipulation o Pigmentation (+ve dipstick but -ve microscopy) • Myoglobinuria • Hemoglobinuria • Porphyria • Look red, but dip and R&M are -ve • Foods: beets, berries, rhubarb • Drugs: pyridium, quinine, rifampin |
|
|
• red urine that is dipstick negative caused by –
|
beets, red berries, food colouring, pyridium, rifampin
|
|
|
Definitions and patterns
|
o Proteinuria = >150 mg/24hr or > 140mg/m2/24hr in kids
o Excretion of > 2gm/24hrs is usually glomerular o Excretion of < 2gm/24hrs is usually tubular, overflow, orthostatic o Nephrotic syndrome = loss of protein exceeds the livers capacity to produce albumin thus leading to hypoalbuminemia and it’s effects: edema |
|
|
Types of Proteinuria
|
• Glomerular proteinuria
o More common o Increased permeability of the glomerular capillaries o Albumin and globulins are lost into urine • Tubular proteinuria o Smaller proteins are not normally reabsorbed in the tubule o Occurs in urinary tract obstruction, sickle cell dz, interstitial nephritis • Overflow proteinuria o Excessive quantities of small proteins in the serum o Light chain Bence Jone proteins in multiple myeloma • Transient proteinuria o Exertion o Stress o Fever • Nephrotic Syndrome o Albumin loss > albumin production in the liver = hypoalbuminemia o Hypercoagulable state from AIII loss: DVT, PE o Hyperlipidemia because you lose lipid binding proteins o Edema is the hallmark of nephrotic syndrome o Adults: ankle edema, face edema, anasarca, ascites, pl. effusions o Kids: FACE EDEMA is a common presentation o Diagnosis: 24h urine for protein and Cr clearance • Urinalysis for lipiduria |
|
|
Causes nephrotic
|
Primary Renal Disease
Multisystem Disease Diabetes mellitus Collagen vascular disease Systemic lupus erythematosus Rheumatoid arthritis Henoch-Schönlein purpura Polyarteritis nodosa Wegener's granulomatosis Amyloidosis Cryoglobulinemia Drugs and Toxins Heroin Captopril Heavy metals Nonsteroidal anti-inflammatory drugs Penicillamine Others Allergens Infection Bacterial Infective endocarditis Poststreptococcal Syphilis Viral Hepatitis B Human immunodeficiency virus Cytomegalovirus Protozoal Malaria Toxoplasmosis Malignancy Solid tumors Multiple myeloma Lymphoma Leukemia Miscellaneous Hereditary nephritis Preeclampsia Malignant hypertension Reflux nephropathy Transplant rejection |
|
|
pre renal
labs |
o Urine Na < 20, FENa < 1%, Cr/BUN ratio <10
|
|
|
pre renal cause
|
Volume Loss
Gastrointestinal: vomiting, diarrhea, nasogastric drainage Renal: diuresis Blood loss Insensible losses Third space sequestration Pancreatitis Peritonitis Trauma Burns Cardiac (think causes of CHF!) Myocardial infarction Valvular disease Cardiomyopathy Decreased effective arterial volume Antihypertensive medication Nitrates Neurogenic Sepsis Anaphylaxis Hypoalbuminemia Nephrotic syndrome Liver disease |
|
|
post renal
|
o Intrarenal and Ureteral: kidney stones, sloughed papillae, malignancies, retroperiotneal fibrosis, uric acid/ocalic acid/myeloma proteins/metotrexate or other precipitants in urine
o Bladder: kidney stone, blood clot, BPH or prostate cancer, bladder cancer, neurogenic bladder (anticholinergics, sympathomimetics) o Urethra: phimosis, stone, stricture, tumor |
|
|
INTRINSIC RENAL FAILURE
|
• Vascular
o Renal afferent arteriole control: NSAIDs inhibit this o Renal efferent arteriole control: ACE-I inhibit this o Renal artery embolism or thrombosis • Endocarditis, angio, afib, trauma, atherosclerosis, fibromuscular hyperplasia, AAA or aortic dissection • Usually needs to be bilateral to cause renal failure o Small vessel • Hemolytic uremic syndrome • Malignant hypertension (now uncommon) • Sclerodermic renal crisis • Pre-eclampsia • Glomerular = Glomerulonephritis o Proteinuria is common and may be in nephrotic range o Hematuria, proteinuria, rbc casts suggest glomerulonephritis o Red cell casts = glomerular dz o Definitive dx usually requires renal bx o Primary glomerulonephritis • Post strep GN • Rapidly progressive GN • Other post infectious GN o Secondary glomerulonephritis • SLE • Endocarditis • Vasulitis: wegener’s, PAN, goodpastures, HSP • Mixed cryoglobulinemia • Interstitial = Acute interstitial Nephritis o Infectious: pyelonephritis, mono, endocarditis o Immunolo |
|
|
ATN cause
|
• Ischemic ATN: any cause of hypotension (septic, hemorragic, hypovolemic, obstructive, cardiac, anaphylactic, endocrine)
• Exogenous Nephrotoxins • Cyclosporin • Amphotericin B • Radiocontrast dye • Methicillin • Solvents: ethylene glycol • Metals: mercury • Aminoglycosides: gent • NSAIDs: afferent arteriole • ACE-I: efferent arteriole • Cisplatin • Endogenous Nephrotoxins • Myoglobin: rhabdomyolysis • Hemoblobin: hemolysis • Proteins: multiple myeloma • Crystals: uric acid, oxalic acid |
|
|
practical investigation for each type
|
o prerenal – N urine, ↑BUN:Cr ratio, ↑urine osmolality, UNa<20
o renal – abN urine microscopy o postrenal – relief with catheter |
|
|
• other organ system effects of uremia –
|
o ↓immune defenses
o pericarditis o neurologic abN (lethargy, confusion, agitation, asterixis, myoclonus, seizures) o pancreatitis o GI bleed o anemia |
|
|
Major Causes of Chronic Renal Failure
|
Vascular
Renal arterial disease Hypertensive nephrosclerosis Glomerular Primary glomerulopathies Focal sclerosing glomerulonephritis (GN) Membranoproliferative GN Membranous GN Crescentic GN IgA nephropathy Secondary glomerulopathies Diabetic nephropathy (most common) Collagen vascular disease Amyloidosis Postinfectious HIV nephropathy Tubulointerstitial Nephrotoxins Analgesic nephropathy Hypercalcemia/nephrocalcinosis Multiple myeloma Reflux nephropathy Sickle nephropathy Chronic pyelonephritis Tuberculosis Obstructive Nephrolithiasis Ureteral tuberculosis Retroperitoneal fibrosis Retroperitoneal tumor Prostatic obstruction Congenital Hereditary Polycystic kidney disease Alport's syndrome Medullary cystic disease |
|
|
uremia • homeostatic derangements –
|
volume overload, ↓↑Na, inability to handle small K load, metabolic acidosis, ↓Ca, ↑PO4
|
|
|
uremia organ problems
|
o CVS – chronic volume overload, anemia, ↑lipids, HTN, pericarditis
o resp – pleural fluid accumulation, pulmonary edema, perihilar infiltrates (bat wing on CXR) o neuro – lethargy, somnolence, seizures, encephalopathy (hiccups, asterixis, myoclonus), restless legs o GI – anorexia, n/v o derm – jaundice, uremic frost, itching o MSK – renal osteodystrophy (Ca/PO4 abN), arthritis, spontaneous tendon rupture, carpal tunnel syndrome o immune – infection secondary to immunocompromised o heme – normochromic normocytic anemia (↓Epo production), ↑bleeding time |
|
|
Reversible Factors and Treatable Causes of Chronic Renal Failure
|
Reversible Factors
Hypovolemia Congestive heart failure Pericardial tamponade Severe hypertension Catabolic state/protein loads Nephrotoxic agents Obstructive disease Reflux disease Treatable Causes Renal artery stenosis Malignant hypertension Acute interstitial nephritis Hypercalcemic nephropathy Multiple myeloma Vasculitis (e.g., systemic lupus erythematosus, Wegener's granulomatosis, polyarteritis nodosa) Obstructive nephropathy Reflux nephropathy |
|
|
• mechanisms of drug-induced renal failure –
|
o intravascular volume depletion (diuretics)
o ↓renal perfusion (antiHTN) o ↑catabolism (tetracycline) o ATN (contrast) o AIN o inhibition renal prostaglandin synthesis (NSAIDs) |
|
|
Mechanisms of Drug Toxicity in Renal Failure
|
Excessive drug level
Impaired renal excretion of drug Impaired renal excretion of active metabolite Impaired hepatic metabolism Increased sensitivity to drug Changes in protein binding Changes in volume of distribution Changes in target organ sensitivity Metabolic loads administered with drug Misinterpretation of measured serum drug level (i.e., change in therapeutic range) |
|
|
Treatment of Pulmonary Edema in Renal Failure
|
Dialysis
Hemodialysis Hemofiltration Peritoneal dialysis Oxygen Nitroglycerin Morphine Diuretics Nitroprusside |
|
|
INDICATIONS FOR EMERGENCY DIALYSIS
|
• A – acidosis that is intractable
• E – electrolytes: hyperK and to a lesser extent hyperCa and hyperMg • I – Intoxications IV STUMBLE NASA o Isopropanol, valproic acid, salicylates, theophylline, uremia, methanol, barbituates, Li, ethylene glycol, nadolol, acebutalol, sotalol, atenolol • O – fluid overload • U – uremia causing encephalopathy, pericaditis |
|
|
Dialysable toxins?
|
• I – Intoxications IV STUMBLE NASA
o Isopropanol, valproic acid, salicylates, theophylline, uremia, methanol, barbituates, Li, ethylene glycol, nadolol, acebutalol, sotalol, atenolol |
|
|
Differential Diagnosis of Hypotension in Hemodialysis Patients
|
Hypovolemia
Excessive fluid removal Hemorrhage Septicemia Cardiogenic shock Dysrhythmia Pericardial tamponade Myocardial infarction Myocardial or valvular dysfunction Electrolyte disorders Hyperkalemia or hypokalemia Hypercalcemia or hypocalcemia Hypermagnesemia Vascular instability Drug related Dialysate related Autonomic neuropathy Excessive access arteriovenous flow Anaphylactoid reaction Air embolism |
|
|
Complications of HD
|
o SOB – volume overload, cardiac causes
o chest pain – MI, tamponade o neuro abN • Disequilibrium syndrome: headache, malaise, n/v, muscle cramps, seizure; due to rapid changes of lytes/fluids • Think: structural, metabolic, disequilibrium syndrome o bleeding from dialysis puncture site – firm pressure, ensure thrill, if no thrill – consult vascular sx o infection – blood cultures, look for other sources, vanco +/- ceftriaxone o ↓BP – resolve on own, small amount NS |
|
|
Differential Diagnosis of Altered Mental Status in Dialysis Patients
|
Structural
Cerebrovascular accident (particularly hemorrhage) Subdural hematoma Intracerebral abscess Brain tumor Metabolic Disequilibrium syndrome Uremia Drug effects Meningitis Hypertensive encephalopathy Hypotension Postictal state Hypernatremia or hyponatremia Hypercalcemia Hypermagnesemia Hypoglycemia Severe hyperglycemia Hypoxemia Dialysis dementia |
|
|
• PERITONEAL DIALYSIS complciation?
|
o peritonitis – tx as outpt, leave PD catheter in; usually Staph aureus or epidermidis
• dx – peritoneal fluid WBC>100 with >50% neutrophils or +Gram stain • Treatment: • Initial loading dose of abx (vancomycin) in the ED • Followed by 10 – 14 days • Consult nephro and discuss f/u • May d/c home for tx at home if patient is well • DON’T assume that abdo pain + PD catheter are associated! Remember to rule out other causes! o catheter leaking o infection at catheter site o malfunctioning/blocked catheter o gradual volume/metabolic derangements – only seen by MD qmonthly |
