Nephrology- Adults Flashcards
Renal function- pathophysiology
Filtration of blood
- removal of waste
- maintain a proper concentration of electrolytes
- acid/base balance
Renal function- cause
Regulating blood volume and BP
Producing erythropoietin
Renal function- epidemiology
Nephron- basic functionality unit of kidney
Glomerulus- site of blood filtration
Renal tubule- H20 & salt resorbed
Renal function- S/S & PE
Proximal Convoluted Tubule (PCT) - reabsorbs 60%
- 65% -> Na, K, Ca
- 80% -> Phosphate, H2O, Bicarbonate
- 100% -> Glucose (>200, will see in urine), Amino Acids
- Secretes drugs/toxins that are too big/protein bound to be filtered
- H2O reabsorbed passively - osmotic gradient
- Ammonia from glutamine (acidifies urine)
Renal function- diagnosis
Loop of Henle
- 4 segments : thin descending, thin ascending, meduallary thick ascending, cortical thick ascending
- Create concentration gradient and form concentrated urine
Renal function- labs & imaging
Distal Convoluted Tubule
- Na and Ca reabsorption
- Na - 5-10%
- Ca - 10-15%
- regulated by PTH and VitD
Renal function- treatment
Collecting Tubule
- NaCl - reabsorbed
- Bicarb - reabsorbed
- H2O - rabsorbed - urine concentration
- K - excretion
- H+ - excertion
- Urea - excreted
- Regulated Urine volume
Acute renal failure/acute kidney injury- pathophysiology
Rapid worsening of renal function
- quick rising BUN/Cr
- accumulation of nitrogenous wastes in blood
Acute renal failure/acute kidney injury- cause
Prerenal
Postrenal
Intrarenal
Acute renal failure/acute kidney injury- epidemiology
No particular race/age
10% of people in hosp
2/3 pt in ICU
1% after surgery
Acute renal failure/acute kidney injury- S/S & PE
Weakness/lethary general malaise, drowsiness Anorexia, N/V, diarrhea Pruritis Hiccups, SOB Dizziness
Signs - point toward underlying cause - prerenal - tachy, hypotensive - Postrenal - distended bladder, CVA tenderness, enlarged prostate Anuria, oliguria Change in volume/wt Change in Mental statu Edema Weakness
Acute renal failure/acute kidney injury- diagnosis
Criteria
- Abrubt (48hrs) absolute inc of serum creatinin of >0.3mg/dl above baseline
OR
- Serum Cr inc >50% w/in 7days OR
- Oligura (small amount of urine) <0.5mg/kg/hr for >6hr
Acute renal failure/acute kidney injury- labs & imaging
BMP - BUN, Cr
UA & urine microscopy - urine culuture
Urine output
Renal U/S - acute vs chronic
- small/shrunken kidney - chronic
Urine spot - osmolality, urine Na, Cr
Acute renal failure/acute kidney injury- treatment
Depends on cause Dialysis if: - serum Cr >5-10mg/dl - unresponsive acidosis - severe electrolyte disorder - fluid overload - uremic complications
Acute renal failure/acute kidney injury- prognosis
Complications - Dialysis Immediately
- Hyperkalemia
- Fluid overload
- Signs of uremia - pericarditis, altered mental status
- Severe metabolic acidosis (pH <7.1)
Prerenal Failure- pathophysiology
Most Common Cause of AKI
Reduced effective blood circulating to kidney
- absolute reduction in fluid volume OR
- Effective volume depletion - CHF, cirrhosis -> just perceived as this:: Respond by reabsorbing Na & others to inc vascular volume -> edema etc is made worse
No actual issue with Kidney
Prerenal Failure- cause
True intravascular volume depletion: hemorrhage, burns, diuretics, dehydration, GI loss, vomiting, diarrhea, anteric fistula
Dec Effective circulating volume: CHF, Cardiac tamponade, aortic stenosis, cirrhosis w/ ascites, nephrotic syndrome
Impaired renal blood flow: ACEI, NSAIDs, renal artery stenosis, renal vein thrombosis
Prerenal Failure- labs & imaging
BUN:Cr ratio - >20:1 Urine Na - <20 meq/L - not peeing it out Fractional Excretion of Na (FENa) - <1% - measure % of Na filtered by the kidney & excreted in urine Urine specific gravity - >1.020
Kidney is responding by inc reabsorption!!
Prerenal Failure- treatment
Correct underlying cause
- CHF - diurese pt
- Dehydration - IVF
- Hemorrhage - Blood + Fluid
Postrenal failure- pathophysiology
Least Common
Ureters, bladder, urethra
- block here -> renal failure
Acute -> fix it - if don’t, can be permanent
- even then - might never be perfect
Postrenal failure- cause
Nephrolithiasis BPH Obstructing tumor w/in GU system Bladder outlet obstruction Blood clots w/in urinary tract Meds Neurogenic bladder
Postrenal failure- S/S & PE
Abdominal or groin pain
Bladder discomfort
Anuria
Rectal exam
Pelvic exam
Postrenal failure- diagnosis
Post void residual >100mL -> bladder outlet obstruction
- > 300 - more worried
- U/S or Cath
U/S or Intravenous pylegram (IVP) - dilated ureters or renal pelvis
Abdominal CT - eval for mass
Postrenal failure- treatment
Relieve Obstruction!!
Cath Nephrostomy tube Stenting Lithotripsy Surgery - remove mass
Intrinsic Renal Failure- pathophysiology
One or both kidneys damaged and not working properly
Some quick, or develop over time
Intrinsic Renal Failure- cause
Acute Tubular necrosis - Most common
Nephrotoxins - NSAIDs, contrast agents, aminoglycosides, cyclosporine A, cisplatin, heme pigments (rhabdo)
Interstitial disease - acute interstitial nephritis, SLE, infection
Glomerrrulonephritis
Vascular dis - polyarteritis nodosa, vasculitis
Intrinsic Renal Failure- labs & imaging
BUN:Cr ratio - 10-15:1
Urine Na - >40 meq/L
FENa - >2%
Urine specific gravity - 1.010-1.020
Acute tubular necrosis (ATN)- pathophysiology
Most common cause of Intrinsic AKI
Acute tubular necrosis (ATN)- cause
Renal ischmia - all severe prerenal disease -> postischemic ATN
Nephrotoxins - aminoglycosides, heme pigmenst, cisplatin, radiocontrast media, pentamindine, mannitol, synthetic cannabinoids, tenofovir, IVIT
Sepsis
Acute tubular necrosis (ATN)- diagnosis
Classic UA - Muddy brown granular epithelial cell casts & free renal tubular epithelial cells
May have - hyperkalemia & metabolic acidosis
Acute tubular necrosis (ATN)- labs & imaging
BUN:Cr ratio - 10-15:1
Urine Na - >40 meq/L
FENa - >2%
Urine specific gravity - 1.010-1.020
Acute tubular necrosis (ATN)- treatment
Hold nephrotoxins
Treat underlying cause
Supportive management
Diuretics - for fluid overload
- not for oliguric
Most will spontaneously recover renal function - better if nonoliguric
Acute tubular necrosis (ATN)- prognosis
May never return to baseline
If during hosp -> higher in-hospital and long-term mortality
Acute Interstitial Nephritis (AIN)- pathophysiology
Immune mediated process of tubulointerstitial injury
- inflammatory infiltrate in interstitium
Acute Interstitial Nephritis (AIN)- cause
Meds - Cephalosporins, penicillins, allopurinol, diuretics, NSAIDs, sulfonamides
Illness - legionella, CMV, streptococcus, myocobacterium, EBC, vandida, SLE, sarcoidosis, Sjogren syndrome
Acute Interstitial Nephritis (AIN)- S/S & PE
Classic - fever, maculopapular rash, eosinophilia
Acute Interstitial Nephritis (AIN)- labs & imaging
UA - WBC, white cell casts, eosinophils, protein
Acute Interstitial Nephritis (AIN)- treatment
Stop offending med
Treat underlying cause
Glucocorticoids
Acute Interstitial Nephritis (AIN)- prognosis
Good
Glomerulonephritis- pathophysiology
Renal glomeruli damaged by deposition of inflammatory proteins in glomerular membrane
Glomerulonephritis- cause
Focal - Henoch-Scholeinpurpura, postinfectious, IgA nephropathy, hereditary nephritis, SLE
Diffuse - Postinfectious, membranoproliferative, SLE, vasculitis, rapidly progressive GN
Glomerulonephritis- S/S & PE
Heamturia
Edema of face/eyes - in morning
Edema Feet/ankles - evening
HTN
Glomerulonephritis- diagnosis
Hemeturia - tea or cola colored
UA - RBC, RBC casts, misshapen RBCs, proteins
Ranl biopsy
Glomerulonephritis- treatment
Steroids
Immunosuppressants/chemo meds
Chronic Kidney Damage (CKD)- pathophysiology
Kidney damage or dec kidney function for >3m
59% of americans develop CKD 3 or higher during life
50% w/ CKD - occurrence of AKI
Chronic Kidney Damage (CKD)- cause
DM
HTN
Chronic Kidney Damage (CKD)- epidemiology
>60yo HTN, DM, CV Fhx of CKD Recurrent UTI Prev AKI Nephrolithiasis Transplant Autoimmune Smoking
Chronic Kidney Damage (CKD)- S/S & PE
Urine Microscopy
- Squamous epithelial cell - sample contaminated
- Renal tubular cells/cast - ATN or AIN
- RBC casts - glomerulonephritis, AIN, vaculitis
- WBC casts - interstitial nephritis, pyelo, inflammation
- Fatty casts - nephrotic syndrome
- Hyaline casts - nl
- Muddy Borwn Casts - ATN
Chronic Kidney Damage (CKD)- diagnosis
Albuminuria
- specific to CKD
- nl - <30 mg/d
- Mod inc - 30-300 mg/day
- Severe inc - >300 mg/day
- Urine albumin:Cr ratio - prefered, yearly screening
- pathognomonic for kidney damage
- detects early CKD - before renal function change
- Higher -> quicker progression to failure
Early detection of med/sever inc in DM -> treat w/ ACEI or ARB and dec amount of albuminuria
- DM - target A1C 7% - prevent/delay progression CKD
U/S
- nl kidney - 10cm
- Shrunken = CKD
- differentiate b/t actue and chronic
Chronic Kidney Damage (CKD)- labs & imaging
Creatinin - product of muscle metabolism, excreted by kidneys
- Nl - 0.6-1.2 mg/dl
GFR - plasma filtration by glomerulus
- nl - >90 ml/min/1.73min2
- inulin clear is gold for meas
- MDRD and Cockcroft-Gault
- MDRD - not used for AKI
- use IBW - obese or fluid overload
Proteinuria - all types of proteins in urine
- nl - <150 mg/d
- gold - 24hr urine -> urine protine:Cr ratio
- causes - Tubular damage, diabetic nephropathy, glomerulonephritis, rhabdo, bence jones proteins
- less concerning - exercise, orthostatic porteinuria, acute sickness
Chronic Kidney Damage (CKD)- treatment
Staging - GFR and albuminuria
Meds to avoid - NSAIDs, contrast, Mg, Phophorous (Fleet’s enemas), Aluminum (Maalox, Rolaids), antimicrobials, DM meds, decongestants, antihypertensives, opioids, & gaba
RENALLY DOSE
Dialysis
- start w/ GFR 10-15 - or unable to control volume status/hyperkalemia
- ArteryVein Fistula needs 2m to mature
- Hemodialysis - 3x/week
- Peritoneal dialysis
- Continuous ambulatotry PD - 4-5x/day
- Continuous cyclic PD - machine cylces at night while asleep
Chronic Kidney Damage (CKD)- prognosis
Complications: HTN Hyperphophatemia - Sevelamer - phosphate binders - foods to avoid - berry, whole grain, dark pop, porgessed foods Hyperparathryoidism - give Vit D Anemia - Erthropoietin, aranesp, iron sup - Goal Hgb - 10-11 Hyperkalemia - Can be fatal!! - low K diet, dialysis - kayexelate - K binder Acidosis - Na bicarb Uremic Encephaolopathy
Nephrotic Syndrome- pathophysiology
Edema
Proteinuria - foamy urine
Low serum albumin
Hyperlipidemia
Nephrotic Syndrome- cause
DM
Minimal change disease
Focal segmental glomerular sclerosis
Membranous nephropathy
Nephritic Syndrome- pathophysiology
HTN
Hematuria
Proteinuria - less then nephrotic
Nephritic Syndrome- cause
Post-inf glomerulonephritis
IgA nephropathy
Membranoproliferative glomerulonephritis
Simple Cysts- pathophysiology
Thin wall without septa, calcifications or solid components
Epithelial cells from renal tubules and collecting ducts
Simple Cysts- epidemiology
M>W
>50yo
Simple Cysts- S/S & PE
“1cyst or multiple & bilateral
Asymptomatic
HTN
Rupture - hematuria, flank pain
- trauma or spontaneous
Infected - form renal abscesss
Simple Cysts- diagnosis
US or CT - incidental finding
Simple Cysts- treatment
Ruptures - IB or Tylenol for pain
Complex Cysts- pathophysiology
Septa, calcifications, solid components
Risk of malignancy
Bosniak classification system
Complex Cysts- diagnosis
CT w/ contrast
Polycystic Kidney Disease- pathophysiology
Inherited disease - cause renal cyst
- progressive renal failure from enlargment of cysts
Autosomal dominant PKD - PKD1 & PKD2
Polycystic Kidney Disease- epidemiology
50% ESRD by 60
Renal function decline by 4th ecade -> decline by 4-6ml/min/year
- progressively losing kidney function every year
Polycystic Kidney Disease- S/S & PE
HTN
Hematuria Proteinuria Renal insufficiency found on labs Flank pain - most common - due to renal hemorrhage, calculi or UTI Nephrolithiasis - uric acid stones - all the rest are Ca Oxalate Renal Cell Carcinoma
Extrarenal Manifestations: Cerebral aneurysm - SAH or ICH most serious complication - 5% younger - 20% >60yo Hepatic Cysts Pancreatic cysts Cardiac valve disease Colonic divertifcula Abdominal wal and inguinal hernia
Polycystic Kidney Disease- labs & imaging
U/S
- large kidneys and extensive bilateral cysts
- Screen for those w/ pos FHx
- US is less reliable in peds -> need genetic testing
CT or MRI - more sensitive
Polycystic Kidney Disease- treatment
HTN - rigorous control of BP - ACEI - prevents progression of renal disease and dec Dietary Na restriction - <2gm per day Statin - treat HLD aggressively - Consider a coronary heart disease risk equivalent - May preserve renal functiton
Tolvaptan - Ssamsca
- 18-55 w/ GFR >25 at high risk for ESRD
- Select via TKV, CT or MRI
- Slow progression of PKD - disease modifying
- Ensure adequate PO H2O intake
- Contra - liver failure, hypovolemia, hypernatremia, dehydrated
- SE - inc LFTs/liver tox, polyuria, polydipsia, chest pain, HA
- Promotes excretion of free water - not losing electrolytes -> lose fluid, inc urin output, dec urine osmolality, restore serum Na level
- Providerss must be registereed, shipped to pt via special pharm
Inc fluid intake
- supresses ADH levels-> inhibits cyst growth
- 3L/day
Dialysis
Kidney transplant
Pain - surgial aspiration or sclerosis of cysts
Polycystic Kidney Disease- prognosis
Die from cardiac issues
Neuro deaths - ruptured intracranial aneurysm & HTN intracerebral hemorrhage
Hypermagnesemia- pathophysiology
Plasma Mg > 2.5 mEq/L
Rare - renal impairment
Mg - is a CCB and block cardiac K channels
Hypermagnesemia- cause
Oral ingestion - laxative abuse, accidental overdose of epson salts
Mg enemas
Mg infusion - preeclampsia or eclampsia
Renal insufficiency
- Mg excreted renally -> inc levels w/ CKD worsens
- Antacids or laxatives in regular doses
Hypermagnesemia- S/S & PE
Asymptocatic -> <4
Neuromuscluar toxicity
4-6 : nasea, flushing, HA, lethargy, drowsiness, dec DTRs
6-10 : somnolence, hypocalcemia, absent DTRs, hypotension, bradycardia, EKG changes
>10: muscle paralysis -> flaccid quadriplegia, apnea, respiratory failure, complete heart block cardiac arrest
Hypermagnesemia- labs & imaging
Mg - order by itself
BMP
EKG - dimished conduction, widened QRS, prolonged PQ interval
Hypermagnesemia- treatment
Nl renal function:
- stop offending agent
- add diuretic to inc renal excretion of Mg - if still urinating
Ca gluconate - IV
- inc action potential threshold -> harder to depolarize -> more stable
Severe + renal impairment - hemodialysis
Hypomagnesemia- pathophysiology
Plasma mg <1.8 mEq/L
Hypomagnesemia- cause
Chronic diuretic therapy - loop, thiazide
Chronic alcoholism
Chronic diarrhea
Hypoparathryoidism
Nutritional deficiencies - prolonged TPN, malnutirtion
Uncontrolled DM
Chronic PPI usage - Cdiff + PPI -> gut flora changes
Hypomagnesemia- S/S & PE
Neurologic
- Tetany - Trousseau and Chvostek sign, muscle spasm, muscle cramps
- seizures
- involuntary movement
Cardiovascular - EKGs
- Mod - Wide QRS & peaked T waves
- Severe - Prolonged PR interval, QRS widening, diminished T wave
- Freq PACs and PVCs -> sustained afib
- Ventricular arrhythmias -> death
Hypomagnesemia- diagnosis
Hypokalemia & Hypocalcemia!
Clinical - if not -> 24hr urine Mg excretion or fraction excretion of magnesium on random urine
- help diff b/t Gi and renal loss
Hypomagnesemia- treatment
Severe - tetany, arrhythmias, seizures
- IV Mg Sulfate
- cont Cardiac monitoring
- Reduce dose if CrCl <30
Asymptomatic/Minimal symptoms
- PO replacement - MG Cl or Mg oxide
- > diarrhea major SE
- intracellular stores take longer to replete -> keep going to 1-2 days after labs normal
Correct underlying disease if possible
Hypercalcemia- pathophysiology
Serum Ca >10.5 mEq/L
Mild - 10.5 - 12
Severe/life threatening >14
Nl - 9-10.5
Hypercalcemia- cause
Malignancy
- ectopic secretion of PTH by tumor
- MM
- Bone Mets
Endocrine
- Hyperparathroid
- MEN
- hyperthyroid
- Pheo
- Adrenal insufficiency
Granulomatous dis - sarcoidosis, TB, histoplamosis, berryliosis, coccidiomycosis
Drugs - Thiazide, Vit A, Vit D, Estrogen, Milk-alkali syndrome, lithium
Misc - dehydration, porlonged immobilization, latrogenic, rhabdomyolysis, familial, lab error
Hypercalcemia- S/S & PE
Asymptomatic till >12
Vague/ nonspcific
non-focal bdominal pain
Constipation, fatigue, diffuse body aches, anorexia, N/V
Intravascular volume depletion - tachy, orthostatic hypotension
Anxiety, depression, confusion, hallucinations
Severe::
- lethargy, altered mental status, seizurres, coma
- Cardiac conduction abnormalities - bradyarrhthmias, sinus arrest, AV blocks, AF, VT, LBBB, RBBB
Painful bones, renal stones, abdominal groans, psychic moans
Hypercalcemia- diagnosis
EKG
- ST elevation
- Stort QT - classic - but not always seen
Hypercalcemia- labs & imaging
Total Ca
- bound and unbound Ca
Ionized/unbound Ca - better represent
- separate lab test OR
- estimate
24hr Urine
Albumin
- might have ““nl”” Ca if labumin is low or vice versa
- correct Ca for albumin levels, or do an ionized Ca level
- Corrected Ca = total Ca + (0.8 x (4-albumin))
1st Serum Ca - Elevated -> repeat ionized or total Ca + corrected albumin - HyperCa confirmed 2nd - Measure PTH - High - primary hyperparathryoid - low -> Check Vit D and PTHrP PTHrP elevated - malignancy
Hypercalcemia- treatment
Crisis - usually dehydrated
- IV access and CV monitoring
- Infuse NS ““wide open”” until BP and perfusion nl
Furosemide - NO LONGER RECOMMEND
- can worsen hyperCa if not yet volumereplete
- adversely affect hemodynamics and renal status
Osteoclast-inhibiting therapies
- Bisphosphonates - hyperCa due to malignancy
- Calcitonin - >14 and symptomatic -> dec serum Ca levels
- Glucocorticoids - dec vit D
Severe - dialysis
Crisis due to primary hyperparathyroid - urgent parathyroidectomy
Hypocalcemia- pathophysiology
Serum <8.5 mg/dL
Ionized <4.6 mg/dL
Hypocalcemia- cause
Hypoparathryoidism - genetic - postsurgical/radiation damage - Hungry bone syndrome - Infiltration of parathryoid gland - Autoimmune Drugs - Bisphosphonates - Ca chelators - EDTA, citrate, phosphate - Phenytoin - Fluoride poisoning Hypomagnesemia Vit D def PTH Resistance Renal Dis Loss of Ca from circulation - Tumor lysis - Acute pancreatitis - Osteoblastic mets - Sepsis or acute severre illness
Hypocalcemia- S/S & PE
Trosseau sign - carpal tunnel spasm after BP cuff applied for 3 min
Chvostek sign - spasm of facial muscle after tapping facial nerve in front of ear
Asymptomatic Mscule spasm orr muscle cramps Tetany Paresthesias Confusion Seizures Dry skin, brittle nails, coarse hair Anxiety, depression, dementia Laryngospasm, bronchospasm EKG - prolonged QT, flatened ST
Hypocalcemia- labs & imaging
Total Ca or Ionized Ca Serum Phosphate Vit D Serum PTH Mg BMP EKG
Hypocalcemia- treatment
Acute & severe - IV calcium gluconate
- treat emergent CV issues
- Tetany, seizures <7.5
Mild - output
- Oral Ca + VitD - Calcitriol/VitD3
FIRST - Treat any concurrent hypomg -> then treat the hypoCa
- Ca problem won’t be fixed until Mg is fixed
Hyperphosphatemia- pathophysiology
Serum >4.5 mg/dL
Hyperphosphatemia- cause
Acute
Acute Renal Failure
Rhabdo
Tumor Lysis syndrome
Acute phosphate load - excess phosphate in TPN, rapid admin of phosphate rich drugs, phosphate containing laxatives, Vit D tox
Hypoparathryoid - parathroidectomy
- infiltration of parathyroid gland, metal overload
Extracellularr shift of phosphate - lactic acidosis, ketoacidosis, respiratory acidosis, crush injuries
Chronic
CKD!!
Hypoparathryoidsm - autoimmune, gene mutations
Pseudohypoparathryoidism
Hyperphosphatemia- S/S & PE
Asymptomatic
Acute/severe -> hypoCa
- tetany, muscle cramps, perioral numbness or tingling, seizures
- Trousseau or Chvostek sign, hyperreflexia, carpopedal spasm, seizure
Uremia
- Fatigue, N/V, pruritis, SOB, sleep distrubances
Painful masses around joints, skin ulcerations, irritated conjunctiva
- ectopic calcifications
Hyperphosphatemia- labs & imaging
Serum P
PTH
Serum Ca
Vit D
Renal U/S?
Hyperphosphatemia- treatment
Acute w/ nl renal function
- Saline + Loop diuretic -> correct phosphaturia
Hypoparrthroid
- Ca + Vit D -> correct hypoCa
AKI::
Phosphate binders when level >6
- ionized Ca low -> Ca based binder - Ca Carbonate orr Ca acetate
- Ionized Ca high -> non-Ca based binder - sevelamer, aluminum hydroxide, lanthanum carbonate
Severe - P >12 or symptomatic
- Dialysis
CKD
- start tx when levels above nl
- Restrict dietary phosphate to 800-1000mg - dark colas, oysters, cheese, milk, organ meats, ice crem, chocolate, nuts/seeds
- Phosphate binders - dec intestinal phosphate absorption
- Dialysis - remove excess phosphate
Hypophosphatemia- pathophysiology
Serum <2.5 mg/dL
Hypophosphatemia- cause
Resp alkalosis Sepsis Refeeding syndrome Alcohol withdrawl Renal transplant HyperCa of malignancy Hyperparthyroid Hereditary rickets Vit D Inhibition of phosphate absorption Inadequate intake
Hypophosphatemia- S/S & PE
Asymptomatic - unless <1mg/dL Metabolic encephalopathy Proximal myopathy Impaired myocardial contractility Dysphagia Resp failure Rhabdo Hemolysis
Hypophosphatemia- labs & imaging
Serum P
Urine P::
24hr or Random speciem + calculate fractional excretion of filtered phosphate
- Exc <100 mg or FEPO4 <5% -> low renal P excretion
-» internal redistubution or dec intestinal absorption
- Ex >100mg or FEPO4 >5% -> renal P wasting
-» Hyperparathyroid, VitD def, renal tubular defect
Hypophosphatemia- treatment
Asymptomatic + P <2
- Oral P
Symptomatic
- 1-1.9 = Oral phosphate - IV if rhabdo, CNS, hemolysis
- <1 = IV phosphate - switch to PO once P >1.5
Urine P wasting - most diff to treat
- Dipyridamole QID - inc P levels
- inc renal P reabsorption
Hyperkalemia- pathophysiology
Serum K >5.0 mEq/L
- not whole body K
Dangerous electrolyte abnormality!!
98% of K is intracellular
2% in blood stream
Nl 3.5-5 - tightly regulated by kidney
Hyperkalemia- cause
Inc intake - PO supplementation, IV K Pseudophyerkalemia - Mechanical trauma from venipuncture - see red serum - true severe intravascular hemolysis - see red serum - Exercise - repeat clenching of fits durign venipuncture - Cooling or deterioration of sample - Thrombocytosis - Plt>500K - Severe leukocytosis - CLL - cells fragile Dec Excretion Renal Failure - acute or chronic - kidney ubale to filter and excrete nl Hypovolemia - dehydration, CHF, cirrhosis - low flow to kidneys Hypoaldosteronism - RTA4 - Adrenal insufficiency Intra/extracellular Shifts Any breakdown of cells - broken cells release K when they lyses - crush injury, trauma, rhabdo, TLS - PseudohyperK Acidosis - H+ moves from blood into cells exchange for K Insulin deficiency or resistance - insulin causes K entry into cells - DM
Hyperkalemia- epidemiology
Meds
- ACEI
- ARBs
- Spironalactone
- Bactrim
- K supplements
- NSAIDs, BetaBlockerrs, digitalis, Succinycholine, Amiloride
Hyperkalemia- S/S & PE
Cardiotoxicity
- inc resting membrane potential of cardiac myocite -> membrane excitability
- high levels - K causes depolarization threshold to rise -> depressed Cardiac function
Vague/varied symptoms
Asymptomatic
N/V, palpitations, lethargy, confusion, parethesias, muscle weakness, paralysis if advanced, arrhythmias/death
Hyperkalemia- diagnosis
Emergency??
- S/S - Most serious - muscle weakness/paralysis, arrhythmias
- K >6.5
- Mod >5.5 + sig renal impairment + ongoing tissue breakdown OR ongling K absorption OR signicant acidosis
Hyperkalemia- labs & imaging
K - repeat if any doubt Serum K >5 BMP - renal function EKG ABG - acidosis?
EKG
- 5.5-6.5 - Peaked T wave
- 6.5-7.5 -> flattned P wave w/ prolonged PR or absent P wave
- 7.5-8 -> Wide QRS
- > 8 -> sine wave pattern - imminent cardiac arrest
Hyperkalemia- treatment
Severe + EKG changes - IV calcium gluconate
Continuous cardiac monitoring
Options to drive K back into cell:
- Insulin + glucose
- Beta-2 adrenergic agonist - inhaled albuterol
- IV Na bicarbonate - temp, not lasting solutions
Remove K from body: GI cation exchanger - bind K in the GI tract in exchange for other cations -> excreted in feces - Na polystyrene sulfonate - Kayexalate - poop it out - Patiromer - Veltassa Diuretics - only if peeing - Loop diuretic - Lasix + saline Hemodiaylsis - HyperrKpt w/ severe renal impairment
Stop K supplements or meds that inc K
Hypokalmeia- pathophysiology
Serum K <3.5
Hypokalmeia- cause
Inc Loss
- Renal - diuretics, hyperaldostteronism
- GI - V/D
K from blood into intracellular compartment
- Insuline excess - put more into cell
- Beta agonist treatment
- Alkalosis
Hypomagnesemia - fix mg first
- Mg & K lost together - diuretics, vomiting
Renal tubular acidosis
- type 1 (distal) & type 2 (proximal) -> K wasting
Meds
- diuretis - except K sparing
- antipsychotics - risperdal, seroquel
- amphotericin B, barium or chlorquine intoxication
Very low cal diets - 200-800cal
Hypokalmeia- S/S & PE
NO patho presenting S/S
Muscle fatigue or weakness
- starts in LE -> trunk/UE -> paralysis
Cramps, rhabdo, myoglobinuria
Resp muscle weakness -> resp failure/death
GI muscle invovement - ileus, constipation, n/v
Hypokalmeia- labs & imaging
BMP Mg EKG - Flattened or inverted T wave - Prominent U waves - V4-V6 - ST depression - Prolonged QT interval -> QU - fusion of T and U wave - Arrhythmia
Hypokalmeia- treatment
Not emergent - unless cardiac menifest or <2.5
- IV K - can cause pain & phlebitis
PO K Cl - perfered for most others
Concurrent hypoMg -> needs to be repleted
Continuous Cardiac monitoring and frequent recheck of K levels
Hypernatremia- pathophysiology
Elevated Serum Na >145 mEq/L
Na is main extracellular cation
Na is charged - need pump
H2O is the only that can freely move back and forth
As Na concentration inc and dec - fluid will follow
- Ince - hypervolemia
- Dec - hypovolemia
- unchanged - euvolemia
Looking at Na in a blood draw, not the wholebody
Hypernatremia- cause
Elderly patients w/ dec thirst and dec access to fluids - highest risk
Inadequate fluid intake
Excess H2O loss - skin, GI tract
- Urine - osmotoic diuresis, diabetes insipidus, diuretics can waste water and/or Na
Diabetes insipidus
- Central - dec pituitary excretion of ADH
- Nephrogenic - dec kidney sensation to ADH
(ADH inc absorption of H2O)
Hypervolemic hypernatremia
- iatrogenic from hypertonic saline or dialysis
- Hyperaldosteronism - inc aldosterone -> inc Na -> inc H2O -> inc volume
Hypovolemic hypernatremia
- renal losses from renal disease or diuretics
- Extrarenal losses
- pt is dehydrated - look volume depleted
Euvolemic hypernatremia
- hypodipsia - dec H2O intake or thirst - lesions
- Diabetes insipidus
Hypernatremia- epidemiology
Chronic - >2 days
- less likely to provoke neurologic s/s
- underlying neuro disease -> imparired thirst
- undergo brain adaption to hyernatremia
Acute - hours
- more likely to provoke neurologic s/s
Hypernatremia- S/S & PE
Early - anorexia, restlessness, N/V
Next - progressive AMS - lethary/irritabolity 1st -> stupor or comas
Neurologic - twitching, hyperreflexia, ataxia, tremor, seizures
- when Na >160
Dec brain volume
- Acute -> rupture of cerebral veins -> hemorrhaging
- OR Demyalating brain lesion
- Chronic - gets used to dec brain mass
S/S of dehyration - dry MM, tenting/poor skin turgor, lack of tears, dec salivation, tachy, hypotension, oliguira/anuria
- ask pt to stick out tongue - good indication
Hypernatremia- diagnosis
Cause - Hx
Hypernatremia- labs & imaging
BMP
- Na >145
- if pt is alert, not dementated, has water young, and Na >150 -> check for lesion
If Etiology unclear
- Urine
- Osmolality - solute per kg in solvant
- looking for extrenal cause
- plasma>urine osmolality -> DI
Hypernatremia- treatment
Dilute fluids to correct deficit - replace ongoing losses
Chronic:
GO SLOW - if not, rapid fluid movement into brain -> cerebral edema -> seizures and coma
Dilute fluid needed - hypotonic
D5W - 1.34mL/hr x weight in kg
- 50kg pt -> 70ml/hr
- goal - lower serum Na by max of 10 mEq/L per 24hr
Recheck Na & glucose 4-6hrs after tx intitation
- correct if dec too fast/slow
Acute: D5W - 3-6mL/kg per hour - can also use 1/2 or 1/4 NS Monitor Na & glucose - Q1-2h until Na <145 - then dec rate to 1 ml/kg per hr -> reach Na of 140 - checking glucose b/c giving dextrose Goal - reduce Na by 1-2mEq/L each hour - get back into a nl range w/in 24 hrs
Hypernatremia- prognosis
High mortality - 40-60%
- w/ underlying disease
Inc M&M
- perioperative 30d mortality
- Perioperative major coronary events
- Pneumonia
- VTE
Hyponatremia- pathophysiology
Na <135mEq/L
Most common electrolyte disorder seen in hosp pts
Hyponatremia- cause
Hypervolemic
- fluid overload
- H2O is added or retained -> Na in serum is diluted
- CHF, cirrhosis, IVF, nephrotic syndrome
Hypovolemic
- H2O and Na is lost - more Na then H2O
- renal losses - duretics -»> THIAZIDES
- Extrarenal losses - diarrhea, sweating, blood loss, fluid shifts
Fluid loss can lead to hypo or hyper Na - depends on how much Na is loss
Euvolemic
Adrenal insufficiency
Polydipsia - primary or psychogenic -
- urinating large amounts
Hypothyroidism
Syndrome of inapprepriate Antidiuretic Hormone (SIADH)
- Intracranial patho - tumor, hemorrhage
- Paraneoplastic syndrome - tumor secretes ADH
- Pulm dis - cancer, COPD, interstitial lung dis
- Meds - SSRI, cyclophsophamide
Resest osmostat - Kidney cant dilute urine
- threshold to release ADH is reset downwards
Hyponatremia- epidemiology
Hypotonic - low solutes - osmolality <280
- SIADH
- Effective arterila blood volume depletion - CHR, cirrhosis, diuretics
- Endocrine d/o: hypothyroid, adrenal insufficiency
- advanced renal failure - extasy, exercise
Isotonic - nl solutes - osmolality 280-295
- Pseudohyponatremia - inc serum lipids or proteins can lead to an erroneous measurement of Na level -> get a fake low Na
Hypertonic - high solutes - osmolality >295
Significant hyperglycemia - cause a false low Na -> need to correct it
- for every 100mg above nl -> add 2ml to Na
Mannitol, maltose, sucrose retention - pulls H2O out of cells -> dilution
Hyponatremia- S/S & PE
Not symptomatic until Na is 125-130
Anorexia, N/V, lethargy, disorientation, HA, seizures
Signs - weakness, agitation, hyporeflexia, orthostatic hypotension, delirium, coma, seizure, respiratory arrest, brainstem herniatiton
Hyponatremia- diagnosis
When started:
Acute - w/in 24hr
Subacute - 24-48hr
Chronic - >48hr
Na level:
Severe - <120 - BE WORRIED
Mod - 121-129
Mild - 130-135
Hyponatremia- labs & imaging
Find underlying cause!!
1st - BMP + serum osmolality
- osmolality can further direct you -> hypotonic, isotonic, hypertonic cause
Urine osmolality & electrolytes - helpful
Further looking:: TSH Plasma cortisol ACTH stimulation test Brain/lung imaging
Hyponatremia- treatment
Identify and treat underlying cause
Symptomatic - even mild - need emerg therapy
- hypertonic saline - 100mL bolus
- raise Na by 4-6 w/in a couple of hours
- should alleviate symptoms & prevent hernia
- check Na every 2H
Non-emergency - goal to Na up slowly
Over rapid correction -> osmotoic demyelination syndrome - central pontine myeinolysis
Hypovolemic - Isotonic saline
Hypervolemic
- CHF, cirrhosis -> diuresis, fluid restrction, Na restriction – DO NOT TAKE SALT TABS
- Renal Failure -> fluid restriction, dialysis, Na restrction
Euvolemic - Fluid restriction
- SIADH - may add salt tabs and/or loop diuretic
- Demeclocycline - off label use - if dont respond to salt tabs or loop diuretics - last ditch effort
- SE: renal toxicity (esp cirrhosis), nephrogenic DI, intracranial hypertension
- Demeclocycline - off label use - if dont respond to salt tabs or loop diuretics - last ditch effort
