HLK week 5 Flashcards
AKI
- definition: over hours to days, decrease in GFRby 25-50%, decrease in SrCr by 75-100%
- S/S: oliguric, normal to large size kidneys, hypervolemia, , maybe uremic syndrome for severe
- MGMT: determine cause and treat, d/c nephrotoxic drugs
Azotemia
- definition: build up of waste products in blood, mostly urea
- s/s: myoclunus, oliguria, fatigue, asterics
uremia
- definition: severe build up of urea
* s/s: urinous breath, pericardial rub, malaise, altered LOC, pale conjuctiva, HTN, SOB
CKD
- definition: over 3 months of kidney dysfunction, decreased GFR
- s/s: asymtomatic until later stages, small kidneys
- causes: diabetes and HTN/ CVD
- staged 1-4, then ESRD
- stage 1: normal or elevated
- stage 2: 60-89
- stage 3a: 45-59
- stage 3b: 30-44
- stage 4: 15-29
- ESRD:
AKI types
- Types: pre-renal, renal, post renal
- most common type: pre-renal
- intrinsic: tubular necrosis, interstitial nephritis, acute glomerulonephritis
- Post-renal: obstruction, males, anticholinergic
CKD Bone changes
- CKD can cause hypocalcemia, hyperphosphorous,
- osteitis fibrosa cystica: hyperparathyroidism (osteoclast activation)MOST COMMON, bone pain, proximal muscle weakness
- osteomalacia: bones done’ mineralize bone pain, or asymptomatic, difficulty walking
- adynamic bone disease: opposite of fibrosa cystica
Kidney transplant life expectancy
living donors: 1-5 yr: 95-80%
Deceased donors: 1-5 yr: 89-66%
nephrotic characteristics
- PROTEINuria! >3 g day in urine
- so no protein in blood – hypoalbumineia
- massive edema
- can be normotensive
- hyperlipidemia
- mechanical issue
- frothy urine
nephritic characteristics
- periorbital and scrotal edema
- HTN!!!
- RBC casts in urine
- injury/ infection issue– angry
- RPGN is severe end
- 1-3 g/ day proteinuria
nephritic examples
post infectious GN -- strp IGA nephropathy-- Berger's-- Asi---- Henouch goodpastures --basement membrane SLE Hep C Pauci-immune --/ all polyangititis interstitial nephritis
nephrotic examples
minimal change disease -- common in kids focal segmental glomerular sclerosis diabetic nephropathy HTN nephropathy amyloidosis HIV assc. nephropathy
goodpasture
basement membrane men>women, think young men 30-40 pulmonary renal syndrome, alveolar hemmoraging/ hemoptysis, RPGM URI can preceed treat w/ plasma exhance
IGA nephropathy (nephritic)
Asians 1-2 days after URI gross hematuria asymptomatic to RPGN can resolve or progress treat w/ ACE/ARB
post-infx GN (nephritic)
1-3 weeks after infx
strep!
hematuria, proteinuria, NEPRHITIC Symptoms
HUMPs on microsopy
treat : supportive, anti-HTN, NO steroids
henouch (nephritic, IGA type)
kids
palpable purple purpura on legs, buttocks
males
GI symptoms, arthralgia
treat w/ aspirin (only time you treat kids w/ this), Rituimab
pauci-immune (nephritic)
all the polyangiitis' ANCA+ can present w/ nodules hemptysis -> hospital refractory sinus infx= wegeners treatment= high dose corticosteroids, plasma exchange
minimal change (nephrotic)
kids 90% of GN in kids in this treat w/ steroids no podocytes in adults= secondary = lymphoma, lithium, NSAIDs
Focal Segmental (nephrotic)
adults no podocytes FOCALLY genetic: Africans treat: symptoms diuretics/ ACE/ARB, statins can develop ESRD
Analgesic Nephropathy (intrinsic AKI)
too many analgesics
s/s: sloughed papilla in urine, ringed shadow sign, volume depletion, hematuria, anemia, sterile pyruia, hyperkalemia. tubular and papilla damage
treat w/ d/c offending rx
intersitial nephritis (intrinsic AKI)
3.3.3.
3 causes: drugs, autoimmune, infx
of immune, 3 S;s: SLE, Sjogrens, sarcoidosis
triad presentation: arthalgias, fever, rash
WBC casts, hematuria, pyuria, proteinuria
treatment: dialysis, treat underlying cause
PKD (intrinsic AKI)
genetic
lots of cysts on the kidney
s/s: ABD flank pain, hematuria, kidney stones, UTIs, family history, HTN
treat: bed rest, supportive, ADH antagonists
acute tubular necrosis (type of AKI)
most common intrinsic AKI
muddy brown casts
Uremia: pericardial effusion/ tamponade, arrhythmias
hyperkalemia, hyperphosphatemia,
treat: diuresis, dialyze, plasma filtration, protein restiction
RAS (prerenal AKI)
renal bruits fibromuscular dyphasia in young woman -- HTN women under 40, beads on a string, asymetric kidney size pre-renal AKI new onset HTN, refractory HTN treat- angioplasty,
diabetic nephropathy
most common cause of ESRD
Lupus nephritis (nephritic)
can be presenting cause of SLE
immune complex deposit? we don’t know – direct cell mediated injury
HTN nephropathy (nephrotic)
HTN nephrosclerosis, from CHRONIC HTn, more common in Africans
amyloidsosis (nephrotic)
protiens clog shit up
cardiorenal syndrome
heart dx causes kidney dx or vice versa
pulmonary renal syndrome
like goodpastures of SLE, wegeners, syndromes involving lung and kidney
hepatorenal syndrome
AKI w/ liver disease, usually portal HTN, poor prognosis
HIV assc nephROathy
African descent thing, can be presenting symptom of HIV
hematuria definition
microscopic= 3 RBC/ HP field on more than 1 occasion
macroscopic= smokey urine
90% non-renal cause
hematuria work up
urine dipstick if + then to UA centerfuge cytology RBC casts= glomerulonephritis CT, ultrasound
hematuria Ddx
cancer
glomerular: Nephritic syndromes
non-glomerular: cysts, stones, intersitial nephritis,
lower GU tract
proteinuria
> 3 g/ day = nephrotic
1 mg/ day = proteinuria
workup: dipstick, UA, protein/cr ratio, kidney biopsy
Function proteinuria: no tx benign
Overload proteinuria: too many proteins like BenceJones
glomerular proteinuria: diabetic nephropaty
tubular proteinuria: ATN, anything intrinsic
creatinine
muscle byproduct, how we estimate GFR
anion gap
normal is 12 +/- 4 –
tells you if acid/base balance is compensated
BUN
blood urea nitrogen– made in liver, urea is nitrogenous waste product from ammonia
measures level of nitrogen in blood indirectly by measuring urea
BUN/CR ratio
only done if BUN OR CR is elevated
hypo natremia: Isotonic
causes: pseudohyponatremia d/t hyperlipidemia, hyperproteinemia, hyperglycemia
hyponatremia: hypertonic
caused by hyperglycemia, mannitol, contrast agents
hypo natremia: hypotonic
causes
check volume status:
hypovolemic: diarrhea, dehydration, hemmohage
Euvolemic: SIADH, beer potomania, ecstacy, polydipsia
hypervolemic: CHF, Cirrhosis
hypo natremia s/s
HA, nausea/ vomitting, malaise, cerebral edema, CNS abnomalities
serum concentration
hypernatremia
always hypovolemic, hyperosmolality
s/s: dehydration! orthostatic hypotension, oliguria, lethargy, irritability, seizures
serum concentration >145
hypo kalemia
U waves,
diuretics, laxitive abuse, diarrhea, Increased aldosterone, polyuria
s/s: muscle weakness, fatigue, constipation, rhabdomyalisis, flacid paralysis
have to correct hypomagnesia to fix this
serum concentration
hyper kalemia
Sharp T waves, wideQRS, PR prolongation,
hypoaldosteronisism, CKD 4/5, ACE/ARBs
arrhtmymias, muscle cramping, weakness, parathesias,
concentration >5
hypo calcemia
s/s perioral numbness, paresthesias, chvostek/ trousseau signs, muscle tetany
prolonged QT interval, torsades
common cause – CKD.
alsohypoalbuminia, respiratory alkalosis, decreased active vitamin D, hypoparathyroidism
concentration
hyper calcemia
causes: hyperparathyroidism, malignancy
s/s: stones, bones, groans, moans, psychiatric overtones
mild >10.5
hypo phosphatemia
causes: alcoholism, alkalosis, diuretics, re-feeding syndrome
s/s/: respiratory failure, muscle weakness, hypoxemia, enchepholapathy
concentration
hyper phosphatemia
causes: CKD, malignancy
s/s: hypocalcemia same
concentration >4.5
hypo magnasemia
causes: diminished absorption/ intake, alcoholism, diabetes, pregnancy,
s/s: tremors, muscle weakness, cramps, babinski, nystagmus, tachycardia
serum
hyper magnasemia
causes: antacid abuse, advanced CKD
s/s: mental obtundation, decreased DTRs, flacid paralysis, hypotension, cardiac arrest
serum >3
