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69 Cards in this Set
- Front
- Back
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inevitable progression of chronic kidney failure can be slowed by
(3) |
low protein diet
blood pressure control ACEs and ARBs |
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the three leading causes of chronic kidney disease
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diabetic nephropathy
hypertensive nephropathy glomerular disease |
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(chronic renal disease)
what are two things that cause intact nephrons to increase their SNGFR as part of their compensatory response to sustained GFR reduction? |
increased capillary surface area
dilation of afferent |
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what 3 bolded terms does Lenny use to describe what the intact nephrons do to compensate against sustained reductions in kidney GFR
[the 1st one he lists helps cause the other two] |
compensatory hypertrophy
increased SNGFR increased reabsorptive and secretory capacities of the tubules |
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(the compensatory response against sustained GFR reductions)...
what 3 things do the proximal tubules of intact nephrons do? ( (in the face of sustained GFR reduction) |
they increase their:
cell size and number surface area reabsorptive and secretory capacities |
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when GFR decreases by 50%,
plasma creatinine and BUN levels do what? why? |
double
because they are primarily handled by filtration alone |
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what is plasma BUN and creatinine's response to GFR reduction ?
what are 4 solutes (or pairs of solutes) Lenny lists, that the kidney can keep within their reference range until GFR is chronically reduced to ____ |
BUN, creatinine
--double if GFR decreases by 50% - - - - - - - - - - - - - - - - - mL/min: phosphate < 25 potassium < 10 plasma pH < 20 Na+ and Cl- < 2-3 |
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FGF-23 and PTH block phosphate reabsorption where in the nephron?
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proximal tubules
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plasma [phosphate] is kept in normal range until GFR < 25 mL/min
what mediator makes this possible? what's its mechanism? |
increased production of FGF-23 and PTH
they block phosphate reabsorption in the proximal tubules |
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plasma [K+] is kept in normal range until GFR < 10 mL/min
what mediator? mechanism? |
aldosterone
increases K+ secretion increases colon excretion of dietary K+ |
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what drugs can cause problems with plasma K+
if given to chronic kidney disease patients? do they cause hyper- or hypo-kalemia? mechanism for their mischief? |
K+ sparing diuretics
ACEs, ARBs hyperkalemia they inhibit aldosterone |
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(chronic kidney disease)
how is plasma pH maintained in the reference range until GFR < 20 |
glutamine synthesis
ammonium secretion |
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in chronic kidney disease, Na+ is normal until GFR < 2-3
increased production of ____ helps keep sodium normal? three things that result? |
PGE2
natriuretic peptides Na+ reabsorption decreases --> Fe Na increases to 30% --> nocturia |
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ability to excrete H2O is maintained until GFR < ____
which breaks down first: the ability to concentrate the urine or the ability to dilute it? what happens to urine osmolality at GFR < ____ |
< 5
the ability to concentrate the urine < 20, urine osmolality is the same as plasma's |
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why is the ability to concentrate urine impaired, at low GFR?
(the answer is 4 lines long) |
solute diuresis--
high [ ] of urea and creatinine in the tubules pull H2O into the tubules and prevent ADH from mediating H2O reabsorption |
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morphologic manifestation of ESRD is _
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small shrunken kidneys
with cortical thinning |
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in chronic renal disease,
what are the two compensatory things the intact nephrons do, that cause them to become injured? |
high SNGFR
high ammonia concentration [? they make more ammonia to get rid of acid. maybe the buildup of nitrogenous wastes also elevates ammonia. ?] |
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the high SNGFR of intact nephrons ultimately damages them
~ 2 mechanisms? 3 pathology terms to describe the resulting injuries |
high pressure -->
hyperfiltration of protein and other macromolecules. these deposit in the mesangium together with ATN II--> mesangial proliferation tubulointerstitial fibrosis ------------------------ PGE2 (afferent dilation) ATII (efferent dilation) --> glomerular epithelial cell injury --> focal glomerulosclerosis |
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intact nephrons get damaged when trying to compensate for chronically decreased GFR.
what immunologic factor causes damage? how does it cause damage? what does it damage? |
high concentration of ammonia
(in the tubules and interstitium) activates alternative complement --> tubular injury |
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Uremic syndrome mechanisms page:
what are the 5 different categories of chemicals that are over- or under-produced? what are the 3, 2, 3, 2, 3 chemicals listed in those categories? |
increased nitrogenous wastes
--urea --aminoguanidine --uric acid increased: --amino acids and small peptides --e.g. insulin 3 vasoactive substances --renin --angiotensin II --endothelin-1 decreased hormone production: --erythropoetin --vitamin D increased hormone production: --aldosterone --ANP --PTH |
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PTH is a potent _____
what's the 6 word mechanism? |
neurotoxin
increases intracellular Ca++ in excitable tissues |
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(uremia mechanisms page)
excess of these 4 things --> hypertension and coronary artery disease/atherosclerosis |
insulin
vasoactive substances: --renin --angiotensin II --endothelin-1 |
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(uremic syndrome)
what's a proposed mechanism for the elevated triglyceride levels? elevated triglycerides cause what? |
hyperinsulinemia-->
impaired action of lipoprotein lipase which elevates triglycerides accelerated atherosclerosis |
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uremic syndrome
what are the 8 big cardiovascular phenomena or clusters of phenomena |
elevated triglycerides
systemic inflammatory state --> coronary artery disease elevation of baseline troponin, CPK, CPK-MB hypertension - - - - - - - - - - - - - - - - - - - - diastolic dysfunction, concentric LVH, cardiac fibrosis pericarditis systolic dysfunction blowing diastolic murmur (pulmonic regurgitation) |
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what are the two main causes of hypertension in uremic syndrome?
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increased intravascular volume
(80% of cases) increased renin production (most of the rest) |
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hypertension in uremic syndrome causes what?
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it's the chief contributing risk factor for LVH
it also causes congestive heart failure |
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blood pressure in uremic syndrome can be controlled by
(4) |
loops
ACEs ARBs dialysis when creatinine clearance is below 5% |
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uremic pericarditis
clinical presentation |
precordial chest pain that
worsens with breathing unlike other types of pericarditis, ST segment elevation is frequently absent |
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uremic syndrome...
5 things that contribute to the development of congestive heart failure |
systemic cytokine elevation
volume overload hypertension chronic anemia myocardial ischemia (?from atherosclerosis?) |
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uremia
GI symptoms |
anorexia
nausea vomiting GI bleeding |
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two causes of GI bleeding in uremia
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upper GI
--superficial mucosal erosions lower GI --uremic colitis --angiodysplasia |
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angiodysplasia
what is it? where does it occur? symptoms? as defined by Goljan p. 344 |
dilation of mucosal and submucosal venules
in cecum and right colon hematochezia |
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hematochezia is
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bright red, bloody stools
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what are the 9 categories of physiological derangement
in uremic syndrome? |
cardiovascular
GI hematologic neurologic metabolic and endocrine acid-base dermatologic immunologic pulmonary |
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uremic syndrome:
4 mechanisms that cause anemia |
Lenny: the major mechanism responsible for anemia is epo.
decreased EPO decreased RBC survival GI bleeding and marrow fibrosis |
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what are the coag results from platelet dysfunction in uremic syndrome?
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PT, PTT are normal
bleeding time is prolonged |
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what are the 4 types of neurologic abnormality seen in uremic syndrome
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distal symmetric polyneuropathy
uremic encephalopathy autonomic dysfunction myopathy |
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uremic encephalopathy sxs
at what GFR? |
AAMC --> DOCS
agitation *asterixis* mood alteration concentration, memory impairment when GFR < 10, it progresses to... dementia obtundation coma seizures |
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how might the myopathy of uremic syndrome help you make the diagnosis?
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it will not help!
muscle wasting will cause plasma creatinine to be lower than expected for a given low GFR |
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muscle wasting in uremic syndrome (once the muscles are totally gone, not while they're breaking down)
causes our plasma creatinine to under/overestimate GFR? since we have chronic kidney disease, we're expecting plasma creatinine and creatinine clearance to be high or low? do we have lower or higher than expected plasma creatinine and creatinine clearance? |
we overestimate GFR
we probably have high plasma creatinine but it's "lower than we would expect" given that we have reduced GFR we probably have low creatinine clearance but it's higher than we would expect given that we have reduced GFR |
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(uremic syndrome)
metabolic and endocrine abnormalities: 10 things Lenny lists |
glucose intolerance
lipid abnormalities protein malnutrition hypogonadism in women primary testicular failure decreased peripheral conversion of T4 to T3 (but normal TSH) secondary hyperparathyroidism osteomalacia osteoporosis extraskeletal calcifications |
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(uremic syndrome)
2 problems related to glucose intolerance |
peripheral insulin resistance
hyperinsulinemia |
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normally, the kidneys metabolize how much insulin?
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6-8 units daily
(1/4 of the total daily pancreatic secretion) |
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(uremic syndrome)
FGF-23 does three things to blast phosphate |
increases phosphate excretion
decreases 1,25 vitamin D synthesis increases PTH secretion |
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the 3 lab hallmarks of secondary hyperparathyroidism
and its chief physical manifestation |
hyperphosphatemia
hypocalcemia PTH elevation osteitis fibrosa cystica |
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First Aid: normally, plasma [Ca++] is __
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8.4-10.2 mg/dL
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two symptoms of osteitis fibrosa cystica
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subperiosteal erosions in the bones of the hand
"salt and pepper" skull |
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_ is a marker for osteoclastic activity
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tartrate-resistant acid phosphatase-5b
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_ is a marker for osteoblastic activity
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alkaline phosphatase
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what's the difference between osteoporosis and osteomalacia?
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osteoporosis
--reduced bone mass --fully mineralized osteomalacia --undermineralized |
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uremic syndrome
two drugs that treat the problems related to secondary hyperparathyroidism |
cinacalcet
sevelamer carbonate |
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cinacalcet
moa |
mimicks Ca++ at chief cell receptors in the parathyroid
(to decrease PTH release) |
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sevelamer carbonate
moa |
binds intestinal phosphate
(to decrease hyperphosphatemia) |
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(uremic syndrome)
the cause of metabolic acidosis |
the damaged kidneys are unable to sufficiently increase
ammoniagenesis |
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(uremic syndrome)
metabolic acidosis affects at least three other body systems how? |
"decreases nitrogen balance and muscle mass"
increases dissolution of bone matrix and mineral --> osteoporosis contributes to insulin resistance |
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(uremic syndrome)
two ways that metabolic acidosis causes muscle breakdown |
it activates
ubiquitin-proteasome pathway branched-chain alpha-keto acid dehydrogenase |
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(uremic syndrome)
what are the 6 mechanisms whereby metabolic acidosis affects bone health? - - - - - - - - - - - - - - - - - - - - what kind of bone problem results? |
increasing:
--cortisol --PTH decreasing --thyroid hormone --growth hormone --1,25 vitamin D buffering of H+ in bone - - - - - - - - - - - - - - dissolution of bone matrix and mineral --> osteoporosis |
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(uremic syndrome)
dermatologic abnormalities include |
brown hyperpigmentation
uremic frost pruritis |
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(uremic syndrome)
three causes of pruritis and each of their mechanisms |
systemic inflammation
--TH1 cytokines (IL-2, IL-6) over-expression of opioid mu receptors (and decreased kappa receptors) --beta endorphin excess histamine production --increased # of dermal mast cells |
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(uremic syndrome)
immunologic abnormalities include defects in 4 big picture immunologic agents or phenomena |
B cell production
cell-mediated immunity neutrophil phagocytosis and chemotaxis fever production |
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(uremic syndrome)
cell-mediated immunity defects cause (3) |
reactivation of TB
reactivation of herpes zoster cutaneous anergy |
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what vaccines should be given to patients with uremic syndrome
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influenza
pneumococcus zoster |
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how common is infection, in patients with chronic kidney failure?
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it's the 2nd most common cause of death
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(uremic syndrome)
infections are somewhat easier to diagnose in patients with uremic syndrome because |
NOT!
the ability to generate fever is impaired in many of these patients |
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(uremic syndrome)
3 pulmonary abnormalities and ~ a couple details about each |
restrictive lung disease
--calcification and fibrosis uremic lung --permeability --edema --x-ray: bat wing appearance pleural effusions --20% of patients |
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manifestations of stages of chronic kidney disease
GFR 60 - 80 mL/min |
parathyroid hormone begins to rise
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manifestations of stages of chronic kidney disease
GFR 30-59 mL/min |
hypertension
LVH CAD anemia protein malnutrition |
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manifestations of stages of chronic kidney disease
GFR 15-29 mL/min |
hyperlipidemia
hyperphosphatemia --advanced bone disease metabolic acidosis hyperkalemia can be a problem [notice that there are 4 "hyper"s, including hyper H+] |
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manifestations of stages of chronic kidney disease
GFR < 15 mL/min |
nausea
vomiting encephalopathy hyperkalemia metabolic acidosis fluid retention edema accelerated hypertension |
