Chronic Kidney Disease Flashcards Preview

Nephrology > Chronic Kidney Disease > Flashcards

Flashcards in Chronic Kidney Disease Deck (41):
1

What is the definition of chronic kidney disease?






• Permanent reduction in glomerular filtration rate
• Usually under 60% is when you start saying there is kidney damage with lowered GFR

2

What is stage FIVE of the CKD stages and what is the indicated treatment?

• Dialysis or transplant
• GFR is under 15 or the patient is on dialysis

3

What is stage FOUR of the CKD stages and what is the indicated treatment?

• GFR is 15-29
• Treatment is prepare pt for renal replacement (dialysis)

4

What is stage THREE of the CKD stages and what is the indicated treatment?

• GFR is 30-59
• Here you treat complications like fluids and electrolytes

5

What is stage TWO of the CKD stages and what is the indicated treatment?

• 60-89 for GFR, and you just estimate progression

6

What is stage one of the CKD stages and what is the indicated treatment?

• Under 90% GFR, diagnose what's causing the damage and treat underlying cause

7

When do symptoms that are directly related to CKD start appearing?

• Unfortunately when there is a ton of damage already
• When GFR falls below 15ml/min/1.73m2
• ESRD is end stage renal disease and that is when dialysis is needed to live

8

What are the most common causes of Chronic Kidney Disease?

CKD is most commonly caused by Diabetic nephropathy
* hypertensive nephrosclerosis and renal vascular disease
*glomerulonephritis
*polycystic kidney disease
*interstitial nephritis
*obstruction

9

What is the "intact nephron hypothesis"

CKD hypothesis that states nephrons functioning in diseased kidneys maintain glomerulotubular balance comparable to all other nephrons. filtration and net excretion are coordinated
*perhaps why GFR is so stinking decreased before azotemia signs are seen

10

What is the "magnification phenomenon"?

In Chronic Kidney disease, the nephrons in the diseased kidney function homogenously.
*however, they alter their handling of given solutes as needed to maintain external balance if possible
*they magnify their excretion of a given solute to maintain balance

11

what is meant by "individual solute control systems"?

Each solute appears to have a specific control system that is geared to maintain external balance in CKD
*each solute system has individual tubular handling and hormonal influences

12

What is the "trade-off" hypothesis?

the mechanisms that are magnified in the diseased kidney to maintain individual solute control may have adverse effects on other systems.
*it's like the body is choosing what to sacrifice to keep one system functioning over another
*increased parathyroid hormone secretion seen in CKD that helps maintain normal serum calcium and enhances renal phosphorus excretion, but it disturbes uric acid balance (sleep, sex, bone disease, anemia, lipidemia, vascular disease)

13

How is the creatinine and urea balance handled in CKD?

• The rate of filtration is maintained for creatinine and urea at the expense of elevated plasma concentrations
• Or, the excretion rates for urea and creatinine remain constant in the face of diminished clearance
• Thus, creeping levels of BUN and creatinine are a good sign that GFR is diminishing and the kidneys aren't too happy

14

How is water balance handled in CKD?

• To maintain balance in a low GFR state, there must be a smaller fraction of water resorbed in CKD
• The result is increased flow per nephron
• As CKD is worse, water excretion is worse and pt. is hypoosmolality
• Urine concentration is fixed around 300mOsm/kg water, leading to dehydration susceptibility
• Prone to both hyper and hyponatremia due to water handling problems

15

How is sodium balance handled in CKD?

• Fraction of sodium resorbed is decreased and fraction excreted is increased
• Humoral natriuretic peptide helps incease sodium excretion in CKD
• No ability to rapidly respond to sodium intake thus major increases can lead to edema
• Also, extrarenal loss can more rapidly deplete total body sodium

16

How is potassium balance handled in CKD?

• Potassium secretion and excretion in cortical collecting duct is increased in high tubular flow
• Also increased potassium excretion in aldosterone rich circumstances with high sodium flow
• Compensation in fecal loss is about 50% of normal daily load at maximum
• Large potassium doses can make CKD patients hyperkalemic

17

How is the H+ ion balance maintained in CKD?

• Functioning nephrons produce more NH4 to compensate for loss of nephron mass
• 4-fold increase in NH4 keeps acid balance normal (traps H+ in urine) until GFR is around 25ml/min
• As it gets worse there is chronic retention of H+, titrating down serum bicarb
• Result is non-anion gap metabolic acidosis

18

What are the three main factors that produce uremia?

• Retained metabolic products
○ Urea and other nitrogenous products play a role and their plasma concentrations are useful in assessing how well dialysis is working
○ No distinct relationship between these and the overall systemic process established
• Overproduction of counter-regulatory hormones
○ Overproduction of parathyroid hormone (response to hypocalcemia)
○ Also too much natriuretic hormone due to volume overload
• Underproduction of renal hormones
○ Decreased EPO and thus anemia
○ Decreased vitamin D processing leads to bone disease and secondary hyperparathyrodism

19

What can uremia look like in terms of neurologic disorders?

Encephalopathy, peripheral neruopathy

20

What can uremia look like in terms of hematological disorders?

• Anemia, bleeding propensity (platelet dysfunction)

21

What can uremia look like in terms of cardiovascular disorders?

• Pericarditis, hypertension, congestive heart failure, CAD, vascular calcification

22

What can uremia look like in Metabolic-Endocrine disorders?

glucose intolerance, hyperlipidemia, hyperuricemia, malnutrition, sexual dysfunction and infertility

23

Bone, Calcium, and Phosphorus levels can be messed up in Uremia how?

hyperphosphatemia, hypocalcemia, dystrophic calcification, secondary hyperparathyroidism, Vitamin D deficiency, osteomalacia, osteitis fibrosa

24

How can uremia affect the skin?

pruritis (itch), hyperpigmentation, easy bruising, purigo nodularis, uremic frost (ppt on skin from so much urea)

25

uremia can present as which Psychological disorders?

depression and anxiety

26

Uremia can cause what fluid and electrolyte disorders?

edema, hyponatremia, hyperkalemia, hypermagnesemia, metabolic acidosis, volume expansion or depletion

27

Why is anemia a marker of CKD?

lack of EPO production, RBC life-span somehow is shorter in uremia, uremic patients bleed easily (especially in the gut), marrow space fibrosis occurs with the soteitis fibrosa of secondary hyperparathyrodism (complication of uremia)

28

What hormone is increased in CKD that affects bone health as well as electrolyte balances?

Parathyroid hormone is released and elevated in CKD.
*regardless the reason, it results in elevated PTH, reduced levels of systemic calcium, and elevated serum phosphate levels

29

in CKD, what important vitamin is unable to be fully processed?

Vitamin D. As GFR falls, renal production of 1,25 vitamin D falls.
*vitamin D normally stimulates teh absorption of calcium and phosphorus from teh intestine and down regulates PTH gene transcription
*the lack of the vitamin leads to decreased calcium levels overall and overproduction of PTH

30

FGF-23 is an example of what and why is it important to CKD?

FGF-23 is a phosphotonin or a phosphorus regulatory hormone.
*released by bone to promote excretion of phosphorus and shut down 1,25 vitamin D production in the kidney

31

What metal is particularly hard to dialyze out?

aluminum is not well eliminated by dialysis but is usually readily excreted by the kidney. Thus, dialysis patients can get aluminum toxicity

32

The most studied evidence that once the kidney starts to fail it will end up totally failing is what phenomenon?

The combined over-compensation of the surviving nephrons (glomerular hyperfiltration and hypertension) that leads eventually to the death of these nephrons

33

What does hypertension look like at the level of the single nephron?

the body is trying to increase GFR at the level of the single nephron (increase SNGFR). And since SNGFR is proportional to the hydrostatic pressure in the capillary, it dilates the afferent arteriole to allow a greater flow and pressure to increase that hydrostatic pressure.
*the increased pressure does eventually damage the nephron, partially explaining why CKD is a progressive disease

34

What are the goals of dialysis?

remove toxins that are normally renally eliminated and to maintain the volume status of the patient
*it is a far cry from the actual kidney

35

what are the two different types of dialysis?

hemodialysis (usually in the hospital) and peritoneal dialysis (usually at home)

36

What are the initial indications for dialysis?

Severe conditions: severe hyperkalemia, volume overload or uremic pericarditis

37

Is there a GFR cutoff for initiating dialysis?

No. though less than 10ml/min is a guaranteed symptom producer, it's still not a mark for initiating dialysis

38

How often and for how long to hemodialysis patients need to be in the dialysis center?

3X a week for 4 hours each time. This...sucks your life

39

What is an AVF in the context of a CKD patient?

AVF is an arterio-venous fistula. A surgical connection of arterial and venous blood attached to a port for easier dialysis access.
*these mean this patient is in ESRD

40

If a newly minted dialysis patient (just started this therapy) is feeling "off" what are you thinking?

Disequilibrium syndrome: headache, somnolence, seizures and sometimes coma

41

What are the two types of peritoneal dialysis?

CAPD (continuous ambulatory, manual process) and CCPD (continuous cycling, it's an automated process)
*both use a highly dextrosed dialysalate in the peritoneal cavity that sucks fluid from the blood into it, filtering kinda like the kidney
*mostly for fluid balance???