Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MS2 Renal > 9/16- Chronic Kidney Disease (CKD) > Flashcards

9/16- Chronic Kidney Disease (CKD) Flashcards

1
Q

What is CKD (vs. AKD)?

A
  • Not reversible (in contrast to AKD)
  • Progressive even after original disease causing kidney damage is treated
  • Associated with other illnesses: heart disease, HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the stages of CKD?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the model explaining progressive kidney failure?

A

Remnant kidney model

Primary renal injury -> loss of nephrons

  • > Hyperfiltration of remaining nephrons
  • > Increased glomerular pressure
  • > Mesangial cell and endothelial cell injury
  • > Mesangial cell and matrix expansion
  • > Focal sclerosis
  • > Loss of nephrons AND REPEAT

Key is to stop the pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is normal GFR?

A

125 mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is normal Na?

A

140 mM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Angiotensin II acts on the ____ (afferent/efferent) arteriole

A

Angiotensin II acts on the efferent arteriole

  • -> constriction
  • Also have increased glomerular pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Important

A

(:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the pathogenesis of CKD (proteinuria and glomerulosclerosis)?

A

(Subtotal nephrectomy in rat is good experimental model) Reduction in functioning nephrons increases systemic hypertension and single nephron glomerular filtration rate (SNGFR)

  • Systemic hypertension accelerates renal arteriolar damage, contributes to micro aneurysm formation
  • Increased glomerular pressure raises SNGFR, but enlarges glom tuft, damages epithelial cells, causing mesangial hyaline deposits, and glomerular thrombi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the pathogenesis of CKD (glomerular and tubulointerstitial damage)?

A

Glomerular sclerosis

  • Glomerular focal sclerosis, and hyalinosis
  • Tubules atrophy
  • Chronic interstitial inflammation

Tubular-interstitial fibrosis end result

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Gross changes seen in CKD?

A
  • Bilateral contracted kidneys
  • Thin renal cortex
  • Multiple cysts (acquired cystic disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some interventions to slow progression of CKD?

A

Control glomerular pressure

  • Low protein diet
  • BP control
  • ACEI and ARBs

(stop Ang II increase in glomerular pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What kind of diet is ideal for slowing progression of CKD? Details?

A

Low protein diet (0.5 g/kg body mass)

  • Loss of renal function limits ability to match intake and output
  • Renal diet may conflict with pt’s previous dietary practices (e.g. diabetic diets)
  • 0.5 g/kg body mass…
  • High biological grade protein
  • Problems with compliance, food choices, blood sugar control, malnutrition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the effects of angiotensin II?

A
  • Vasoconstriction
  • Aldosterone production
  • > Sodium retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ACEI and ARB may cause what in diabetics?

A

Bump in creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are results of kidney failure in terms of:

  • Toxin accumulation
  • Abnormal electrolyte levels
  • Endocrine system
A

Toxin accumulation

  • High BUN and creatinine

Abnormal electrolyte levels

  • Fluid retention, CHF…
  • Hyponatremia
  • Hyper/hypo-kalemia
  • Acidosis
  • Hyperphosphatemia

Endocrine system

  • Low Vit D -> hypocalcemia (no activation of Vit D 25 to 1,25)
  • Anemia (decreased EPO production)
  • Hypoglycemia (failure to metabolize insulin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some signs and symptoms of chronic kidney disease (broad categories)?

A
  • Sodium and volume mgmt:
  • Phosphorus and bone disease
  • Anemia
17
Q

What are some signs and symptoms of chronic kidney disease in terms of sodium and volume mgmt?

A
  • High Na diet -> volume retention in kidney failure
  • Water restriction without sodium -> thirst
  • Use a low sodium diet and diuretics to control volume (say no salt rather than more water!)
18
Q

What are some signs and symptoms of chronic kidney disease in terms of phosphorus and bone disease?

A
  • Hyperphosphatemia: Pi binds to Ca++ and precipitates in vasculature
  • PTH elevated, osteodystrophy, vascular calcification
  • 1,25 dihydroxyVitD suppresses PTH but increases gut Ca absorption
  • Pi found in most foods, restriction limits dietary choices
19
Q

How to deal with hyperphosphatemia, calcium, vitamin D and PTH in CKD?

A

Phosphate binders- trap Pi in gut

  • Al, Mg, iron, and Ca salts are excellent binders
  • Mg is toxic, Al is bone toxic, Ca results in hyper calcemia
  • Sevelamer expensive, works poorly

Vitamin D- suppresses PTH

  • Works poorly
  • Causes hypercalcemia

Cinacalcet- sensitizes PTH gland to Ca, decreasing PTH secretion

  • Can cause low turnover in bone disease
20
Q

How to manage anemia (in CKD)?

A

Have decreased EPO levels with CRF; long and short acting EPO/ESA available

  • Anemia to Hb of 8 g/dL is tolerated
  • Excessive epo dosing causes HTN, thrombosis and can accelerate tumor growth!
  • Aim for Hb of 10 (not 14!)
21
Q

Why might EPO not work in anemia due to CKD?

A
  • Chronic blood loss (e.g. GI bleeding)
  • Chronic inflammation (e.g. hyper-PTH, chronic infections) suppresses RBC production
  • Relative or absolute iron deficiency
22
Q

What are the main causes of diabetic nephropathy?

A
  1. DM
  2. HTN
  3. GN (Other)
23
Q

What are the stages of diabetic nephropathy Type I diabetics?

A
  • Initially high GFR
  • Control of diabetes -> drop in GFR
  • After years of mgmt, may have fall in GFR (helped by Anti-HTN treatment)
24
Q

What are components of the normal glomerulus?

A
  • Bowman’s space
  • Capillary lumen
  • Filtration membrane
  • Mesangium
  • Tubules
25
Q

What is seen here?

A

Left: normal glomerulus

Right: glomerulus in diabetes

26
Q

What are the changes in renal (micro)anatomy due to DM?

A
  • Mesangial expansion and thickening of glomerular basement membrane
  • Nodule formation (25 to 30% of patients)
  • Thickening of Bowman’s capsule
  • Exudative hyaline lesions in Bowman’s capsule, mesangium, dilated capillaries
27
Q

Why does diabetes damage the kidney?

A

Renal effects of diabetes:

  • Glomerular hypertension (GFR initially elevated)
  • Glomerular vascular damage
  • Proliferative/fibrotic renal changes
28
Q

How to manage/treat diabetic damage to the kidney?

A

Tightly control glucose

Lower glomerular pressure

  • Low protein diet if tolerated
  • Aggressive hypertension control
  • ACEI or ARB
29
Q

What are some end stage kidney failure symptoms/findings?

  • General
  • GI
  • Cardiac
  • Pulmonary
  • Peripheral nerves
  • CNS
A
  • General: Tired, apathy, itching, copper penny taste - GI: Nausea, vomiting, anorexia, loss of wt
  • Cardiac: Pericarditis, uremic myocarditis
  • Pulmonary: Edema, pleural effusion
  • Peripheral nerves
  • Increased conduction times, axonal loss, demyelination
  • Paresthesia, restless leg syndrome, cramps
  • CNS
  • Apathy, confusion, drowsiness
  • Eventually coma, seizures
30
Q

What are the indications for dialysis?

A

Renal Clearance: GFR of ~ 10mL/min/1.73m2

Could wait if:

  • Stable or increased edema-free weight
  • Protein intake > 0.8 g/kg/d
  • No clinical signs / symptoms of uremia

Earlier initiation for Diabetics (GFR 15 ml/min) may be beneficial

  • However, early initiation of dialysis adds risks and complications for patient
31
Q

Flow scheme hemodialysis (picture)

A
32
Q

T/F: There are methods to do chronic hemodialysis

A

True

  • Routine access to vasculature is possible
  • Complications include bleeding and thrombosis
33
Q

What is an AV fistula/graft?

A
  • No foreign body (internal)
  • Grafts of gortex
34
Q

What is a hemodialysis catheter?

A
  • Dual lumen
  • Provides quick easy access

Many complications:

  • Sepsis, endocarditis
  • Great vessel thrombosis
  • Frequently clot, missed treatments
  • Substance abuse

Avoid when possible

35
Q

How is peritoneal dialysis done?

A

Fluid put in peritoneal cavity and peritoneal membrane acts as filtration barrier

36
Q

Where are renal transplants located? What happens to old kidney? Lifetime treatment?

A
  • Can use cadaveric or living donor
  • Kidney placed over iliacs!
  • Native kidneys not typically removed
  • Lifetime immunosuppressive therapy
37
Q

Summary:

  • CKD is common ( > 7% of the population)
  • Pathophysiology of CKD: progressive glomerular sclerosis and kidney fibrosis
  • CKD affects many organ systems
  • Clinical interventions for CKD reviewed
  • Options for renal replacement therapy
  • Transplantation (when possible) is best treatment
  • Home dialysis, HD, or PD next best Tx
  • Essentially all ESKD pts spend some time on dialysis
A

(:

MS2 Renal (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions