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Renal - Gupta > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

T or F: Creatinine lab values are great indicators of kidney function all of the time?

A

False, Creatinine may make kidney function appear more stable than it actually is

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2
Q

Why should you be weary of saying that a creatinine value of 1.0 g/dL is normal?

A

• You must take into account the PATIENT, a big ass athlete may have a normal creatinine of 1.5 g/dL while a little old man might have a normal of 0.6 g/dL

(YOU MUST take age, gender, and muscle mass into account)

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3
Q

Even in the absence of creatinine levels, what tests/findings can be indicative of CHRONIC kidney injury?

A

• SMALL trunckated (ECHOGENIC) kidney’s that are less than 9cm tells you that its a CHRONIC process

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4
Q

T or F: acute injury is more likely to be symptomatic than chronic injury

A

True

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5
Q

What is PATHOPNEUMONIC for glomerular damage leading to renal failure?
• what is a good indicator of tubular dysfunction?

A

GLOMERULAR:
• Red Blood Cell Casts**
• pts. will also have proteinuria

TUBULAR:
• Inability to concentrate the urine

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6
Q

What disease is often implicated with WBCs in the urine, but negative urine cultures?

A

ALLERGIC (and tubular) cause of Kidney Failure

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7
Q

What are the symptoms of uremia?

• what is the px. of CKD with uremia?

A

Symptoms:
• Nausea, Vomiting, Fluid Retention

Px:
• BAD prognosis, Kidney disease will kill these people

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8
Q

What creates Hyaline deposits?

A

• Hyaline - created from protein crossing podocytes

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9
Q

What are two VERY important factors we try to control in CKD?

A

HYPERTENSION
• this is pretty easy to control with drugs

SODIUM (=poison)
• harder to control

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10
Q

Why are ACE inhibitors and ARBs good for lowering proteinuria?
• why is important to lower proteinuria in CKD?

A

Why are they good:
• they PREVENT angiotensin II mediated constriction of the efferent arteriole (which increases intraglomerular pressure)

Proteinuria is a BAD px. indicator of CKD

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11
Q

Why do most people die before they can even get put on dialysis?
• pathophysiology?

A

CARDIOVASCULAR dysfunction secondary to kidney dysfunction

Pathophysiology:
• LV hypertrophy occurs from increased Na+ rentention leading to inc. ECFV (=> inc. preload => inc. afterload => hrt. failure)

UREMIA CAUSES PERICARDIDITIS

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12
Q

T or F: uremia is a strong indicator for dialysis.

A

True, you need to prevent pericarditis etc.

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13
Q

Why are people with CKD more likely to experience fasting fasting hypoglycemia?

A

Insulin is excreted in the kidney so people with CKD get a build up of serum insulin

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14
Q

What is one of the 1st symptoms of CKD?

A

• Early morning nausea (really just empty stomach nausea in general)

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15
Q

What is Calciphylaxis?

• when does this occur?

A

Calciphylaxis
• calcium lines and blocks up the blood vessels ultimately leading to skin breakdown and ulceration

This is a late stage probelm

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16
Q

What is the last mineral to become dysregulated in CKD?

A

•POTASSIUM

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17
Q

T or F: in CKD almost everyone starts to develop metabolic acidosis

A

True

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18
Q 
What is expected in the following for CKD?
• Hx
• Physical Exam.
• Lab data
• Imaging Studies
A

Hx:
• Voiding Complaints
• Abnormal Appearance of urine

Physical:
• HTN
• Edema

Lab Data:
• elevated Creatinine and BUN

Imaging:
• Ultrasound

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19
Q

What are some key factors in determining if CKD is acute or chronic?

A
  • Peripheral Neuropathy
  • Bone Changes consistent with longstanding hyperparathyroidism
  • Small kidneys on ultrasound
  • waxy casts
20
Q

What are 4 main factors that suggest Tubular Etiology of renal failure more so than Glomerular?

A
  • Absence of Heavy Proteinuria
  • Can’t concentrate urine (specific gravity 1.010 and osmolarity of ~300 mosm/kg)
  • HYPERKALEMIA and Metabolic Acidosis out of proportion to renal insufficiency
21
Q

What is THE MOST IMPORTANT component to differentiating glomerular and tubular disease?

A

Urinalysis

*lots of protein (2+), RBC casts, specific gravity greater than or equl to 1.015 suggest glomerular etiology

22
Q

What pathology is typically associated with active inflammation of the tubules?
• glomerulus?

A

Tubulointerstitial Nephritis:
• Pyelonephritis
• Allergic interstitial nephritis

Glomerulonephritis:
• all of the Nephritic syndromes

23
Q

T or F: Chronic kidney disease tends to be inexorably progressive, even if the initial injuring stimulus is removed

A

True

24
Q

What are the most common etiologies of advanced kidney disease in the US?

A
  • DIABETES MELLITUS*** #1
  • hypertensive nephrosclerosis
  • acute and chronic glomerular diseases
  • polycystic kidney disease
  • tubulointerstitial diseases
25
Q

What is the renal response to nephron loss?

A
  1. Compensatory Glomerular Hypertrophy
  2. Compensatory Hyperfiltration

*50% decrease in renal mass results in only 20-30% reduction in GFR b/c residual nephrons pick up the slck

26
Q

What are some side effects that increase in a dose dependent manner in response to loss in nephron mass greater than 50%?

A
  • HTN

* Proteinuria

27
Q

Compare HTN in CKD to 1º HTN.

A

CKD HTN is more often due to volume overload rather than

28
Q

What is the best indicator of overall kidney function?

• how do we estimate this?

A

GFR - best index of overall kidney function

Estimate:
• via creatinine

29
Q

Why might CKD progress even in the absence of original underlying disease?

A

Increased stress put on remaining nephrons could lead to kidney dysfunction

30
Q

Is Diabetic Nephropathy more associated with Type 1 or Type 2 diabetics?
• why does diabetes lead to nephropathy?

A

Type I

Hyperfiltration Results in Glomerular Capillary HTN and Glomerular hypertrophy

31
Q

Why are ACE inihibitors better than diuretics or direct vasodilators at preventing albuminemia?

A

They lower capillary pressure systemically (reducing afferent arterial flow) but ALSO act to vasodilate the efferent arteriole

32
Q

Differentiate between the Trade off and Intact nephron hypothesis.

A

Intact Nephron Hypothesis:
• Damage nephrons generally function how they should so loss of renal homeostasis is 2º to a decreased number of nephrons

Chonic Kidney disease = decreased number of normally functioning nephrons

Trade Off Hypothesis:
• Secondary events occur to assist in homeostasis with the addition of adverse side effects

33
Q

What are some of the compensatory changes made according to the trade off hypothesis?

A

Compensatory Changes:
• Calcium/phosphorus | secondary Hyperparathyroidism

  • Na+ balance | HTN
  • K+ balance | Hyperaldosteronism and HTN
  • Remaining nephrons pick up the slack | increased filtration by resisdual nephrons causing injury
34
Q

T or F: urinary flow rate is a good secondary marker of renal function

A

FALSE

35
Q

What is a simple equation for estimating GFR by taking into accound age and sex?

A

(140 - age)/Creatinine x (0.85 - if female)

36
Q

Describe the 5 stages of CKD.

A
  1. Kidney Damage with Normal or High GFR
  2. Kidney Damage with Low GFR
  3. Moderate low GFR
  4. Severe low GFR
  5. Kidney Failure
37
Q

T or F: you should treat patients with CKD as if they are in the highest risk group for CVD.

A

True

38
Q

What are some of the nervous system effects of CKD?

A
  • Difficulty Concentrating
  • Encephalopathy manifested by ASTERIXIS
  • PERIPHERAL NEUROPATHY
39
Q

How does HTN help to compensate for low GFR?

A
  • Low GFR = less ability to filter Na+
  • Na+ is retained
  • HTN increases pressure natriuresis promoting ability to maintain Na+ balance
40
Q

Why is CKD associated with anemia?

• when does this occur?

A

These people have significantly less blood cell synthesis b/c of less EPO

• Occurs at 30% of normal GFR

41
Q

Why do people develop PROTEIN calorie malnutrition when they have CKD?

A

• They have a LOSS of APPETITE and concurrent decrease in protein intake

42
Q

Why do people with CKD excrete increasing amounts of PTH?

A
  • PHOSPHATE builds up
  • Kidney is dysfunctional

Leads to…

• Down regulation of 1-alpha-hydroxylase and less Calcitriol production

which leads to…

• Increase PTH secretion

43
Q

What derangements happen in phosphorus metabolism in CKD?

A
  • PO4 complexes with Ca2+ leading to decreased serum Ca2+ conc.
  • Inhibits 1-alpha-hydroxylase
  • Metastatic Calcification
  • Enhancement of PTH secretion
44
Q

T or F: Potassium homeostasis can be maintained until GFR is below 15 ml/min

A

True

45
Q

Do people with CKD tend to progess toward metabolic acidosis or alkalosis?
*Explain

A

Acidosis:
• decreased NH4+ production from decreased numbers of nephrons

This will be acidosis with normal ion gap

Renal - Gupta (17 decks)

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