11.2: Clinical II Flashcards

1
Q

What is chronic kidney disease?

A
  • Progressive decline in GFR
  • At least 3 months
  • w/ or w/o proteinuria
  • 75% cause by Htn. or TIIDM
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2
Q

What does CKD put you at risk for?

A
  • All forms of CV disease
  • Only 2% require RRT: renal replacement therapy
  • Number is so low because MOST DIE FROM CVD
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3
Q

Five stages of CKD?

A
I: > 90, with some kidney damage
II: 60 - 89 GFR
III: 30 - 59 GFR, most common group
IV: 15 -29 GFR
V:
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4
Q

What are the main causes of CKD in the US?

A

TII DM and HTN: 75% of cases!

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5
Q

How does diabetes cause CKD?

A
  • Leads to angiopathy of the glomerular capillaries
  • Causes diffuse glomerular sclerosis
  • Leads to nephrotic range proteinuria
  • Occurs 15 - 25 yrs post diagnose with uncontrolled sugar and htn accelerating progress
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6
Q

What is leading cause of death in young diabetics?

A
  • CKD cause from angiopathy of glomerular capillaries
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7
Q

How does Htn lead to nephropathy?

A
  • Causes hyaline arteriolar sclerosis of renal vessels
  • Resulting ischemia damages tubes and glomerulus
  • Protein/hematuria can occur but are not common
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8
Q

What is renovascular htn?

A
  • NOT THE SAME as hypertensive nephropathy
  • Form of secondary htn. from renal artery stenosis
  • In comparison, hypertensive nephropathy occurs in small vessels
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9
Q

Other names for hypertensive nephropathy?

A
  1. Hypertensive nephrosclerosis

2. Benign nephrosclerosis

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10
Q

5 types of glomerulonephritis?

A
  1. IgA nephropathy: most common cause
  2. Post-infectious glomerulonephritis
  3. Membranoproliferative glomerulonephritis
  4. Lupus nephritis
  5. Rapidly progressive glomerulonephritis
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11
Q

What is IgA nephropathy?

A
  • IgA deposits on glomeruli leading to CKD 25%

- Presents as hematuria 1 - 2 days post URI

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12
Q

Person with bronchitis, peeing blood, dysmorphic RBCs in urine with high BUN and Cr.?

A

IgA nephropathy

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13
Q

What is post-infectious glomerulonephritis?

A
  • Usually from strep skin infection (impetigo) or strep pharyngitis
  • IC get lodged in glomerular basement membrane
  • Complement activation leads to destruction of GBM
  • 2 - 4 weeks post initial infection
  • ASO titre high w/ low serum complement
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14
Q

What is the following characteristic of?

  • 2 - 4 weeks post initial infection
  • ASO titre high w/ low serum complement
A

Post-infectious glomerulonephritis

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15
Q

What is Membranoproliferative glomerulonephritis?

A
  • Deposits in GBM and mesangium
  • Complement activation leading to glomerular destruction
  • DOES NOT effect mesangium
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16
Q

What is thrombophilia?

A

Tendency to form blood clots

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17
Q

What is RPGN?

A

“Rapidly progressive glomerulonephritis”

- High numbers crescents seen on biopsy

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18
Q

What are crescents on biopsy indicative of?

A

RPGN

19
Q

Common causes of RPGN”

A
  1. Goodpasture syndrome
  2. Wegener’s granulomatosis
  3. SLE
20
Q

4 Types of nephrotic syndrome?

A
  1. MCD
  2. FSGS
  3. Membranous nephropathy
  4. Amyloidosis
21
Q

Characteristics of nephrotic syndrome?

A
  • Proteinuria
  • Bland histology
  • Lack of urinary sediment
22
Q

What is MCD?

A
  • Type of nephROTIC syndrome common in kids
  • More common in history of autoimmunity
  • Steroid and ACEI can treat for good outcome
23
Q

What is FSGS?

A
  • Most common cause of nephrOTIC syndrome in adults
  • Can appear secondary to HIV, heroin use
  • Poor response to therapy
24
Q

What is membranous nephropathy?

A
  • Can be seen in stage V lupus, heb B, drugs, tumors

- Treated with immunosuppression

25
Q

What are clinical features of amyloidosis?

A
  1. Heart failure
  2. Enlarged tongue
  3. Skin lesions
  4. GI disease
  5. Polyneuropathy: Carpal tunnel
26
Q

What is heart failure with, carpal tunnel and enlarged tongue characteristic of?

A

Nephropathy from amyloidosis

27
Q

What is cholesterol atheroembolic disease?

A
  • Cholesterol released from plaque into blood stream
  • Usually occurs after surgical or interventional
  • Happens weeks after procedure
28
Q

Symptoms of cholesterol atheroembolic disease?

A
  1. Fever / malaise
  2. Digital gangrene
  3. Livedo reticularis: rash
  4. Renal failure
29
Q

What is livedo reticularis?

A

Rash characteristic of cholesterol atheroembolic disease?

30
Q

How to treat stage II / III CKD?

A

“Conservative renoprotection”

  1. Promote healthy living: no smoking, exercise, weight loss
  2. BP and lipid control
  3. Glycemic control
  4. ACEI / ARB
31
Q

Management of stage IV CKD?

A
  1. Nephrology referral

2. BP

32
Q

When to call nephrologist in CK?

A

Stage IV

33
Q

How does CDK lead to mineral bone disorders?

A
  • Decrease P excretion, increased serum P levels
  • Decreased Vit. D activation decreases serum Ca and Ca absorption
  • End result increase in serum PTH leading to secondary hyperparathyroidism
34
Q

How to treat hyperparathyroidism?

A
  • Restrict dietary phosphate or with meds
35
Q

What contributes to anemia in CDK/

A
  1. Decreased EPO synthesis
  2. Blood loss
  3. Lower RBC half life
36
Q

Treatment goals for anemia?

A

Hgb: 10 - 12
Transferrin saturation: 20 - 50%
Ferritin: 100- 800

37
Q

Outcomes with ESRD?

A
  • 20% die in within first two years on hemodialysis

- 13 hospital days and 2 admission on avg per year

38
Q

Why are ESRD death rates higher in US than in Europe and Japan?

A
  • US ptns often have higher rate of CVD as well

- Different dialysis practice

39
Q

How to treat ESRD?

A
  1. HgB 10 - 12
  2. Use arteriovenous fistulas whenever possible
  3. Ca 8.4 -9.5
  4. P: 3.5
  5. Albumin > 4
  6. Nutrition consult
40
Q

Benefits of arteriovenous fistulas?

A
  • Eliminate central venous catheter use
  • Less bacteremia and venous thrombosis
  • *Nearly impossible to place of ptn. has vascular disease
  • **Takes months to prep before it can be used
41
Q

What is hemodialysis?

A
  • Diffusion of molecules in solution across semipermeable membrane along electrochemical gradient
  • Restores body fluids resembling normal renal environment
  • Urea moves out, bicarb moves in
42
Q

What is ultrafiltration?

A
  • Goal of removing excess body water
  • Hydrostatics and osmotics drive process
  • No change in solute []s
43
Q

What are the sequelae of ESRD?

A

Uremic cardiovascular disease leading to:
• Medial vascular calcification
• Arterial stiffness
• LV hypertrophy
• Higher risk of cardiac arrest and heart failure