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
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
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:
4
Q
What are the main causes of CKD in the US?
A
TII DM and HTN: 75% of cases!
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
6
Q
What is leading cause of death in young diabetics?
A
- CKD cause from angiopathy of glomerular capillaries
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
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
9
Q
Other names for hypertensive nephropathy?
A
- Hypertensive nephrosclerosis
2. Benign nephrosclerosis
10
Q
5 types of glomerulonephritis?
A
- IgA nephropathy: most common cause
- Post-infectious glomerulonephritis
- Membranoproliferative glomerulonephritis
- Lupus nephritis
- Rapidly progressive glomerulonephritis
11
Q
What is IgA nephropathy?
A
- IgA deposits on glomeruli leading to CKD 25%
- Presents as hematuria 1 - 2 days post URI
12
Q
Person with bronchitis, peeing blood, dysmorphic RBCs in urine with high BUN and Cr.?
A
IgA nephropathy
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
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
15
Q
What is Membranoproliferative glomerulonephritis?
A
- Deposits in GBM and mesangium
- Complement activation leading to glomerular destruction
- DOES NOT effect mesangium
16
Q
What is thrombophilia?
A
Tendency to form blood clots
17
Q
What is RPGN?
A
“Rapidly progressive glomerulonephritis”
- High numbers crescents seen on biopsy
18
Q
What are crescents on biopsy indicative of?
A
RPGN
19
Q
Common causes of RPGN”
A
- Goodpasture syndrome
- Wegener’s granulomatosis
- SLE
20
Q
4 Types of nephrotic syndrome?
A
- MCD
- FSGS
- Membranous nephropathy
- 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
What are clinical features of amyloidosis?
1. Heart failure
2. Enlarged tongue
3. Skin lesions
4. GI disease
5. Polyneuropathy: Carpal tunnel
26
What is heart failure with, carpal tunnel and enlarged tongue characteristic of?
Nephropathy from amyloidosis
27
What is cholesterol atheroembolic disease?
- Cholesterol released from plaque into blood stream
- Usually occurs after surgical or interventional
- Happens weeks after procedure
28
Symptoms of cholesterol atheroembolic disease?
1. Fever / malaise
2. Digital gangrene
3. Livedo reticularis: rash
4. Renal failure
29
What is livedo reticularis?
Rash characteristic of cholesterol atheroembolic disease?
30
How to treat stage II / III CKD?
"Conservative renoprotection"
1. Promote healthy living: no smoking, exercise, weight loss
2. BP and lipid control
3. Glycemic control
4. ACEI / ARB
31
Management of stage IV CKD?
1. Nephrology referral
| 2. BP
32
When to call nephrologist in CK?
Stage IV
33
How does CDK lead to mineral bone disorders?
- 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
How to treat hyperparathyroidism?
- Restrict dietary phosphate or with meds
35
What contributes to anemia in CDK/
1. Decreased EPO synthesis
2. Blood loss
3. Lower RBC half life
36
Treatment goals for anemia?
Hgb: 10 - 12
Transferrin saturation: 20 - 50%
Ferritin: 100- 800
37
Outcomes with ESRD?
- 20% die in within first two years on hemodialysis
| - 13 hospital days and 2 admission on avg per year
38
Why are ESRD death rates higher in US than in Europe and Japan?
- US ptns often have higher rate of CVD as well
| - Different dialysis practice
39
How to treat ESRD?
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
Benefits of arteriovenous fistulas?
- 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
What is hemodialysis?
- 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
What is ultrafiltration?
- Goal of removing excess body water
- Hydrostatics and osmotics drive process
- No change in solute []s
43
What are the sequelae of ESRD?
Uremic cardiovascular disease leading to:
• Medial vascular calcification
• Arterial stiffness
• LV hypertrophy
• Higher risk of cardiac arrest and heart failure
