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Clin Med GI > CKD Lecture 1 (INC) > Flashcards

CKD Lecture 1 (INC) Flashcards

1
Q

What defines CKD?

A

GFR is <60 for 3+ months w/ or w/out kidney dmg

OR

Presence of markers of kidney dmg for 3+ months despite GFR

structural problems, abnormality in blood/urine, imaging issues etc

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2
Q

For CKD, what happens with kidney function after treatment, and how does this differ it from AKI?

A

CKD will result in decline in function even if underlying issue is removed d/t chronic nephron overwork.

AKI typically results in normal kidney function after addressing underlying issue

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3
Q

Explain the 5 steps that make up the pathophys of CKD

A
  1. Hyperfilitration, meaning that BUN and creatinine are normal
  2. Hypertrophy of remaining nephrons
  3. RAAS system tries to maintain homeostasis
  4. Glomerular architecture becomes distorted (especially in glomeluruls) d/t hypertrophy hindering filtering abilities
  5. Inflammation and fibroblast puts in scar tissue, destroying the function in the kidney
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4
Q

What is the renal rebound?

A
  1. Lifestyle/meds lead to improvement in BUN creatinine, GFR (improved DM, hydration, control other disease)
  2. Recovery does not reflect restoration of renal tissue, just means that the nephrons that are left have a lower workload.
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5
Q

Prevalence of CKD

A

15%,
9 out of 10 adults are unaware they have CKD!

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6
Q

70% of ESRD (stage 5) CKD is caused by these two chronic diseases

A

DM
HTN/vascular disease

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7
Q

How does CKD lead to CVD?

A

Proteinuric CKD - ↑ risk of CV mortality

Many CKD pts die from CVD before progressing to ESRD!

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8
Q

What are the risk factors for CKD?

A

Old
sub-Sarahan African ancestry

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9
Q

Explain cardiorenal syndrome

A

Deterioration of one organ results in deterioration of the other.

The underlying conditions of acute kidney stuff causes problems with CV, but as you get to chronic, the kidneys start affecting the CV directly

Because they require the same things to be healthy

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10
Q

In the past, what is the staging of kidneys solely reliant on?

A

GFR

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11
Q

What is the new recommendation of staging CKD

A

GFR and albuminuria

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12
Q

What are the GFR stages of CKD?

A
  1. > = 90
  2. 60-89
  3. 45-59
    3a. 30-44
  4. 15-29
  5. <15
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13
Q

What are the 3 albuminuria?

A

A1: <30
A2: 30-300
A3: 300+

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14
Q

Where do most patients fall for CKD?

A

G1 A1 with underlying condition causing kidney issues

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15
Q

A patient with a GFR of 38 mL/min and urine albumin of 100 mg/g =

A

Stage 3b, A2

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16
Q

A patient with a GFR of 96 mL/min and urine albumin of 38 mg/g

A

Stage 1, A2

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17
Q

A patient with a GFR of 10 mL/min and urine albumin of 350 mg/g =

A

Stage 5, A3

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18
Q

A patient with a GFR of 110 mL/min and urine albumin of 12 mg/g =

A

Normal as long as there is nothing else going on

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19
Q

What are the s/s of early-mid CKD, and what about when it progresses

A

Start asymptomatic
Eventually slow onset of non-specific s/s
MC is HTN d/t activating RAAS system
Later stages = volume overload d/t RAAS system retaining fluid
Late CKD = waste build up - leads to uremia

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20
Q

If a patient is at CKD stage 5 and does not do dialysis, what can happen to their skin?

A

Uremic frost d/t urea excreted in swear

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21
Q

Why do patients become anemic with CKD?

A

No erythropoietin

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22
Q

What happens to BUN and creatinine and GFR in CKD?

A

BUN and creatinine increase
GFR decreases

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23
Q

What do you see in UA for CKD and why?

A

Proteinuria sometimes
Broad waxy cast d/t dilated nephrons

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24
Q

What is the pH status of CKD and why?

A

metabolic acidosis d/t not being able to excrete H+

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25
Q

What are the s/s of stage 1 and 2?

A

sometimes HTN but usually asymptomatic

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26
Q

What are the s/s of stage 3 and 4?

A

More likely to have s/s
organ systems are affected
anemia, fatigue
abnormal electrolytes

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27
Q

What are the s/s of stage 5?

A

marked disturbance in ADL, well being, nutrition, water and electrolyte homeostasis

Uremic syndrome

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28
Q

What are the 3 abnormal renal imaging interpretations that are indicative of CKD despite normal GFR?

A

Polycystic kidneys

Small kidneys ( < 9-10 cm)

Asymmetric kidneys (vascular disease)

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29
Q

What does the primary treatment of CKD depend on?

A

Slowing progression
Finding underlying disease
Control BP (ACEs and ARBs, not used in AKI because you want kidneys to have as much blood as possible)
Control proteinuria (ACE/ARBs, diet)
Avoid kidney stones
DM control BG with SGLT-2 inhibitors
Adjust med doses based on renal function

30
Q

What are the order of abnormalities based on progression of CKD

A

HTN
PTH
Anemia
Phosphorus
Acidosis, hyperkalemia
Uremic syndrome

31
Q

What do most CKD patients die by?

A

CV disease
primarily from HTN

32
Q

What is the goal BP of patients with HTN and CKD?

A

<130-80 or 140-90

33
Q

How do you manage HTN with CKD?

A

diet, exercise, wt loss, low sodium diet <2300

34
Q

What do ACE and ARBs d/t creatinine and potassium

A

Tend to increase both

35
Q

Why do you use diuretics for CKD?

A

Nearly always needed because the kidneys try to have body retain as much fluid as possible

36
Q

What diuretic do you start with first for CKD and when is this changed?

A

Thiazides - early CKD
Loop - more effective in later CKD (GFR < 30)

anti-HTN rx - CCBs, BBs are sometimes indicated

37
Q

What is the most common problem with cholesterol if you have CKD? How do you treat?

A

Hypertriglyceridemia

Typically use a statin, can use PSK9 inhibitors as adjunct therapy

38
Q

How does CKD lead to HF?

A

HTN, volume overload, anemia, atherosclerosis, leading to LVH

39
Q

How do you treat HF with CKD

A

ACE/ARBs
monitor for hyperkalemia

40
Q

How do you treat A-fib with CKD?

A

1-4 stage = treat normal
stage 5 = higher bleeding risk with anticoagultion

41
Q

What can lead to pericarditis and what should they be put on?

A

Uremic patients
Put on hemodialysis

42
Q

What is the typical pattern of mineral metabolism disorders in CKD?

A

Hyperphosphetmia
hypo
Hypocalcemia (secondary hyperparthyroidism d/t low calcium)

sometimes you just see hyperparathyroidism w/out low calcium d/t PTH kicking in

43
Q

What is osteitis fibrosa cystica

A

bones get eaten by osteoclast (high bone turnorver), leading to bone pain and muscle weakness

44
Q

Adynamic bone disease

A

low bone turnover
Suppression of PTH or low endobonegenous PTH

45
Q

Osteomalacia

A
  • lack of bone mineralization
    In the past → aluminum toxicity
    Currently → due to hypovitaminosis D, bisphosphonates
46
Q

What is a brown tumor?

A

Osteitis fibrosa cystica
Areas of bone have more calcium pulling out

47
Q

What does osteomalacia look like on CT?

A

Look over exposed, but it is just d/t low calcium

48
Q

If you have mineral metabolism problems, what should control first

A

Control phosphorus
less meats, dark colas, baked goods, frozen dinners

If this does not work, you go to oral phosphorus binders

49
Q

What are the oral phosphate binders?

A

Calcium carbonate/acetate (with each meal)
Non-calcium-based (sevelamer or lanthanum)
Aluminum hydroxide (but can lead to osteomalacia, only for really sick patients)
Iron-based agents

50
Q

After getting phosphorus under control, what should you control next?

A

Manage hyperparathyroidism

51
Q

What meds do you use for hyperparathyroidism and what do you measure?

A

Vitamin D3 (calcitro, animal-derivedl)
Cinacalcet to

52
Q

If a patient has iron deficiency, what do you do?

A

Oral iron or IV iron if needed

53
Q

What is the goal Hb if you have EPO?

A

10-11

Watch for HTN

54
Q

How does CKD lead to hypocoaguability?

A

Normally controlling anemia helps platelets, we don’t treat this typically

55
Q

Why can severe proteinuria lead to hypercoagubility?

A

Losing protein C and S

55
Q

When does hyperkalemia typically manifest?

A

Stage 4-5

56
Q

How do you manage chronic hyperkalemia?

A

List of low and high potassium foods

Loop diuretics can decrease potassium

57
Q

How can CKD lead to metabolic acidosis?

A

Not enough tubules to get rid of acid

58
Q

What type of food should you not eat with metabolic acidosis? What if this does not work by itself?

A

Less meat, eggs

Can give sodium bicarbonate, but can lead to swelling

59
Q

How to treat uremic encephalopathy?

A

Dialysis

60
Q

How do you treat uremic neuropathy?

A

dialysis
control of neuropathic pain with (TCAs and anticonvulsants)

present the same as DM neuropathy

61
Q

Dietary restrictions in CKD

A

Decrease protein
Decrease sodium (if decreased too far, they get volume depleted and BP goes down)

62
Q

What meds should we not use in CKD?

A

Magnesium or phosphorus containing laxiditives
NSAIDs
IV contrast
Nephrotoxic agents
Renally excreted drugs

63
Q

When do you consider dialysis?

A

Considered at 10

Normally based on uremic symptoms

fluid overload unresponsive

can’t be controlled essentially

64
Q

What are the two types of dyalsis?

A

Hemodyalsis
Periodyalsis (through peritenum)

65
Q

After transplanting kidney, what do you need to do?

A

Need to put on immunosuppressive regimen

Need to be along with a specialistic

66
Q

What do you use to filter blood for hemodialysis?

A

Dialysate that is based on the patient’s electrolyte

67
Q

How do you allow vascular access for hemodyalsis?

A

Arteriovenous fistula (preferred)
Lasts longest
Requires 6-8 wks for maturation after surgical construction

Prosthetic graft
Shorter duration, but only needs 2 wks to mature
Higher risk of infection, thrombosis, aneurysm than fistulas

Indwelling vascular catheter
Very high risk of infection
Temporary only

68
Q

What is the MC dyalsis?

A

Hemodyalsis

69
Q

What is peritonitis?

A

MC complication of dialysis d/t infection of peritoneum of staph

leads to abdominal pain, cloudy urine, treatment based on AB therapy

70
Q
A

Clin Med GI (10 decks)

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