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PHARM 343 > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

Chronic Kidney Disease Definition

A

Damage to kidney
or
GFR less than 60 for more than 3 months

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2
Q

Stage 1 CKD

A

Kidney damage with Normal GFR
- GFR greater than 90

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3
Q

Stage 2 CKD

A

Kidney damage with mild reduced GFR
- GFR 60-89

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4
Q

Stage 3 CKD

A

Moderate Reduced GFR
- 3a: GFR 45-59
- 3b: GFR 30-44

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5
Q

Stage 4 CKD

A

Severe Reduced GFR
- GFR 15-29

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6
Q

Stage 5 CKD

A

Kidney Failure / End Stage Renal Disease
- GFR less than 15 or DIalysis

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7
Q

CKD Staging Via ACR

A

ACR = Albumin:Creatinine Ratio

A1: Normal/mild increase
- ACR is less than 3.0
A2: Moderate increase
- ACR 3.0-30
A3: Severe increase
- ACR is greater than 30

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8
Q

How to assess CKD (abbreviation)

A

C: Cause
G: Glomerular Filtration
A: Albuminuria Category

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9
Q

How to evaluate for causes of CKD

A

Physical Exam
Nephrotoxic Drugs
Medical History
Family History
Social History
Symptoms and Signs (Systemic Disease)
Symptoms and Signs (Urinary Tract Abnormal)
Lab Tests

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10
Q

What are the major causes of CKD

A

1: Type 2 Diabetes

#2: Hypertension

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11
Q

What is the leading cause of death in CKD patients

A

Cardiovascular Disease

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12
Q

CKD
- Overview

A

Hypertension + T2DM causes Glomerulosclerosis
- Loss of nephron mass
- Proteinuria
- Glomerular Hypertension

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13
Q

CKD (Hypertension)
- How does it occur

A

Mainly driven by RAAS system leading to kidney injury

Vasculature
- Endothelial damage
- Endothelial cell damage
Glomerulus
- Glomerular hypertension
- Glomerular cell hypertrophy
Tubule
- Tubular damage
- Tubular cell injury
Interitem
- Inflammation
- Oxidative stress

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14
Q

RAAS System response to low BP

A
  1. Low BP
  2. JG Cells in Kidney stimulate release of renin
  3. Angiotensinogen from liver is converted by renin into Angiotensin I
  4. ACE converts Angiotensin I into Angiotensin II
  5. Angiotensin II acts on adrenal cortex to produce aldosterone and acts on arterioles to constrict
  6. BP increases
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15
Q

Angiotensin II role

A
  • Vasoconstriction
  • Increase blood pressure
  • Increases filtration of plasma protein, leads to renal scarring
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16
Q

How does Diabetic Neuropathy affect CKD

A

Glomerular Hyperfiltration
Altered Glomerular Composition
Renal Hypertrophy
Glomerular Hypertension
Proteinuria
–> All of this leads to glomerular scarring

17
Q

Progression factors of CKD

A

Hyperglycemia
Hypertension
Smoking
Obesity
Proteinuria

18
Q

Proteinuria and CKD

A

Proteinuria is a strong risk factor of cardiovascular mortality
- High proteinuria = Higher risk of end stage renal disease
- Glomerular Dysfunction –> Glomerular Hyperfiltration

19
Q

Persistient Proteinuria and Transient and CKD

A

Persistient proteinuria is an indicator of kidney damage and renal disease

Transient proteinuria can be an indicator of some sort of underlying issue (UTI, heavy exercise, dehydration, pregnancy)

20
Q

Symptoms of CKD

A
  1. Edema/Fluid Overload
    - Glomerular Hyperfiltration causes too much proteins to go through. Reduction in kidneys filtering ability. Fluid buildup
  2. Pruritus
    - Waste is retained leading to itching
  3. Restless Leg
    - Electrolyte abnormalities
  4. Anemia
    - Kidneys do not produce erythropoietin
21
Q

CKD Lifestyle Management

A
  1. Exercise
  2. Weight Loss
  3. Smoking Cessation
  4. Low Sodium Diet
  5. Limit Protein Intake in CKD G3-5 (Do not do if patient is metabolically unstable)
  6. Limit alcohol
22
Q

ACEi Drugs

A

Perindopril
Ramipril
Lisinopril

23
Q

ARB Drugs

A

Candesartan
Irbesartan
Valsartan

24
Q

When are ARBs and ACEi recommended

A

Always use in diabetic patients (unless contraindicated)

For non diabetic patient used if ACR is greater than 3.0 (proteinuria) (unless contraindicated)

25
Q

ACEi and ARBs mechanism

A

Reduces hyperfiltration
Reduce glomerular hypertension (less stress on glomerulus)
Reduce/stabilize proteinuria

Renoprotective
- Benefits are independent from BP lowering effects

26
Q

ACEi and ARBs considerations

A

Do not use in AKI (Due to hemodynamic effect)

Contraindications:
- Pregnancy
- Angioedema history
- Bilateral renal artery stenosis

27
Q

ACEi and ARBs Adverse Effects

A

ACEi
- Dry cough

ACEi and ARB
- Angioedema

28
Q

ACEi and ARB monitoring

A

Start with low dose and taper slowley

Will get worse first before patient gets better
- Serum Creatinine will spike up (due to decrease in GFR)

Be careful of potassium (hyperkalemia)

29
Q

Proteinuria
- Treatment

A

ARBs and ACEi

Can use Spironolactone in some patients (Be careful of hyperkalemia)

Diltiazem and Verapamil have some effectiveness (Calcium Channel Blockers)

30
Q

SGLT-2 Inhibitor Drugs

A

Empagliflozin
Dapagliflozin
Canagliflozin

31
Q

SGLT-2 Inhibitor Mechanism

A

Renoprotective

Prevents reabsorption of glucose
- Lowers plasma concentration of glucose by excreting it

Reduces sodium reabsorption
- Sodium gets delivered to macula densa, glomerular feedback is restored, blood flow in kidney is reduced , decreases glomerular hyperfiltration, reducing intraglomerular pressure

32
Q

SGLT-2 Inhibitors effects on patients with diabetes vs no diabetes

A

Reduction in glucose reabsorption mainly benefits DM Patients

Reduction in intraglomerular pressure benefits both DM and non-DM patients
- Dapagliflozin

33
Q

SGLT-2 Inhibitors Considerations

A

Initiate as an add on therapy to ACEi and ARBs for patients with T2DM and CKD
- When GFR is greater than 20
- Reasonable to keep using even if GFR falls under 20

Do not initiate in patients undergoing dialysis

34
Q

SGLT-2 Inhibitor Adverse Effects

A

Genital Mycotic Yeast Infections (Due to excrerion of sugars)

UTI

Increased urination and thirst

Diabetic Ketoacidosi
- Occurs during acute illness (should put therapy on hold in this case)

35
Q

Non-Steroidal Mineralocorticoid Receptor Antagonist drugs

A

Steroid MRA = Spironolactone

Non-Steroidal MRA = Finerenone

36
Q

Non-Steroidal Mineralocorticoid Receptor Antagonist considerations

A

Can be added on to ARB/ACEi + SGLT-2 Inhibitor
- In patients with persistient albuminuria (ACR greater than 30)
- In patients with normal potassium

Renal and CV benefits for patients with
CKD + T2DM + Greater than 25 GFR

37
Q

GLP-1 considerations

A

Used to manage glycemic control in patients not responding to metformin or SGLT-2 inhibitors

38
Q

CKD and reducing CV risk

A

Statins
- Prescribe for all patients older than 50 with CKD
- Prescribe for patients 18-49 if at moderate-high risk of CV disease

ASA
- Secondary prevention of atherosclerotic cardiovascular disease and ischemic CV disease

39
Q

CKD SIckday management

A

If patient is ill and unable to replenish their fluids hold the following nephrotoxic drugs

Sulfonylurea
ACEi
Diuretics
Metformin
ARBS
NSAIDs
SGLT2 Inhibitors

PHARM 343 (23 decks)

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