Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Therapeutics + Fall 2022 > Cardio/Renal - Final Exam > Flashcards

Cardio/Renal - Final Exam Flashcards

1
Q

What is the difference between AKI and AKD?

A

AKI: acute kidney injury - abrupt decline in kidney function over 7 day or less
AKD: acute kidney disease - AKI between 7 to 90 days, precedes CKD diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

KDIGO staging of AKI

A

Stage 1: 1.5-1.9x baseline SCr OR 0.3+ mg/dL increase in SCr
Stage 2: 2.0-2.9x baseline SCr
Stage 3: 3x baseline SCr OR 4.0+ mg/dL increase in SCr OR initiating renal replacement therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the traditional biomarkers of AKI? What are the novel biomarkers?

A

Traditional: SCr and BUN
Novel: NGAL, TIMP2 & IGFBP7, KIMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the most common trigger of AKI?

A

NSAID use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are 6 risk factors of AKI?

A
  1. Age > 65 years
  2. Black ethnicity
  3. Existing CKD
  4. DM
  5. Nephrotoxin use (ie. NSAIDs)
  6. Decreased circulatory volume (HF, cirrhosis, nephrotic syndrome, blood loss)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are 3 GENERAL prevention measures against AKI?

A
  1. Maintain euvolemia and normal electrolytes (balanced isotonic crystalloids)
  2. Maintain organ perfusion (MAP>65)
  3. Avoid nephrotoxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When would we use diuretics in an AKI patient?

A

Edema management, hyperkalemia/electrolyte abnormalities

Note: may cause hypovolemia, hypotension, or diuretic resistance (loop)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

T/F Dopamine and fenoldopam improve AKI outcomes

A

FALSE - increases arrhythmias and hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What medications should be temporarily held during hemodynamic AKI?

A

ACEi/ARBS, NSAIDs, SGLT2is, calcineurin inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What meds should you temporarily hold for pre-renal AKI?

A

Loop diuretic, thiazide diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What diseases cause intrinsic AKI?

A

Glomerulonephritis, acute tubular nephritis, tubulointerstitial nephritis, vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do you treat pre-renal AKI?

A

Intravascular volume repletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do you treat intrinsic AKI?

A

If caused by a medication, stop immediately and do not restart and list as allergy
If caused by disease state, treat that state accordingly (immunosuppression, supportive care, glucocorticoids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you treat post-renal AKI?

A

Relieve obstruction (acute - catheter, chronic - treat underlying cause)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Kidney Replacement Therapy (KRT)? What are the two ways to conduct it?

A

Treatment for prolonged/severe AKI
1. Continuous Kidney Replacement Therapy (CKRT)
2. Intermittent Hemodialysis (IHD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the best marker of kidney function in AKI (hint: not GFR or SCr!)

A

Urine output
GFR and SCr are NOT RELIABLE! (fluctuate often depending on clinical context)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

eGFR and eCrCl (Cockcroft-Gault) are both used for kidney function assessment for drug dosing. How do you decide how to recommend a dose?

A

Since eGFR and eCrCl may cause 20-30% dosing disparities, use the method that was STUDIED during DEVELOPMENT.

Cockcroft-Gault is most often used!
BUT newer drugs are using eGFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

If the drug dosed has a wide therapeutic index, is less than 30% renally excreted, and has inactive metabolites, then what changes need to be made in a patient with kidney dysfunction?

A

Nothing! These drugs need not be renally dosed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does kidney dysfunction affect non-renal clearance?

A

Uremic toxins inhibit hepatic CYP enzymes and transporters in the gut/liver.

Altered first pass - less metabolism = more active drug
Reduced Phase I metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Drugs with toxic metabolites should be _________
Drugs with active metabolites should be _____ ____ ______
Drugs with inactive (but have) metabolites should be ________

A

Toxic = avoided
Active = used with caution
Inactive - monitored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does kidney dysfunction affect opioid PK/PD?

A

PK = opioids undergo phase II metabolism, so altered duration and peak concentration

PD = increased opioid receptor sensitivity, increased BBB permeability and CNS effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What 2 opioids are ok to use in renal dysfunction? What 3 are ok to use with caution? What 3 are contraindicated?

A

OK = fentanyl, methadone
Caution = hydromorphone, oxycodone, hydrocodone
AVOID = morphine, codeine, meperidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the loading dose formula? What is the most important variable?

A

LD = (desired change in concentration) x Vd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the maintenance dosing equation? Which variable is most important?

A

MD = Css,desired x (CL x T) / F
Clearance is most important

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What SEVEN antimicrobials DO NOT require renal dose adjustment? (MEMORIZE!)

A

*Clindamycin
*Azithromycin
*Linezolid
*Metronidazole

*Ceftriaxone
*Doxycycline
*Moxifloxacin

CALM CDM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does volume of distribution change with edematous states in kidney dysfunction? With wasting/volume depletion?

A

Edematous = increased Vd
Wasting = decreased Vd

As renal function decreases, it decreases the ability to remove fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Phenytoin concentration is obscured by renal dysfunction due to alterations in ________ ________, Vd and free fraction. It also has a ______ therapeutic index and many DDIs.

A

Protein binding
Narrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the target total [phenytoin]? What is the target free [phenytoin]?

A

Total target = 10 - 20 mcg/mL
Free target = 1 - 2 mcg/mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What anticoagulants do NOT need renal dosing?

A

Warfarin, argatroban, heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the ranking of least to most renally cleared DOAC?

A

Least:

Apixaban
Rivaroxaban
Edoxaban
Dabigatran

Most:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the Cockcroft-Gault equation?

A

(140-Age) x IBW / (72 x SCr) [x 0.85 for women]

IBW = 50 [45.5 for women] + (2.3 x inches > 60)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

______ diuretics and _____________ diuretics should be avoided is CrCl < 30 ml/min

A

Thiazides
Potassium-sparing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

When dosing a loop diuretic, if the patient has a CrCl of:

25 - 50 ml/min = __ x the dose
<25 ml/min = __ x the dose

A

25 - 50 ml/min = 2x the dose
<25 ml/min = 4x the dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What analgesics should absolutely be avoided in CKD?

A

NSAIDs

Use Tylenol instead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is dialysis? What is CKD5?

A

Dialysis = removal of waste products/fluids from the body on the basis of particle differences passing through a membrane

CKD5 is when GFR<15
CKD5D is another name for “dialysis”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the qualifications for ESRD?

A

Dialysis required for >3 months
GFR<15 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are some methods of drug removal in dialysis?

A

Diffusion (passive)
Convection (due to pressure, not concentration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the 3 dialysis modalities?

A

Hemodialysis
Peritoneal dialysis
Continuous Kidney Replacement Therapy (CKRT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the three ways to conduct hemodialysis from lowest risk to highest?

A
  1. Arteriovenous fistula (preferred for long-term)
    • where vein and artery are connected
  2. Arteriovenous graft
    • graft into nearby vein and artery
  3. Central venous catheter
    • tube into vena cava (last line)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is peritoneal dialysis?

A

Infuse dialysate into peritoneal cavity, let it sit then remove (“dirty”)

Extracts urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is continuous kidney replacement therapy?

A

Aka “Slow hemodialysis”
For critically ill, Hemodynamically unstable patients
Includes CVVH (Continuous venovenous) and CVVHD (usually convection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Hemodialysis mostly uses ______ clearance mechanism, while hemofiltration and hemodialfiltration mostly use ______ clearance.

A
  1. Diffusion
  2. Convection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the steps for HD drug concentration monitoring?

A
  1. Obtain drug concentration prior to HD
  2. Estimate HD drug removal
  3. Based on post HD estimates, adjust dose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the general schedule of hemodialysis?

A

HD = 3 times per week, each session is 3-4 hours long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Drug removal is ______ efficient with HD compared to peritoneal dialysis.

A

More
PD has much smaller pores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Name 6 complications of hemodialysis

A

Fatigue
Bleeding
Infection
Thrombosis
Cramping
Hypotension

F BITCH (lol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What causes hypotension in hemodialysis?

A

Hypovolemia, excess fluid removal, antihypertensives before HD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What fluids/medication do we use to manage HD hypotension?

A

Small saline bolus
Decrease fluid removal
MIDORINE
- a-1 agonist = increased vasoconstriction (increases BP)
- 2.5 - 10 mg by mouth 30 minutes before HD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What causes cramping in hemodialysis? What drugs/fluids do you use to manage?

A

Causes: hypovolemia (less muscle perfusion)
Fluid treatment: small saline bolus
Drugs:
- Vitamin E (400 IU PO at bedtime)
- Quinine (324 mg PO daily) [not for leg cramping!]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What drugs should be used to manage thrombosis in hemodialysis?

A

Prevention: heparin with dialysis
Drugs: Alteplase 2 mg/mL instilled for 30-120 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the minimum vancomycin concentration for post-HD?

A

15-20 mg/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What percent of vancomycin does hemodialysis usually remove?

A

30 - 70%
(We will use 40%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the best measure of anemia? What is the cutoff for this measure of anemia in CKD?

A

Hemoglobin
Males: Hb < 13 g/dL
Females: Hb < 12 g/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the 4 goals of therapy for CKD anemia?

A
  1. Increase oxygen-carrying capacity
  2. Improve quality of life
  3. Prevent symptoms and complications of anemia
  4. Decrease need for blood transfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

T/F: Decreased mortality is a goal of treatment

A

False!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

When GFR is < ____ ml/min/1.73m2 anemia begins to develop

A

45

57
Q

Which two labs are used to decide on treatment for anemia?

A

TSat (transferrin saturation)
Serum Ferritin

58
Q

What does hepcidin do?

A

It allows for iron uptake
(If hepcidin is low, then iron cannot be taken into cells)

59
Q

What is the most common cause of erythropoietin resistance?

A

Iron deficiency

60
Q

How often should an iron panel be taken for ESRD patients?

A

Every 3 months

61
Q

What is the goal of therapy for anemia in CKD?

A

TSat > 30%
Serum Ferritin > 500 ng/mL

62
Q

What are some key points of oral iron therapy? (Absorption, AEs, adherence, price, speed of iron distribution)

A
  • Poor absorption (10-15%)
    -AEs: GI (nausea, constipation, dark stools)
  • Bad adherence (<50%)
  • Cheap
  • Slow iron replenishment
63
Q

What are some key points of parenteral/IV iron replacement therapy? (Absorption, AEs, adherence, price, speed of iron distribution)

A
  • Good absorption
  • AEs (infusion reactions/anaphylaxis)
    AVOID IN INFECTION
  • Adherence: usually inpatient only
  • Expensive!!
  • Quick replenishment
64
Q

What is the most commonly used oral iron supplement?

A

Ferrous sulfate

65
Q

What are the oral iron supplements?

A

Ferrous sulfate*
Ferrous fumarate
Ferrous gluconate
Polysaccharide iron
Ferric citrate

66
Q

What is the dosing regimen of oral iron supplements?

A

Once daily or every other day

67
Q

What are the IV formulations of iron replacement therapy? Which is the most common?

A

Iron Dextran (REQUIRES TEST DOSE! Anaphylaxis risk)
*Ferric Gluconate
*Iron Sucrose

Ferumoxytol
Ferric carboxymaltose
(These are more common outpatient, more expensive but require fewer doses)

68
Q

If a patient is on dialysis, which type of iron replacement is preferred?

A

IV iron is preferred

69
Q

What are erythropoesis-stimulating agents (ESAs)?

A

Type of colony-stimulating agent, promote differentiation of erythrocytes, reticulocytes are biomarkers

70
Q

What are the 4 types ESAs?

A
  1. Epoetin alfa [Epogen] (SQ preferred)
  2. Darbepoetin alfa (200x more potent than epo alfa)
  3. Methoxy polyethylene glycol epoetin beta (longest acting)
  4. Epoetin alfa epbx [Retacrit] (cheaper, biosimilar of Epogen)
71
Q

What is the Hb goal for ESA treatments?

A

Hb: 10-11 (do not exceed 11.5, BBW for >11)

72
Q

What are some adverse effects of using ESAs?

A

Hypertension
Increased thrombosis (DVT, PE, MI, CVA)
Headache, edema, fatigue

PRBCA: Pure red blood cell aplasia (dangerous!)

73
Q

While we try to avoid blood transfusions as much as possible, when would you want to use one?

A

Administer packed red blood cells in SEVERE ANEMIA (Hb <7 g/dL)

74
Q

As GFR declines, MBD worsens. What are some symptoms MBD?

A

USUALLY ASYMPTOMATIC
Identified through routine lab testing

75
Q

What 3 parameters should be monitored in CKD-MBD?

A
  1. Calcium + Phosphorus
  2. iPTH
  3. 25-OH Vitamin D
76
Q

What is the corrected calcium equation?

A

Correct Ca+2 = measured Ca + 0.8 x (4 - albumin)

77
Q

What are 3 consequences of CKD-MBD?

A

CV disease
Bone disease
Calciphylaxis (CUA)

78
Q

What are the goals of treatment of CKD-MBD?

A
  • prevent CV disease and calcification
  • prevent secondary hyperparathyroidism and renal osteodystrophy
  • maintain critical parameters (calcium, phosphate, PTH)
  • Prevent mortality (but no treatments help w mortality)
79
Q

What are the three steps in treatment of CKD-MBD?

A
  1. Phosphate binders
  2. Activated vitamin D
  3. Calcimimetic
80
Q

In CKD-MBD, when using PHOSPHATE BINDERS you use _________ if calcium is normal or high and ________ if calcium is low.

A

Normal-high: non-calcium based binder
Low: calcium based binder

81
Q

Name the 4 major calcium-based binders (phosphate binders) and when each would be preferrred

A
  1. Sevelamer carbonate (Renvela) = 1st line
  2. Lanthanum (Fosrenol) = chewable
  3. Ferric citrate (Auryxia) = if iodine deficiency (mild), $ and 6 tabs QD
  4. Sucroferric oxyhydroxide (Velphoro) = good if pill burden is high
82
Q

What are the two main calcium-based binders (phosphate binders)? Which is 1st line?

A
  1. Calcium acetate (1st line) = more $, but less Ca = lower hypercalcemia risk
  2. Calcium carbonate = cheaper, high Ca may risk hypercalcemia
83
Q

In CKD-MBD, when using PTH LOWERING AGENTS you use _________ if calcium is high and ________ if calcium is low.

A

High = Calcimimetic
Low = Activated vitamin D + analogs

84
Q

What are the two calcimimetics to know? Which is PO and which is IV?

A

PO: Cinacalcet (Sensipar)
IV: Etelcalcitide (Parsabiv)

Calcimimetics pretend to be Ca, causes downregulation calcium synthesis

85
Q

What are the three Vitamin Ds? Which one is endogenous/active and which two are not?

A

Calcitriol = endogenous and active!

Non-endogenous:

Paricalcitol
Doxcalciferol
(Contain less calcium and phosphate)

86
Q

Goals for treatment of secondary hyperparathyroidism are: (4)

A
  1. Avoid hypercalcemia from overcorrection
  2. Get phosphorus into normal range
  3. Ca x Phos <55 (not recommended to use this)
  4. iPTH < 2 - 9x ULN for assay
87
Q

Phosphate binders should ALWAYS be taken _______ _______

A

With food!

88
Q

What are some adverse effects of calcium-based phosphate binders?

A

Abdominal pain/GI discomfort and Nephrolithiasis
“Bones got Stones and abdominal groans”

Also calciphylaxis

89
Q

What drugs have DDIs with calcium-based phosphate binders? (3) How long is the required windows between administrations?

A

DDIs:
Fluoroquinolone
Levothyroxine
Iron

Separate by ~2 hours

90
Q

What is the dosing for non-calcium based binder Sevelamer?
Does it affect any other condition (dyslipidemia)?

A

If SPhos is:

5.5 - 7.5 mg/dL = 800 mg TID
7.5 - 9 mg/dL = 1200 - 1600 mg TID
>9 mg/dL = 1600 mg TID

Also helps lower LDL and increase HDL!

91
Q

What is the dosing for Lanthanum carbonate?

A

Initial dose = 500 mg TID
MUST CHEW

A little more potent than sevelamer

92
Q

What is the dosing for ferric citrate? (As a Phosphate binder)
What are some AEs? What is it’s benefit?

A

420 mg (two 210 mg tabs) TID
AEs: GI, diarrhea, iron overload, stool discoloration

Benefit = moderate TSat and ferritin increase (8.6%, 114 ng/mL)

93
Q

Aluminum based phosphate binders exist and bind to phosphate extremely effectively. Why don’t we use them?

A

They are last line because there are serious AEs (GI, CNS toxicity, aluminum toxicity, microcytic anemia)

94
Q

For ESRD patients, every 1 mg/dL increase in PHOSPHORUS above normal increases mortality risky by ____%!

A

18

95
Q

Vitamin D2 = ______
Vitamin D3 = ________
1,25-OH D3 = ___________

A

D2 = Ergocalciferol
D3 = Cholecalciferol
1,25-OH D3 = calcitriol (active)

96
Q

When should calcitriol NOT be used to stabilize secondary hyperparathyroidism?

A

When the patient has hypercalcemia or hyperphosphatemia (use calcimimetics)

97
Q

Ergocalciferol and cholecalciferol are _______ forms of vitamin D. They are available OTC and are (cheap/expensive). Recommended for vitamin D deficiency.

A

Inactive, cheap

98
Q

What is calcifediol?

A

A prohormone of calcidiol
Approved in CKD stages 3 and 4 (not ESRD!)
Available as ER capsule
AEs: hypercalcemia/hyperphosphatemia
SCa < 9.8, SPhos < 5.5

99
Q

What is the MOA of calcitriol?

A

Suppresses PTH by increasing calcium concentrations = direct stimulation of parathyroid VDR and suppression of PTH release

100
Q

Vitamin D analogs have what advantages?

A

Less hypercalcemia
Less hyperphosphatemia
Highly effective

101
Q

What is cinacalcet dosing? What is the time frame for titration up?

A

Dose: 30 mg/day PO
Titration up over 2 - 4 weeks

102
Q

Cinacalcet is metabolized by ________ and has a (large/small) Vd. It is (not highly/highly) protein bound.

A

CYP3A4
Large
Highly

103
Q

What are major AEs and DDIs of cinacalcet?

A

GI = N/V in ~50%
Hypocalcemia (bc Calcimimetic)
QTc prolongation

Potent CYP2D6 inhibition
CYP3A4 inhibitors increase cinacalcet concentration

104
Q

What is Etelcalcitide and what are it’s adverse effects?

A

IV Calcimimetic (as opposed to cinacalcet) and is dosed at hemodialysis
Less GI effects, still some N/V

105
Q

When classifying CKD, what are the GFR stages and cutoffs?

A

G1: >90
G2: 60-89 (mild)
G3a: 45-59 (mild/mod)
G3b: 30-44 (mod/severe)
G4: 15-29 (severe)
G5: <15 (failure)

106
Q

When classifying CKD, what are the albuminuria cutoffs?

A

A1: <30 mg/g (mild)
A2: 30-300 mg/g (moderate)
A3: >300 mg/g (severe)

107
Q

What is the “CGA” that dictates CKD classification?

A

Cause
GFR
Albuminuria category

108
Q

What is the intact nephron hypothesis? (From patho)

A

When there is moderate nephron loss, the remaining nephrons work harder to filter urine, causing kidneys to appear “healthy”. Nephron loss is replaced by fibrotic tissue.

109
Q

What 4 major conditions cause CKD?

A
  1. Diabetes
  2. Hypertension
  3. Glomerulonephritis
  4. Polycystic kidney disease
110
Q

What is the first sign of diabetic nephropathy?

A

Elevated albumin

111
Q

What are modifiable risk factors for CKD?

A
  • Diabetes
  • HTN
  • protenuria
  • hyperlipidemia
  • tobacco use
112
Q

What is the MOST important predictor of CKD progression?

A

Management of underlying causes of CKD

113
Q

What are the first, second and third line agents for diabetics with CKD?

A
  1. SGLT-2i and Metformin
  2. GLP1-RA (weight loss benefits, no renal benefits)
  3. Other diabetic drugs
114
Q

What are the first, second (2), and third line agents to treat CKD in patients with HTN?

A
  1. ACE/ARBs
  2. Finerinone (non-steroid MCRA)
    OR
  3. DHP CCB [diltiazem, verapamil]
  4. Steroidal MCRA (spironolactone)
115
Q

What are the first and second line agents to treat CKD in patients with hyperlipidemia?

A
  1. Moderate-high intensity statin
  2. Antiplatelet agents (P2Y12s, aspirin)
    OR
  3. Ezetimibe, PCSK9i, icosapentyl ethyl
116
Q

What is the BP goal of KDIGO?

A

Systole < 120 mmHg (aggressive!)

117
Q

What are some non-pharmacological treatments for HTN in CKD patients according to KDIGO?

A

Limit Na intake to <2g a day
Moderate intensity exercise
Weight loss to 20-25 BMI
Limit alcohol to 1-2 drinks daily

118
Q

Are statin drugs renally eliminated? Would this make it more or less likely to be used in treatment of hyperlipidemia with CKD?

A

They are NOT significantly renally eliminated. It’s first line for hyperlipidemia with CKD.

119
Q

Should we initiate statins for CKD stage 5 patients on dialysis?

A

Do NOT initiate!

120
Q

For general CKD management/slowing progression, what is the first-second-third line treatments?

A

1st = ACE/ARBs
2nd = SGLT2is
3rd = Finerinone

121
Q

We target proteinuria reduction of ____ to ____ % on CKD patients

A

30-50%

122
Q

What drugs are best at reduction proteinuria in CKD patients?

A

ACEis/ARBS

123
Q

Which ACEis are short acting?

A

Captopril
Enalapril

124
Q

Which ARBs** are short acting?

A

Trick question! They’re all relatively long acting compared to short-acting ACEis

125
Q

Should we initiate dual RAAS inhibition?

A

In most cases, NO! ACEi + ARB can be dangerous (hypotension). Instead combine one ACEi/ARB with Finerinone

126
Q

What is Aliskiren?

A

A direct renin inhibitor (RAAS), dosed at 150-300 mg PO daily
CI in preganancy or combination with ACEi/ARB
Not as commonly used

127
Q

What are ABSOLUTE CONTRAINDICATIONS of RAAS inhibition in CKD?

A

Pregnancy
Bilateral** renal artery stenosis
History of ACEi/ARB angioedema

128
Q

What are conditions to USE CAUTION when using RAAS inhibitors in CKD?

A

Unilateral* renal artery stenosis
Hyperkalemia
Dehydration/hypovolemia
Hypotension
Kidney dysfunction (SCr>3)

129
Q

What labs would you monitor for RAAS inhibitor use in CKD and when?

A

K+ and SCr within 1-2 weeks if high risk, or 4 weeks if normal

130
Q

What are some AEs that come with RAAS drugs?

A

Hypotension
Orthostasis
Dizziness
Cough
Hyperkalemia

131
Q

Quinapril (an ACEi) contains magnesium. What two drug classes should be avoided?

A

Fluoroquinolones, tetracyclines

132
Q

T/F: SGLT2is should only be administered if a CKD patient is diabetic

A

False! Second line regardless of diabetes status!

133
Q

Who should AVOID SGLT2is of the CKD patients?

A

THose with Type I diabetes! May cause euglycemic diabetic ketoacidosis

134
Q

What is the dosing for Finerinone?

A

10-20 mg PO daily

135
Q

What are some potential AEs of Finerinone?

A

Hyperkalemia (often potassium sparing)
Hypotension (MCRAs are used in HTN)

136
Q

What drug (also used to decrease uric acid) can be used to slow CKD? [technically KDIGO says there is insufficient evidence]

A

Allopurinol

137
Q

What drug may slow metabolic acidosis in CKD patients?

A

Sodium bicarbonate

138
Q

What are some consequences of secondary hyperparathyroidism? (7)

A

ESA resistance
LV hypertrophy
Parathyroid hyperplasia
Myocardial fibrosis
Immune dysfunction
Lipid metabolism
Renal Osteodystrophy

Therapeutics + Fall 2022 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions