Brainscape's Knowledge GenomeTM

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


See full index

ClinMed II Exam 5 GU/Renal > Chronic kidney disease (CKD) > Flashcards

Chronic kidney disease (CKD) Flashcards

1
Q

What is one of the leading causes of death in the US?

A

kidney diseases

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

What is one of the leading causes of kidney failure (3/4 cases)?

A

DM and high BP

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

Chronic kidney disease is more prevalent in which populations?

A

Older, Women, Racial minorities, Lower socioeconomic status, DM and HTN

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

Median wait time for individuals first kidney transplant?

A

3.6 yrs

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

Characteristics of acute kidney disease?

A

Rapid loss of function, commonly reversible
-usually caused by: dehydration, blood loss, meds, IV contrast, obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Characteristics of chronic kidney disease?

A

Progressive loss of function or presence of damage that lasts 3+ months, commonly irreversible
-usually caused by: long term chronic systemic/autoimmune/genetic diseases (DM, HTN, Lupus, PKD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Chronic kidney disease results in an inability to maintain what?

A

Acid-base balance, fluid/electrolyte balance, excretion of nitrogenous waste

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

As CKD progresses, what happens to glomerular filtration?

A

Decreases

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

The most accurate measure of GFR is using what?

A

plasma or urinary clearance of an exogenous filtration marker (ex. insulin) *not routinely performed

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

Normal value for GFR?

A

90+

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

What value of GFR indicated a treatment plan for kidney failure (dialysis or kidney transplant)?

A

Below 15

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

In clinical practice, estimated GFR is calculated using what?

A

Endogenous filtration markers such as serum CR +/- cystatin C level, in combo w/ demographic factors such as age and gender

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

What is the recommended calculation of eGFR?

A

2021 CKD EPI equation

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

How does the 2021 CKD EPI equation estimate GFR?

A

Serum Cr, age, sex
(+/- cystatin)

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

Stage 0 of CKD?

A

Increased risk (DM, HTN, etc.) GFR: >/=90

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

Stage 1 of CKD?

A

Kidney damage w/ normal or inc. GFR (>/=90)

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

Stage 2 of CKD?

A

Kidney damage w/ mildly reduced GFR (60-89)

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

Stage 3 of CKD?

A

Moderately reduced GFR (30-59)

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

Stage 4 of CKD?

A

Severely reduced GFR (15-29)

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

Stage 5 of CKD?

A

Overt renal failure (dialysis) GFR: <15

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

Individuals may often remain _____ until kidney disease is far advanced?

A

Asymptomatic

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

PMH to gather for CKD?

A

BP and glucose control, family/personal hx of: HTN, DM, genetic/autoimmune kidney disease, abnormal kidney imaging/urine studies, cancer/chemo/radiation

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

Med history for CKD?

A

Review meds, potentially nephrotoxic agents (even if not currently taking)

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

Social history for CKD?

A

Human immunodeficiency, Hep C/B, IV drug use, STDs, occupational contaminants (lead, pesticides)
Pts w/ risk factors: test for presence of these viruses if underlying cause not clear

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

Physical exam for CKD?

A

Evaluate for:
-volume imbalance/third spacing (edema, inc. JVP)
-microvascular injury (AV nicking, retinopathy –> chronic microvascular dz, peripheral neuropathy –> diabetic microvascular dz)
Auscultate:
-Abd bruit
Palpate:
-abnormal distal pulses (Renal artery stenosis/RAS)
-enlarged kidneys (polycystic KD)

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

CBC/CMP findings in CKD?

A

Elevated BUN & Cr
Hyperkalemia, Hyperphosphatemia, Hypocalcemia, Low hemoglobin/hematocrit

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

Urinalysis/microscopy for CKD?

A

Proteinuria/albuminuria, RBC/casts, WBC/casts

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

As kidney function decreases, what happens to Cr levels?

A

Increase (waste product develops from normal wear/tear on body muscles)

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

Normal levels of Cr vary depending on what?

A

Age, race, body size

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

What Cr level in men may be an early sign of kidneys not functioning properly?

A

> 1.4

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

What Cr level in women may be an early sign of kidneys not functioning properly?

A

> 1.2

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

BUN measures what?

A

Amount of nitrogen in blood (waste product of urea)

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

When is urea made in the body?

A

When protein is broken down

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

What happens to BUN levels as kidney function decreases?

A

Increase

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

Multiple lab abnormalities and declining GFR function may require what?

A

Direct evaluation and management by nephrologist to conduct serologic testing +/- renal bx

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

Lab data for albuminuria and proteinuria in CKD?

A

Albumin spot samples (common) or 24hr urine collection
Mod inc: 30-300 (spot) and 300mg/24hrs
Severely inc. >300

Dipstick urine
Mod increase: 1+
Severe: >1+

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

Additional diagnostics for CKD?

A

EKG changes (electrolyte abnormalities)
+/- US (CKD late stage: small echogenic kidneys bilaterally), r/o obstruction, r/o RAS

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

What to monitor in progression of CKD?

A

Proteinuria/Albuminuria, Cr/BUN, Na+ and volume, Posph/Calcium balance & PTH, Hematocrit/Erthropoietin (EPO), K+, Acid-base

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

The RAAS pathway is initiated in response to what?

A

Lifesaving measures, fluid/electrolyte imbalance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What does RAAS regulate?

A

Aldosterone secretion (aldosterone regulates blood volume, BP, Na+, K+, H+ in blood)

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

What causes the juxtaglomerular cells of the kidneys to increase renin?

A

Dehydration, Na+ deficiency, hemorrhage –> dec. in blood volume —> dec. BP
(Liver also releases angiotensinogen)

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

Increased renin/angiotensinogen will increase angiotensin I, leading to what?

A

ACE converting angiotensin I to angiotensin II in the lungs

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

Effects of angiotensin II?

A

Vasoconstricts arterioles (increasing BP until normal), acts on adrenal cortex (as well as extracellular K+) to inc. aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What does increased aldosterone lead to?

A

In kidneys, increase Na+ and water reabsorption/K+ and H+ excretion in urine —> inc. blood volume to act on BP

45
Q

What is tubuloglomerular feedback?

A

Macula densa (area of specialized cell) senses NaCl conc and GFR —> works w/ RAAS to regulate renal BF/GFR
*high NaCl: increased GFR
*low NaCl: decreased GFR

46
Q

When renal BF/GFR is reduced, or if there is a decrease/dilution of Na and Cl ion concentration in filtrate, what occurs?

A

Release of prostaglandins –> releases renin –> activates RAAS to inc. BP and volume –> increases retention of Na+, fluid via aldosterone

47
Q

If afferent arterioles are constricted, what will happen in the capillaries?

A

BP will drop in capillaries of kidneys and GFR is reduced

48
Q

When angiotensin II levels increase d/t activation of RAAS, most arteries in the body experience what? What do efferent arterioles do to compensate?

A

Vasoconstriction in order to maintain adequate systemic BP (reduced BF/pressure to the kidneys)
TO compensate: efferent arterioles constrict to greater degree in response to elevated angio II

49
Q

Efferent arteriole constriction increases what?

A

Hydrostatic pressure in glomerular capillaries/drives more filtrate into bowmans capsule, increasing the GFR
*hyperfiltration

50
Q

In initial nephron injury, the remaining functioning nephrons experience what?

A

Hyperfiltration (to compensate for loss of non-functioning units and maintain GFR)

51
Q

What is a consequence of hyperfiltration by remaining functional nephrons?

A

Glomerular capillary HTN

52
Q

How does hyperfiltration further the RAAS cycle?

A

Efferent arteriole vasoconstriction causes stimulation of RAAS –> initiates cycle to inc. blood volume/BP –> causes further glomerular injury from inc. capillary pressure

53
Q

What is glomerular pore size altered by?

A

Angio II (increases protein leak across glomerular BM) –> leads to inc. in glomerular permeability/excess protein filtration

54
Q

What results as a consequence of repeated/continued activation of RAAS in kidney pathology?

A

Albuminuria/proteinuria

55
Q

Excess protein excretion in the urine contributes to what?

A

Progressive kidney damage: proteins in urine are toxic to tubules (cause tubular injury, tubulointerstitial inflammation, scarring)

56
Q

What are the underlying causes of injury that develop in the renal parenchyma?

A

Proinflammatory/Profibrotic effects of Angio II and aldosterone

57
Q

What promotes fibrosis and scarring in the kidneys?

A

Inflammatory mediators

58
Q

What ultimately occurs in kidney injury that promotes CKD?

A

glomerulosclerosis and tubulointerstitial fibrosis

59
Q

Risk factors for CKD?

A

DM** (leading cause of CKD/ESRD), HTN, Glomerulonephritis, Tubulointerstitial nephritis, Genetic disease, Obstructive nephropathies, Vascular disease

60
Q

What is a clinical diagnosis of a diabetic patient w/ renal injury?

A

DKD

61
Q

What reduces the progression of kidney disease w/ DM?

A

Intensive insulin therapy to maintain HbA1c levels

62
Q

Poorly controlled diabetes leads to what?

A

Renal injury w/ albuminuria +/- reduced GFR and activation/re-activation of RAAS pathway (leading to poor BP control)

63
Q

Normal glucose handling in the kidneys?

A

Filtration of glucose w/ 100% reabsorption of glucose

64
Q

Glucose handling w/ DM in the kidneys?

A

High filtered loads of glucose, filtered load exceeds reabsorption capacity, glucose excreted in urine, polyuria

65
Q

What is diabetic nephropathy/diabetic kidney disease (DKD)?

A

Elevated blood glucose rises beyond kidneys capacity of reabsorption

66
Q

What does non-reabsorbed glucose raise?

A

osmotic pressure, causing more water to be carried out –> inc. volume of urine–> dilutes NaCl in filtrate/signals RAAS

67
Q

Treatment goal of poor glucose control?

A

Halt progression to diabetic nephropathy or DKD (glycemic control, BP control, lifestyle modifications)

68
Q

DKD patients have a high rate of progression to what?

A

CKD, cardiovascular disease, mortality

69
Q

Most common comorbidity in DKD?

A

HTN

70
Q

Recommended BP in DKD?

A

<130/80
*reduced CV morbidity/mortality

71
Q

Be flexible with target BP in DKD if patient is at risk for what?

A

Hypotension

72
Q

In DKD, glycemic control slows disease progression to what?

A

ESRD

73
Q

Target HbA1c in DKD?

A

6.5-8%

74
Q

Be flexible with target HbA1c if patient with DKD is at risk for what?

A

Hypoglycemia

75
Q

Pharmacologic tx for glycemic control in DKD?

A

Metformin (1st line, cost effective)
SGLT2i (first line)
GLP-1 RA (second line)
other options: insulin/other antidiabetic agents

76
Q

Pharmacologic tx for HTN control in DKD?

A

ACEi or ARB (1st line)
*titrate to max dose tolerated, do not use both simultaneously
*combo therapy w/ diff HTN agents may be necessary for BP control

77
Q

Renal protective qualities of ACEi and ARBs?

A

Block RAAS pathway/delay DKD progression in pts w/ albuminuria and HTN

78
Q

What other pharmacologic tx can be considered for DKD?

A

Statins

79
Q

What is the secondary leading cause of ESRD?

A

Hypertensive nephropathy or hypertensive kidney disease

80
Q

Sustained HTN leads to what?

A

Renal injury and worsening BP control

81
Q

Mechanisms of HTN in CKD include what?

A

Volume overload, Sympathetic overactivity, salt retention, endothelial dysfunction, alterations in hormone systems that regulate BP

82
Q

Treatment goal w/ HTN for kidney dz?

A

halt progression into Hypertensive nephropathy or hypertensive kidney disease

83
Q

Target BP in Hypertensive nephropathy or hypertensive kidney disease?

A

<130/80

84
Q

Treatment for pts with HTN and albuminuria in Hypertensive nephropathy or hypertensive kidney disease?

A

First line: ACEi and ARB
2nd/3rd line if volume overload: Loop diuretic +/- CCB

85
Q

Both ACEi and ARBs reduce what?

A

Glomerular permeability barrier to proteins (limit proteinuria, filtered protein-dependent inflammatory signals) and decrease glomerular intra-capillary pressure

86
Q

Caution with ACEi and ARBs w/ Cr and GFR?

A

Expect worsening Cr levels up to 30% and acute reduction in GFR from baseline a few days after starting meds
(safe to continue if values stabilize after initial rise)

87
Q

Caution with ACEi and ARBs w/ K+ levels?

A

Expect raise in K+ levels
if hyperkalemia (>6mmol/L), stop any other harmful drugs (reduce K+ sparing drugs)
If it still continues: stop ACEi/ARB

88
Q

Monitoring w/ ACEi & ARBs?

A

Monitor serum Cr and K+ conc. prior to initiation, w/in 1 week of starting, w/in 1 week of increase in doses
After: monthly, q3 months, then quarterly

89
Q

Common ADRs w/ ACEi & ARBs?

A

Hypotension, cough (ACEi), hyperkalemia, headache, dizziness, fatigue, nausea

90
Q

Contraindications of ACEi or ARBs?

A

-Previous angioedema or renal artery stenosis
-Pregnancy category D: avoid

91
Q

When should kidney disease be referred to a nephrologist?

A

eGFR <60 (stage 3), GFR <30 (CKD stage 4 and beyond), persistent albumin/Cr ratio (>/= 300), abnormal urine microscopy, hx of systemic autoimmune/genetic dz, large/cystic kidneys on imaging/exam, rapid progression of loss of kidney function, difficulty managing labs, Single kidney w/ eGFR <60, resistant HTN, pregnancy, young pt w/ unclear cause of CKD

92
Q

ESRD treatment?

A

Dialysis, transplant

93
Q

Dialysis is an artificial replacement for what?

A

Lost kidney function in those w/ CKD stage 5

94
Q

Dialysis is regarded as a holding measure for what patients?

A

Those awaiting kidney transplant

95
Q

Dialysis is sometimes the only supportive measure in which patients?

A

Those in which kidney transplant is not appropriate

96
Q

Dialysis process?

A

Using machine patients blood is pumped through blood compartment of dialyzer –> exposed to partial permeable membrane (thousands of tiny synthetic hollow fibers) –> solution flows around outside of fibers/water & wastes move between –> cleansed blood returns to body via circuit

97
Q

How is ultrafiltration achieved in dialysis?

A

Increasing hydrostatic pressure across dialyzer membrane (apply negative pressure to dialysate compartment of dialyzer)
*allows several excess L’s of fluid to be removed during typical 4 hr treatment

98
Q

What is peritoneal dialysis?

A

Sterile solution containing glucose (dialysate) is run through a tube into peritoneal cavity –> peritoneal membrane acts as partially permeable membrane

99
Q

What is the process of peritoneal dialysis?

A

Diffusion/osmosis drive waste products & excess fluid through peritoneum into dialysate until dialysate approaches equilibrium w/ body’s fluids
–> dialysate then drained, discarded, replaced w/ fresh dialysate
*repeated 4-5x a day (automatic systems can run more frequently overnight)

100
Q

How is the net effect of removal of waste products of salt and water similar in hemodialysis and peritoneal dialysis?

A

Because peritoneal dialysis is carried out for such a long period of time

101
Q

Organ donors for kidney transplant may be in what condition?

A

Living, brain dead, or dead via circulatory death

102
Q

How long after cessation of heart beat may a kidney be recovered from a donor?

A

24 hrs

103
Q

How does kidney transplant remove the need for dialysis?

A

Transplanted kidney takes over work of both failure kidneys
*often kidney will start making urine as soon as bloodflow starts

104
Q

Indication for kidney transplant?

A

ESRD regardless of primary cause

105
Q

Majority of kidney transplant recipients are on ______ at time of transplant?

A

Peritoneal or hemodialysis

106
Q

Who may undergo pre-emptive kidney transplant before dialysis is needed?

A

Those with chronic renal failure who have a living donor available

107
Q

Complications of kidney transplant?

A

Rejection (immune response to transplanted organ) with possible need for immediate removal of organ

108
Q

When possible, kidney transplant rejection can be reduced by what?

A

Serotyping to determine the most appropriate donor-recipient match & use of immunosuppressant drugs

ClinMed II Exam 5 GU/Renal (4 decks)

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