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Renal > Renal Exam 2 > Flashcards

Renal Exam 2 Flashcards

1
Q

Define acute kidney injury

A
  • Reduction in GFR resulting in azotemia. Absence of chronic uremia. Size of kidney preserved.
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2
Q

Diagnostic criteria for acute kidney injury

A
  • Abrupt (within 48 hours) reduction in kidney function:
    a. Absolute increase in serum Cr level of 0.3 mg/dl OR
    b. % increase in serum Cr level of >= 50% (1.5 fold from baseline) OR
    c. Reduction in urine output
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3
Q

Define oliguria

A
  • UOP
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4
Q

Define anuria

A
  • UOP
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5
Q

What is uremia?

A
  • Illness accompanying kidney failure resulting from toxic effects of abnormally high [] of nitrogenous waste in blood.
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6
Q

When consulting a cardiologist, you share EKG findings? What is this for nephrologists?

A
  • UA
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7
Q

Relationship between GFR and Cr? Describe how this relationship is unique at certain concentrations of Cr.

A
  • Inversely proportional
  • At high concentrations of Cr, rise in Cr does not produce clinically significant reduction in GFR. However at lower concentrations, small rise in Cr result in significant reduction in GFR. Eg. 2 -> 3 = 50% reduction in GFR from 50 -> 25 ml/min
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8
Q

What is normal GFR?

A
  • ~100-110 ml/min
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9
Q

What are casts?

A
  • Trappings of cellular elements in matrix of protein secreted by renal tubule cells
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10
Q

Effect of NSAIDs on GFR

A
  • Block PGs = inability to vasodilate afferent arteriole = reduction in GFR
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11
Q

Effect of ACEi on GFR

A
  • Inhibits vasoconstriction at efferent arteriole = reduction in GFR
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12
Q

Effect of ARBs on GFR

A
  • Inhibits vasoconstriction at efferent arteriole = reduction in GFR
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13
Q

Three categories of AKI and etiologies

A
  1. Pre-renal: decreased renal perfusion without ischemia. VOLUME DEPLETION
  2. Renal: intrinsic renal dz.
  3. Post-renal: obstruction of urinary flow. OBSTRUCTION
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14
Q

BUN/Cr ratio in pre-renal AKI

A
  • > 20:1
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15
Q

Describe UA in pre-renal AKI

A
  • “Bland” = no hematuria, no proteinuria. Will be concentrated, have ketones perhaps. Casts: +/- hyaline casts.
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16
Q

FENa in pre-renal AKI

A

-

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17
Q

Most common cause of AKI?

A
  • Renal AKI, specifically ATN (acute tubular necrosis)
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18
Q

FENa in renal AKI (ie. ATN)

A
  • > 2% usually
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19
Q

Causes of ATN

A
  • Ischemia, toxins
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20
Q

Casts found in acute tubular necrosis

A
  • *

- Granular casts (muddy brown urine)

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21
Q

Describe microscopic morphological features of ATN

A
  • Tubular dilatation, attenuation of tubular epithelium, loss of epithelial cell brush border, granular cast material, mitotic figures (regeneration occurring)
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22
Q

Type of receptors found in prostate smooth muscle

A
  • Alpha-1A
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23
Q

What is the transition zone of the prostate?

A
  • Tissue that surrounds the urethra
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24
Q

What is the central zone of the prostate?

A
  • Tissue that surrounds the ejaculatory ducts as they pass through prostate
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25
Q

What is the peripheral zone of the prostate?

A
  • Glandular tissue that is most felt during the DRE
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26
Q

Location of prostate where BPH develops

A
  • Transition zone
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27
Q

Location of prostate from where majority of prostate cancer develops

A
  • 70% of cancers from the peripheral zone
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28
Q

Function of testosterone in prostate

A
  • Prostate growth and differentiation

- 5-alpha reductase converts free T into DHT that acts here

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29
Q

Most common neoplastic process in men

A
  • BPH
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30
Q

What is AUASI score?

A
  • Americal urological association sx index score. Subjective parameters to assess BPH.
  • Don’t need to know scoring
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31
Q

What is decision to treat BPH based on?

A
  • Patient’s level of bother and willingness / ability to comply with therapy.
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32
Q

Complications of BPH

A
  • Acute urinary retention, renal insufficiency, chronic/recurrent UTIs, uncontrolled gross hematuria/clot retention, bladder calculi
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33
Q

When is watchful waiting appropriate as a mgmt. option in BPH?

A
  • Mild sx (
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34
Q

Pharmacologic tx for BPH

A
  1. Alpha-1 antagonists: relax prostate and bladder neck SM. Agents = terazosin and doxazosin are non-selective. Alfuzosin, tamsulosin and silodosin are alpha-1a selective antagonists preferred in elderly where vascular side effects concerning.
  2. 5-alpha reductase inhibitors: prevent conversion of free T to DHT = decreased cell proliferation and stimulation of apoptosis. Agents = finasteride and dutasteride. Get PSA at baseline as this can decrease it by half.

** Note: combination treatment is most beneficial in reducing clinical progression of BPH (esp. with large glands!) versus monotherapy.

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35
Q

Side effects of alpha-1 antagonists used in BPH

A
  • Orthostatic HoTN, fall risk, dizziness, tiredness, nasal congestion, retrograde ejaculation, intraoperative floppy iris syndrome
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36
Q

Absolute and relative indications for prostate surgery in BPH

A
  1. Absolute: acute urinary retention, recurrent UTIs, refractory gross hematuria/clot retention, bladder stones, azotemia
  2. Relative: progression of dz on meds or desire to stop meds, incomplete bladder emptying, inability to tolerate PO therapy
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37
Q

Gold standard surgery in BPH

A
  • TURP: transurethral resection of prostate
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38
Q

Most common solid organ cancer in men

A
  • Prostate cancer
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39
Q

Which population has the highest chance of prostate cancer? What else is significant about the prostate cancer in this group?

A
  • AAs. Higher grade/stage. 2x more likely to die of dz.
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40
Q

How does risk for prostate cancer change with relatives with hx?

A
  • 2-fold risk increase with one 1st degree relative

- 5-10 fold risk increase with two to three 1st degree relatives

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41
Q

Sx with prostate cancer

A
  • Early: no symptoms

- Late: mets = bone pain; bladder outlet symptoms

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42
Q

What is the controversy surrounding prostate cancer screening?

A
  • USPSTF: no screening
  • AUA w/ACS: strongly disagrees with USPSTF as mortality of prostate cancer decreased as well as patients presenting with advanced and metastatic dz.
  • Benefit: PSA most reliable tumor marker now, mortality of prostate cancer decreased, incidence of advanced and metastatic dz decreased
  • Harm: screening results in overdiagnosis (detected of cancer that otherwise would have remained clinically silent) = unnecessary biopsies, treatments with risks/side effects with potentially no benefit in years of life saved
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43
Q

AUA position on screening

A
  • 70 yo: no screening in this group or in men with
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44
Q

What is PSA? Function?

A
  • Enzyme produced by prostatic epithelial cells that liquefies seminal fluid.
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45
Q

What can cause PSA to be elevated?

A
  • Any disruption of normal prostatic cellular architecture (BPH, inflammation, manipulation, surgery etc.)
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46
Q

Are PSA levels diagnostic?

A
  • No safe range for PSA determined.
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47
Q

When screening for prostate cancer, is DRE or PSA recommended alone?

A
  • Both must be used. Neither diagnostic for prostate cancer, but indications to proceed with biopsy, which provides definitive diagnosis for prostate cancer. Abnormalities of either screening (PSA or DRE) should prompt referral to urologist.
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48
Q

How many suspicious palpable lesions on DRE are cancer?

A
  • > 50%.
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49
Q

When is prostate biopsy indicated?

A
  • Abnormal DRE and / or PSA
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50
Q

What type of cancer are most prostate cancers?

A
  • > 95% are adenocarcinoma. Remember found in glandular peripheral zone.
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51
Q

How are prostate cancer patients risk stratified?

A
  • Stratified into low, intermediate and high risk based on:
    1. PSA
    2. Gleason score (pathology report)
    3. DRE result (palpable or not)
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52
Q

Treatment for localized prostate cancer (just in prostate)

A
  • Watchful waiting/active surveillance: low grade dz, low volume dz,
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53
Q

What is the follow up protocol for prostate cancer?

A
  • After prostatectomy, PSA > 0.2 = recurrence. Follow PSA forever.
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54
Q

Met sites for prostate cancer

A
  • Pelvic LNs -> bone (osteoblastic lesions, not osteolytic lesions) -> lung -> liver
    • Stepwise progression
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55
Q

Tx for metastatic prostate cancer

A
  • Hormone therapy: decrease androgens circulating in blood stream
  • Nearly all men progress to androgen-independent dz typically within 2-3 years. Can use systemic chemo.
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56
Q

Lymphatic drainage of testes

A
  • To retroperitoneal LNs. Arises in retroperitoneal space
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57
Q

Which scrotal masses are painful? Painless?

A
  • Painful: testicular torsion, epididymitis/orchitis, scrotal abscess, incarcerated inguinal hernia, testicular tumor, trauma
  • Painless: testicular tumor, hydrocele, spermatocele/epididymal cyst, varicocele, inguinal hernia
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58
Q

In what direction do testicles prefer to torsion?

A
  • Lateral to medial
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59
Q

What is Bell-clapper deformity? Significance?

A
  • Inappropriately high fixation of tunica vaginalis (peritoneum) to testes. This predisposes to testicular torsion, typically bilateral.
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60
Q

Sx of testicular torsion

A
  • Sudden onset of acute scrotal pain and swelling. Exquisitely tender and high-riding.
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61
Q

Most sensitive PE test in testicular torsion

A
  • Cremasteric reflex. Absence = testicular torsion.
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62
Q

Tx of testicular torsion

A
  • True vascular emergency. Send to surgery (orchiectomy if testis dead, if viable fixate to overlying fascia, always to bilateral d/t frequency of bilateral Bell-clapper deformity)
  • May try manual detorsion (open the book, un-torsion from medial to lateral) to buy time, but still needs surgery.
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63
Q

What is blue dot sign?

A
  • Twisting of testicular / epididymal appendage, which doesn’t require surgery. Pain resolves with anti-inflammatories. See good testicular blood flow on US.
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64
Q

Sx of epididymitis

A
  • Progressive, gradual onset pain (greater than 24 hours) +/- fever or irritative voiding sx
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65
Q

Etiology of epididymitis

A
  1. Infectious: young = STDS, older = bacterial GU infection

2. Non-infectious/inflammatory: meds, urinary reflux within ejaculatory ducts

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66
Q

PE findings in epididymitis

A
  • Tender mass posterolateral to testicle
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67
Q

Tx of epididymitis

A
  • Abx, anti-inflammatories, analgesics, rest, scrotal elevation (briefs), surgical drainage/orchiectomy if abscess
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68
Q

What is Fournier’s gangrene?

A
  • Fasciitis of scrotum, groin and perineum
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69
Q

In what patient population is Fournier’s gangrene commonly seen?

A
  • Immunocompromised or diabetic
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70
Q

PE findings on Fournier’s gangrene

A
  • Enlargement of scrotum, thickening and erythema, NECROTIC BLACK / ECCHYMOTIC PATCHES, CREPITUS, DISHWATER DRAINAGE
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71
Q

Why is Fournier’s gangrene so dangerous?

A
  • If left untreated will progress within hours to overwhelming bacterial sepsis with an associated high mortality
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72
Q

Tx of Fournier’s gangrene

A
  • Broad spectrum abx with aerobic and anaerobic organisms

- Surgical drainage and debridement

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73
Q

Define hydrocele vs spermatocele

A
  • Hydrocele: fluid collection bw parietal and visceral layers of tunica vaginalis surrounding testicle
  • Spermatocele: cyst arising from epididymis which contains spermatozoa
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74
Q

Are hydroceles painful? How are they found on PE?

A
  • Painless typically. Transilluminates on exam.
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75
Q

Tx of hydrocele

A
  • Congenital: surgical correction via inguinal exploration to close patent processus vaginalis and also correcting possible coexisting inguinal hernia
  • Acquired: Surgical drainage via scrotal incision.
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76
Q

Presentation of spermatocele

A
  • Painless mass above / posterior to testes (double testicle sign)
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77
Q

Tx of spermatocele

A
  • No surgical excision unless large and discomfort
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78
Q

What is a varicocele?

A
  • Abnormal dilation of veins in pampiniform plexus of spermatic cord d/t elevated venous pressure and/or incompetent valves. Most common cause of infertility in men.
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79
Q

What is most common cause for infertility in men?

A
  • Varicocele
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80
Q

Most common location for varicocele

A
  • Left. Left gonadal vein inserts into left renal vein at a right angle w/increased incidence of incompetent valves.
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81
Q

Indications for surgery on varicocele?

A
  • Painful symptomatic varicocele, significant testicular atrophy, infertility
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82
Q

Indications for exploration after blunt trauma to testicle

A
  • Disruption of tunica albuginea
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83
Q

One of the most curable solid neoplasms in men

A
  • Testicular cancer. This is most common solid tumor in ages 15-35
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84
Q

Presentation of local vs metastatic testicular cancer

A
  • Local: painless mass (most commonly!), swelling/firmness/heaviness, pain d/t bleeding/infarction, often detected by partner
  • Metastatic: depends on mets, back/abdominal pain, cough/SOB, gynecomastia/breast tenderness, LE edema, neck mass
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85
Q

Scrotal US findings in testicular cancer

A
  • Heterogenous mass
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86
Q

Tumor markers of testicular cancer

A
  • AFP (never pure seminoma), beta HCG, LDH (advanced seminoma)
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87
Q

When should testicular cancer markers be obtained?

A
  • Prior to tx, check after to make sure it resolves.
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88
Q

Describe tx for testicular cancer

A
  • All tumors initially receive a radical orchiectomy via inguinal approach and w/ high ligation of spermatic cord at internal inguinal ring! Trans-scrotal bx is to be condemned.
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89
Q

Staging of testicular cancer should make sure to check where?

A
  • Retroperitoneal space (d/t LN drainage), CXR, CT of abdomen/pelvis
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90
Q

First site of testicular cancer met

A
  • Retroperitoneal LNs
  • Right: interaortacaval
  • Left: para-aortic
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91
Q

Physiological processes of erection

A
  1. Neurologically mediated increase in penile arterial flow
  2. Relaxation of cavernous smooth muscle
  3. Restriction of venous outflow

**Overall: stimulus = NO release (PSNS) = cGMP formation (induces Ca decrease) = vascular SM relaxation = influx of blood in cavernous sinusoids

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92
Q

Relationship between ED and vascular dz

A
  • Well established. ED may be first identified sx of vascular dz. Smaller cavernosal arteries make them more susceptible to occlusion.
  • Early tx and lifestyle modification before dz severe or life threatening.
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93
Q

Vascular causes of ED

A
  1. Atherosclerosis and associated risk factors: HTN, DM, dyslipidemia, smoking, obesity, sedentary lifestyle
  2. Venous leak
  3. Vascular surgery
  4. Pelvic/perineal trauma
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94
Q

Mechanism for vascular dysfunction that leads to ED

A
  1. Phase 1: Oxidative stress (from various risk factors) = impaired NO production at endothelial cell
  2. Phase 2: Endothelial cell early vascular damage (continued assault d/t risk factors) = atherosclerotic changes. ED seen here.
  3. Phase 3: Endothelial cell late endothelial dysfunction (continued assault) = CAD, thrombosis, PVD, CVA, worsening ED.
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95
Q

Medication causes of ED

A
  1. Beta-blockers
  2. SSRIs

** many others

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96
Q

First line therapy for ED

A
  1. Lifestyle modification: stop smoking, limit/avoid etoh, follow healthy diet, exercise regularly
  2. Modification of drugs: change / reduce beta-blockers, SSRIs if possible
  3. Counselling, androgen replacement therapy

** for exam, if answer choice about being a really good doctor and talking about lifestyle etc, choose that one

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97
Q

Medications used for ED? MOA?

A
  • PDE5 inhibitors: inhibits degradation of cGMP by PDE5 = increases cGMP [] = facilitates SM relaxation in cavernous smooth muscle. Note: does not work on penis in absence of stimulation because NO and cGMP levels low in flaccid state.
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98
Q

Adverse effects of PDE5 inhibitors

A
  • HA, flushing, rhinitis, dyspepsia, visual changes, back pain
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99
Q

Contraindications to PDE5 inhibitors

A
  • Nitrate use, active coronary ischemia, cardiac conditions, life-threatening CV event in past 6 months, hypotension, retinitis pigmentosa, caution with alpha-blocker use
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100
Q

When should ED patients be referred to urologist?

A
  • Failure of first line therapy
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101
Q

Define normal BP and pre-HTN

A
  • Normal:
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102
Q

Define HTN per JNC7

A
  • Stage 1: 140 – 159 or 90 – 99

- Stage 2: > = 160 or >= 100

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103
Q

Define primary vs secondary HTN. Which is most common?

A
  • Primary (aka essential or idiopathic): no known cause
  • Secondary: associated with underlying primary dz
  • Most common = primary 90%. Secondary = 10%.
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104
Q

Define isolated systolic vs isolated diastolic HTN

A
  • Isolated systolic (ISH) = > 140 SBP with nml DBP

- Isolate diastolic = nml SBP with > 90 DBP

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105
Q

What is masked HTN?

A
  • BP consistently elevated out of office, but not with office readings
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106
Q

Define HTNsive emergency vs HTNsive urgency

A
  • Emergency: DBP > 120 with evidence of end-organ damage

- Urgency: DBP > 120 without end-organ damage/asymptomatic

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107
Q

How is HTN diagnosed?

A
  • Pt must have elevated BP on at least an initial screen and then 2 or more repeat visits (see certain exceptions). BP twice at each visit with correct size cuff and if > 10 mmHg different, repeat a third time.
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108
Q

T/F. HTN is most common primary diagnosis in America.

A
  • True. Note: 48% of people have adequate control.
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109
Q

Define target organ damage from HTN

A
  1. Brain: stroke, TIA, vascular dementia
  2. Eye: retinopathy
  3. Heart: LVH, MI (or angina), CHF
  4. Kidney: CKD
  5. PAD
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110
Q

Most common cause of blindness in developed societies

A
  • Diabetic retinopathy
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111
Q

Define grading of HTNsive retinopathy

A
  • Grade 1: generalized arteriolar narrowing
  • Grade 2: severe generalized narrowing, focal areas of arteriolar narrowing & AV nicking
  • Grade 3 (moderate): previous grades + retinal hemorrhages, microaneurysms, hard exudates and cotton-wool spots
  • Grade 4 (severe/malignant): HTNsive retinopathy, grades 1-3 + optic disk swelling (papilledema) and macular edema
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112
Q

Most common reason of ESRD? Second most common?

A
  • Most common = DM

- Second most common = HTN

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113
Q

How to screen for PAD?

A
  • ABI
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114
Q

What percentage of people have pre-HTN in USA?

A
  • 25%
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115
Q

What percentage of people have HTN in USA?

A
  • 31%
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116
Q

Risk factors for primary (essential) HTN?

A
  • Age, AA, family hx, excess etoh use, obesity, hyperlipidemia, certain personality traits, increased salt intake, sedentary lifestyle, vit D deficiency
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117
Q

In what group is isolated systolic HTN more common in?

A
  • Elderly
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118
Q

Cause of isolated systolic HTN

A
  • D/t diminished arterial compliance

- Increased CO d/t: anemia, hyperthyroidism, aortic insufficiency, AV fistula, Paget dz of bone

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119
Q

Causes of seconday HTN

A
  • Mnemonic: ABCDE
  • A: apnea, aldosteronism
  • B: bruits, bad kidneys (renal parenchymal dz)
  • C: catecholamines, coarctation, Cushing’s syndrome
  • D: drugs, diet
  • E: erythropoietin, endocrine disorders
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120
Q

What are the clinical clues suggestive of secondary HTN?

A
  1. Poor response to therapy
  2. Worsening control in previously stable HTNsive patient
  3. BP > 180 or > 120
  4. Onset of HTN in persons younger than 30 or older than age 50
  5. Significant HTNsive target organ damage
  6. Lack of family hx of HTN
  7. Findings of hx, PE, or lab testing that suggests a secondary cause
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121
Q

% of OSA patients with HTN

A
  • 50%
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122
Q

Sx of OSA

A
  • Daytime somnolence, obesity, snoring, LE edema, morning HAs, nocturia
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123
Q

How is OSA diagnosed?

A
  • Epworth sleepiness scale/sleep apnea clinical score

- Polysomnography is formal diagnosis

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124
Q

How is primary hyperaldosteronism diagnosed?

A
  • Best initial test = aldosterone:renin ratio
  • PAC/PRA ratio: plasma aldosterone [] : plasma renin activity ratio
  • PAC:PRA ratio > 30 = primary hyperaldosteronism. Consider event > 20.
  • Follow up Adrenal CT
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125
Q

If you see a 30% jump in Cr after starting ACE/ARB, what should you think?

A
  • Bilateral kidney disease. Note: 10-15% rise after starting an ACE/ARB in patient without RAS (renal arterial stenosis)
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126
Q

HTNsive patient with unexplained CHF/acute (flash) pulmonary edema think…

A
  • Think renovascular disease
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127
Q

Causes of renovascular HTN

A
  • Atherosclerosis

- Fibromuscular dysplasia (common in women 15-50 yo)

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128
Q

How is renovascular HTN diagnosed?

A
  • Abdominal bruit (50%)
  • Screen duplex Doppler US
  • 50+: MRA, CTA
  • Gold standard = renal arteriography
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129
Q

When is surgery an option for renovascular HTN?

A
  • With complex anatomic lesions
    1. Short duration of BP elevation prior to diagnosis of renovascular dz, since this is the strongest clinical predictor of a fall in BP after renal revascularization
    2. Failure of optimal medical therapy to control the BP
    3. Intolerance to optimal medical therapy
    4. Recurrent flash pulmonary edema and/or refractory heart failure
    5. Unexplained progressive renal insufficiency
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130
Q

Why would HTN be sustained after anatomic correction (surgery)?

A
  • Damage to contralateral kidney

- Vascular remodeling

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131
Q

What is the most common cause of HTN in preadolescent children? 2nd Most?

A
  • Most: Renal dz

- 2nd most: Coarctation of aorta

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132
Q

How is renal parenchymal dz diagnosed?

A
  • Increased Cr (decreased GFR)

- US to determine chronicity (small kidneys = chronic)

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133
Q

With what is HTN d/t renal parenchymal dz caused?

A
  • ACEi
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134
Q

You HTN patient’s eye exam shows evidence of mild arteriolar narrowing. You correct diagnose him with:

A
  • Grade 1 HTN retinopathy
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135
Q

Typical hx seen with coarctation of aorta

A
  • HTN and SOB on exertion
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136
Q

How is coarctation of aorta diagnosed?

A
  • PE (delay between brachial and DP pulses, weak/absent femoral pulse)
  • Check arm/leg BP. If > 20 systolic difference.
  • Do echo in children
  • Consider MRI in adult
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137
Q

Drugs that can cause HTN

A
  • Antidepressants: SSRI/SNRIs (venlafaxine, fluoxetine), TCAs
  • NSAIDs
  • OCPs (esp combo)
  • Steroids
  • Decongestants (diphenhydramine, phenylephrine, pseudoephrine)
  • Triptans (for migraines)
  • Weight loss drugs
  • Illegal stimulant drugs
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138
Q

How is pheochromocytoma diagnosed?

A
  • 24 hour urine metanephrines and catecholamines (have low index of suspicion)
  • Plasma for fractionated metanephrines (high index of suspicion OR children – high false +)
  • If +ve, do: clonidine suppression test (to help distinguish false +ve), CT/MRI abdomen/adrenal glands
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139
Q

What is important to remember with tx of pheochromocytoma?

A
  • Pre-treat with alpha-1 blocker (phenoxy or prazosin)

- Beta-blocker (don’t use alone d/t unopposed alpha stimulation which will further elevation of BP)

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140
Q

Steps in diagnosing and mgmt. of HTN

A
  • Step 1: diagnosis
  • Step 2: BP classification
  • Step 3: look for CVD risk factors
  • Step 4: look for target organ damage
  • Step 5: assess for identifiable causes of HTN
  • Step 6: treatment
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141
Q

Exceptions to diagnosing HTN without using 3 occasions

A
  • > 210 systolic OR HTN accompanied by target organ damage
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142
Q

How to diagnose HTN if white coat HTN or masked HTN?

A
  • Have patient purchase BP cuff and monitor at home

- 24 hr ambulatory BP monitor (HTN is above 135/85, daytime avg above 140/90, nighttime avg above 125/75)

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143
Q

CVD risk factors to look for in HTNsive patients

A
  • Cigarette smoking, obesity, physical inactivity, dyslipidemia, DM, microalbuminuria (GFR
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144
Q

Review 24-27 cases

A

Review 24-27 cases

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145
Q

Routine ancillary studies to do in HTN

A
  • EKG, UA, BGL, CBC, CMP, lipid profile, +/- TSH
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146
Q

Review reasons for further investigation L24-27

A

Review reasons for further investigation L24-27

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147
Q

JNC8 goals for treating HTN

A
  • All patients require lifestyle changes

- Age >= 60 (w/ no DM/CKD): goal

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148
Q

What are the lifestyle changes/modifications necessary/recommendation in HTN patients?

A
  • *

- Weight reduction, DASH eating plan, dietary sodium reduction, physical activity, moderation of etoh consumption

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149
Q

Which diuretic should be used in patient with Cr clearance > 30 ml/min?

A
  • Thiazide
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150
Q

Which diuretic should be used in patient with Cr clearance

A
  • Loop diuretic or combo
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151
Q

HTN meds used in ISH elderly patients?

A
  • DHP CCB (-dipine)
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152
Q

What are the non-DHP CCBs used for?

A
  • HTN, also arrhythmias
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153
Q

Preferred anti-HTN in heart failure patients (d/t systolic dysfunction) and patients with DM w/proteinuria?

A
  • ACEi. Useful after MI with low EF
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154
Q

Common side effects with ACEi

A
  • Cough
  • Hyperkalemia
  • Reversible acute renal failure
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155
Q

Are ACEi effective in AAs?

A
  • Low efficacy
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156
Q

Patients experiencing cough with ACEi should be placed on what antihypertensive?

A
  • ARB
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157
Q

Benefits of beta-blockers

A
  • Decrease CV morbidity and mortality in non-elderly

- Non-ISA (not pindolol) decrease risk of reinfarction / sudden death in post-MI patients

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158
Q

In which patients should beta-blockers be avoided?

A
  • Reactive airway disease, elderly, DM, 2nd/3rd degree heart block
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159
Q

Should alpha blockers be used as monotherapy in HTN?

A
  • No

- Useful as add-on. Useful in patients with dyslipidemia.

160
Q

Antihypertensive to be used in pregnancy?

A
  • Methyldopa
161
Q

Adverse effects of diuretics

A
  • ** Muscle cramps, impotence, gout (esp. thiazides), dyslipidemia, glucose intolerance, hypokalemia (unless K sparing), hyperuricemia, hypomagnesemia
162
Q

Adverse effects of beta-blockers

A
  • **Depression, sleep disorders, exercise tolerance, dyslipidemia, glucose intolerance, impotence
163
Q

Adverse effects of CCBs

A
  • **Edema, flushing, HA, dizziness, GI disorders (constipation), changes in HR
164
Q

Adverse effects of ACEi

A
  • **Cough, angioedema (don’t give in hx), hyperkalemia
165
Q

First line drug choice in HTNsive AA patients without CKD

A
  • Thiazide or CCB. Not ACE or ARB
166
Q

First line drug choice in HTNsive non-AA patients without CKD

A
  • Thiazide, ACE/ARB or CCB
167
Q

First line drug choice in HTNsive all races with CKD

A
  • ACE/ARB
168
Q

In which patients are ACEi and ARBs contraindicated?

A
  • Pregnant or those who are likely to become
169
Q

Option for starting HTNsive meds

A
  • A: start 1 drug and titrate to max dose
  • B: start 1 then add second for achieving max dose of 1st. If goal BP is not met, titrate both drugs to max dose to achieve (do this one at a time)
  • C: start 2 drugs > 160 / 100 and titrate up to max dose. If goal not met, start 3rd and titrate to max.
170
Q

When should 2 drugs be started for HTN diagnosis?

A
  • SBP > 160 / 100 (above goal 20 / 10)
171
Q

Patient presents with HTN and hypokalemia. This is concerning for: essential HTN, Cushings, OSA, primary aldosteronism, hyperparathyroidism?

A
  • Primary aldosteronism
172
Q

Your patient just started a new BP pill and is now presenting with depression. What meds could have this side effect: metoprolol, lisinopril, amlodipine, HCTZ?

A
  • Answer = metoprolol
173
Q

Patient presents with HTN and hypercalcemia. This is concerning for: essential HTN, Cushings, OSA, primary aldosteronism and hyperparathyroidism?

A
  • Hyperparathyroidism
174
Q

Which drug should be avoided in elderly?

A
  • Beta-blocker
175
Q

Drugs that are safe to be used in pregnant women with HTN

A
  • Methyldopa, BBs and vasodilators. No ACEi or ARBs!
176
Q

Define HTN in children/adolescents

A
  • 95% percentile or greater adjusted for age, height, gender

- Note: uncomplicated HTN is not a contraindication to physical activity

177
Q

Goal of mgmt. in HTNsive urgencies? Meds?

A
  • Reduce BP to
178
Q

Goals and Tx of HTNsive emergencies? Meds?

A
  • Requires immediate BP reduction to prevent or limit organ damage
  • Maximal initial fall in DBP of 25% over 2-6 hours. Switch to PO drugs after control
  • Vasodilators: nitroprusside (watch for cyanide poisoning), nicardipine, fenoldopam, NG, enalaprilat, hydralazine
  • Adrenergic inhibitors: labetalol, esmolol, phentolamine
179
Q

Define tx goals in HTN in acute CVA patient

A
  • If eligible for lytic therapy: BP 220 / > 120. Don’t lower > 15%.
180
Q

MYCASST’S charting

A
  • Meds, Years diagnosed, Control, Appointment (last), Specialist, Sx of dz, Testing, Satisfaction
181
Q

In what age group does the prevalence of UTIs in uncircumcised boys exceed that of girls and circumcised boys?

A
  • 0-3 month group

- In general, 4-8 times increased risk for UTI in uncircumcised males under 1 years of age

182
Q

Which UTI pathogen has an increased risk of renal scarring?

A
  • Any other bacteria than E.coli
183
Q

Risk factors for UTIs in pediatric patients

A
  • Age (boys younger than 1, girls younger than 4), lack of circumcision, female, race (white), genetics (if first degree relative), urinary obstruction, BBD (bladder/bowel dysfunction), vesicoureteral reflux, sexual activity, bladder catheterization
  • In different section he listed the following risk factors: abdominal pain, back pain, fever w/no other apparent source, ill-appearing, suprapubic tenderness, fever > 24 hrs, non-black race
184
Q

Presentation of renal scarring?

A
  • Complication of UTI. Causes HTN, proteinuria and renal failure.
185
Q

Which children are at risk for renal scarring?

A
  • Children with pyelonephritis, not simple cystitics
  • Risk factors: recurrent febrile UTIs, delay in tx, BBD, obstructive malformations, vesicoureteral reflux, any pathogen other than E.coli, Temp > 39, inflammatory markers, abnormal renal bladder US
186
Q

T/F. Presence of another source of fever rule out UTI

A
  • False
187
Q

When should urine sample for lab evaluation of UTI be obtained?

A
  1. Girls and uncircumcised boys 2 yo with any urinary sx

4. Circumcised boys > 2 yo with multiple urinary sx

188
Q

Define pyuria from UA

A
  • WBC > 5/hpf; any bacteria
189
Q

Gold standard for diagnosing UTI

A
  • Urine culture
190
Q

Tests not helpful for diagnosing UTI

A
  • Inflammatory markers, serum creatinine (unless hx of multiple UTIs and you are suspecting renal scarring), blood culture, LP. Note: blood culture and LP warranted in neonates (must).
191
Q

When is hospitalization for UTI indicated in pediatric population?

A
  • Age > 2 months, urosepsis (toxic, hypotension, poor cap refill), immunocompromised patients, vomiting/unable to tolerate PO meds, lack of outpatient follow-up, failure of outpatient therapy
192
Q

When do UTIs in neonates typically present?

A
  • 2nd-3rd week

- Greater risk in preterm infants

193
Q

Risk factors for UTIs in neonates

A

**

  • Uncircumcised males (10 X increased incidence)
  • Kidney or renal tract abnormalities
194
Q

What pathogen is involved in UTIs of preterm infants vs term infants?

A
  • *
  • Preterm: coag neg Staph and Klebsiella, NOT E.COLI. More hematogenous spread than ascending, therefore more sepsis in this group.
  • Term: E.coli most common. From ascending spreading more than from hematogenous spread, therefore more pyelonephritis.
195
Q

Most reliable method for urine culture in neonate UTI group?

A
  • Suprapubic aspiration
196
Q

Describe workup in neonate UTI group

A
  • Always urine and blood cultures (r/o urosepsis, which is more common)
  • Always get LP if ill-appearing
  • Always get renal US to r/o abnormalities
  • Always get VCUG (voiding cystourethrogram) if renal US abnormal
197
Q

Tx for UTI in neonate

A
  • IV Ampicillin (covers non-gram negs) + gentamicin (for gram-pos) for 10-14 days.
198
Q

First line tx of pediatric UTI? Tx if hospitalized?

A
  • 3rd gen cephalosporins and aminoglycosides. If enterococcus suspected, add amoxicillin.
  • Hospitalized: gentamycin alone or with ampicillin
199
Q

If pediatric patient fails to respond to abx therapy, how do you proceed?

A
  • Obtain renal and bladder US, obtain urine c/s
200
Q

With recurrent UTIs in pediatric patient, what should you rule out?

A
  • VUR
  • BBD (constipation, daytime wetting, frequency and urgency)
  • Note: give Prophy abx if 3 febrile UTIs in 6 months or 4 in 1 year (Bactrim or nitrofurantoin)
201
Q

What is VUR?

A
  • *

- Retrograde passage of urine from bladder into upper urinary tract. Most common urologic finding in children.

202
Q

What is the most common urologic finding in children?

A
  • VUR
203
Q

Risk factors for VUR

A
  • 3 x more likely in whites than blacks, 2 x more likely in girls (less if circumcisions present), more like
204
Q

Most common form of VUR

A
  • Primary
205
Q

Define primary vs secondary VUR. Which is more serious?

A
  • Primary: incompetent closure of UVJ (ureterovesical junction) d/t shortening of intravesical ureter (genetically determined). Spontaneously resolves.
  • Secondary: anatomic or functional bladder obstruction leading to abnormally high pressure in bladder resulting in failure of closure of UVJ. More serious!
206
Q

Grades of VUR

A
  1. Grade I: reflux fills ureter, no dilation of ureter
  2. Grade II: reflux fills ureter and collecting system, no dilation of ureter or collecting system
  3. Grade III: reflux fills ureter and collecting system mildly dilating them and blunting calyces.
  4. Grade IV: reflux fills ureter and collecting system grossly dilating them and blunting calyces. Some tortuosity of ureter also present.
  5. Grade V: massive reflux grossly dilates collecting system. All calyces blunted with loss of papillary impression and intrarenal reflux may be present. There is significant ureteral dilation.
207
Q

Test of choice to diagnose VUR

A
  • VCUG (voiding cystourethrogram)
208
Q

Identify mgmt. of VUR

A
  • Identify if sx are present indicative of BBD
  • UA to detect proteinuria or pyuria. If pyuria or bacteria, do urine culture.
  • If bilateral VUR, check serum Cr to assess renal function
  • Always get US
209
Q

Tx of VUR

A
  1. Medical: daily abx prophylaxis tx to lower risk of recurrence & periodic monitoring by cystrography
  2. Surgical
210
Q

When is VCUG indicated?

A
  1. Children of any age with 2 or more febrile UTIs
  2. Children of any age with 1 febrile UTI and:
    a. US abnormalities
    b. Fever > 39 (102.2) and pathogen other than E.coli
    c. Poor growth
    d. HTN

**Note: do when patient is asymptomatic

211
Q

Tx of BBD with recurrent UTIs

A
  • Timed voiding, double voiding (pee twice before going to bed), avoid Cs (carbonated drinks, citrus, chocolate and colorants), laxatives if constipated. Refer to urologist if failure to respond.
212
Q

When should GU pediatric problems be referred to urologist/nephro?

A
  • VUR (grades III-IV), obstructive uropathy, renal abnormalities, HTN, impaired kidney function, refractory BBD
213
Q

Effect of genetics, age/race/sex, geographical location, diet, occupation and drugs on nephrolithiasis increased risk

A
  • Genetics: familial clustering higher for stone
  • Age: elderly white men
  • Geographical location: hot environments
  • Diet:
    a. Increased risk: oxalate, sucrose/fructose, sodium, vit C, calcium supplements; OBESITY
    b. Decreased risk: calcium in diet, K, mag, phytate, beverages (coffee, tea, beer, OJ)
  • Occupation
  • Drugs: prednisone, acetazolamide, Topamax
214
Q

DDx of nephrolithiasis

A
  • Cholecystitis, appendicitis, cystitis, diverticulitis, acute pyelonephritis, MSK, herpes zoster, duodenal ulcer, AAA, gynecologic, papillary necrosis/blood clot
215
Q

6 factors causing stone formation

A
  1. Decreased urine volume: increased urinary concentration of stone-forming substances
  2. Excessive excretion of stone forming substances
  3. Anatomic abnormalities
  4. Urine pH: either alkaline or acid
  5. Presence/absence of urinary inhibitors: citrate, mg, pyrophosphate, trace metals and endogenous
  6. Urinary potentiators: crystal nidus
216
Q

What is the most common kidney stone?

A
  • Calcium oxalate
217
Q

How does diarrhea / malabsorption lead to kidney stone formation?

A
  • These conditions lead to excretion or lack of absorption of bicarb = chronic metabolic acidosis. This results in acidic urine that precipitates stones (esp. uric acid stone).
  • This will be exam question!
218
Q

What type of stone does fat malabsorption (d/t pancreatitis, intestinal bypass surgery etc.) lead to? How?

A
  • Fat malabsorption leads to more fat within GI tract. Fat binds Ca leaving oxalate free to be absorbed into the blood. Hyperoxaluria and oxalate stones result.
219
Q

Gold standard for detecting kidney stones

A
  • Helical CT
220
Q

What kidney stones are missed via imaging?

A
  • Uric acid and cysteine stones are radiolucent
221
Q

Risk factors for Ca-based stones

A
  • Low urine volume, high pH, hypercalciuria (most common cause = primary hyperparathyroidism), hyperoxaluria, hypocitraturia, hyperuricosuria, anatomical (MSK: medullary sponge kidney).
222
Q

Causes of hypercalciuria

A
  1. Most common = primary hyperparathyroidism
  2. Dent’s dz: x-linked defect in CLCN5 (Cl channel) of PCT leading to hypercalciuria, nephrocalcinosis, nephrolithiasis, rickets and proteinuria. Kidney failure occurs in 3-5th decade of life.
  3. CYP 24A1 mutation
  4. FHHNC
223
Q

Therapy for calcium stones associated with hypercalciuria

A
  • Treat underlying cause
  • Fluid intake 2-3L / day, dietary modification, thiazide diuretics (to decrease urinary Ca excretion, ie. increase reabsorption), K citrate, bisphosphonates (increases Ca uptake into bone, used in osteoporosis)
224
Q

Link between salt and hypercalciuria? Why do I care?

A
  • When Na excretion decreases, there is a decrease in urine Ca excretion.
  • Thiazide diuretic: decrease Na and Cl reabsorption in DCT, while at the same time decreasing Ca excretion (more Ca reabsorbed).
225
Q

Tx for calcium kidney stones associated with hyperoxaluria

A
  1. Tx underlying dz
  2. Add calcium to diet to bind extra oxalate
  3. Pyridoxine, K-Mg citrate, urophos K, oxasorb, high fluid intake.
226
Q

Long term sequelae and metabolic associations with nephrolithiasis

A
  • HTN, obesity, metabolic syndrome, CAD (women), osteoporosis, CKD
  • This is why we ultimately treat nephrolithiasis
227
Q

Risk factors for CKD in patients with nephrolithiasis

A
  • Struvite stones and / or UTIs, recurrent obstruction, hyperoxaluria, uric acid nephropathy
228
Q

Causes of struvite (aka triple phosphate) kidney stones

A
  1. Infection: specifically with urea-splitting organisms such as proteus mirabilis
  2. Alkaline urine: *diagnostic clue
  3. Staghorn calculi: stone that takes up entire calyceal space
229
Q

Problem with struvite stones

A
  • Risk for urosepsis, perinephric abscess, intractable UTI, CKD/ESRD, difficult to treat as bacteria live inside stone
230
Q

Tx for struvite/infection stones

A
  • Medical: ATB, acetohydroxamic acid
  • Surgery
  • SWL: shock wave lithotripsy
231
Q

Causes of uric acid stones

A
  • Gout (dietary purine overconsumption), hyperuricemia/hyperuricosuria (d/t HGPRT deficiency as seen in Leschy-Nyan or Kelley-Seegmiller), chronic diarrhea (volume depleted, loss of bicarb, metabolic acidosis = acidic urine), acidic urine, low urine volumes
232
Q

Tx of uric acid stones

A
  • Dietary modification, alkalinize urine, allopurinol (Xanthine oxidase inhibitor = reduction in uric acid production), increase urinary volume
233
Q

Causes of cystine stones

A
  • Inherited disorder, defect in transport of COAL amino acids in PCT (cystine is insoluble)
234
Q

Tx of cystine stones

A
  • OVER 4 LITERS OF FLUIDS/DAY, fruits and vegetables, acetazolamide, K citrate, dietary sodium restriction
  • Medical: penicillamine, captopril, mercaptopropionylglycine – these all make cystine more soluble.
235
Q

Other types of stones

A
  • Triamterene, indinavir, phenazopyridine, melamine, xanthine, adenine phosphoribosyltransferase
236
Q

General tx of acute kidney stones

A
  • 90% will pass (
237
Q

Most common cause of nephrotic syndrome in children

A
  • MCD: minimal change dz
238
Q

SSx of glomerulonephritis (nephritic syndrome)

A
  • Edema (d/t extracellular volume expansion): retention of salt
  • Gross hematuria (RBC casts and/or dysmorphic RBCs). Note: RBC casts always from kidney.
  • Lipiduria
  • Proteinuria (> 150 mg/day, can be nephrotic levels depending on amt of damage)
  • Renal failure
239
Q

Biopsy findings in asymptomatic hematuria

A
  • Normal, thin basement membrane nephropathy or IgA nephropathy
240
Q

Criteria for asymptomatic hematuria

A
  • Hematuria, proteinuria
241
Q

Skin condition associated with IgA nephropathy

A
  • Henoch-Schönlein purpura
242
Q

Presentation of IgA nephropathy

A
  • Asymptomatic hematuria with proteinuria
  • Hematuria associated with URI
  • Henoch-Schönlein purpura
243
Q

Biopsy findings for IgA nephropathy

A
  • Mesangial cell proliferation, IgA in mesangial region
244
Q

Presentation of rapidly progressive GN

A
  • Renal failure, oliguria, edema, HTN, proteinuria, hematuria (RBCs and casts)

**Medical emergency

245
Q

Biopsy findings in rapidly progressive GN

A
  • Cellular crescents, which are proliferation of parietal epithelial cells. Pathologic description of this = crescentic GN.
246
Q

Biopsy findings in rapidly progressive GN

A
  • Cellular crescents, which are proliferation of parietal epithelial cells. Pathologic description of this = crescentic GN.
247
Q

Causes of rapidly progressive GN

A
  1. Direct Ig attack: anti-GBM dz (Goodpasture syndrome)
  2. Immune complex deposition: SLE nephritis class III and IV, post-infectious GN, IgA nephropathy (w/Henoch-Schönlein purpura) etc.
  3. Pauci-immune: granulomatosis w/polyangiitis (GPA aka Wegeners), Eosinophilic granulomatosis with polyangiitis (EGPA aka Churg-Strauss syndrome), microscopic polyangiitis (MPA)
248
Q

Immunofluorescent finding in kidney specimen of patient with Goodpasture syndrome

A
  • Continuous linear deposits of IgG in GBM
249
Q

Immunofluorescent finding in kidney specimen of patient with immune complex destruction type of rapidly progressive GN

A
  • Granular pattern of immune complex deposition
250
Q

Immunofluorescent findings in kidney specimen of patient with pauci-immune GN

A
  • No If findings
251
Q

Most common cause of acute GN worldwide

A
  • Post-infectious GN (PSGN)
252
Q

Histologic findings in post-infectious GN

A
  • Subepithelial electron-dense deposits, which deposits of immune complexes against antigens of pathogen.
253
Q

Examples of pulmonary – renal syndromes

A
  • Anti-GBM dz (Goodpasture’s)
  • Systemic vasculitis (eg. GPA)
  • Lupus
  • Etc.
254
Q

Immunofluorescent findings in kidney specimen of class III/IV lupus nephritis. What is specifically being stained?

A
  • Remember this is immune complex deposition. Specifically consists of IgG, IgA and IgM with C3 and C1q. This is known as full house pattern.
255
Q

Review L30 cases

A

Review L30 cases

256
Q

SSx of nephrotic syndrome

A
  • Massive proteinuria (> 3.5 g/day), hypoproteinemia/hypoalbuminemia (albumin
257
Q

Complications of nephrotic syndrome

A
  • Thrombosis (d/t loss of hemostasis proteins)
  • Infections (d/t loss of Igs)
  • Accelerated atherosclerosis (? Why)
  • Protein malnutrition
  • Iron-resistant microcytic hypochromic anemia (d/t transferrin loss)
  • Hypocalcemia and secondary hyperparathyroidism (d/t urinary excretion of cholecalciferol-binding proteins and therefore loss of vit D)
  • Depressed thyroxine levels
258
Q

Etiologies of nephrotic syndrome

A
  1. Primary: MCD, FSGS, membranous glomerulopathy

2. Secondary: diabetic glomerulopathy, amyloidosis

259
Q

Histological findings for MCD

A
  • Effaced foot processes
260
Q

Variants of FSGS

A
  1. May be related to MCD
  2. HIV: collapsing variant
  3. Other CKD causes
261
Q

Histological findings in membranous glomerulopathy

A
  • Subepithelial deposits (spikes) in granular pattern, thickened BM, effaced foot processes
262
Q

Most common cause of nephrotic syndrome in USA

A
  • Diabetic glomerulopathy
263
Q

Histological findings in diabetic nephropathy

A
  • Kimmelstiel-Wilson nodules (increase in mesangial matrix from damage as a result of non-enzymatic glycosylation of proteins), BM thickening
264
Q

Patients over the age of 50 presenting with nephrotic syndrome should be evaluated for what?

A
  • Presence of malignancy. Occurrence of glomerular syndromes associated with malignancy is rare.
265
Q

Most common malignancy associated with membranous glomerulopathy

A
  • Carcinoma of lung
266
Q

Mechanisms of glomerular injury

A
  1. Immunologic
    a. Antibody mediated: autoantibodies, immune complexes
  2. Non-immunologic
    a. Metabolic: example = diabetes
    b. Hemodynamic glomerular injury: HTN (systemic or glomerular)
267
Q

Why is blockade of RAAS important to alleviate glomerular injury?

A
  • In cases of glomerular HTN, intraglomerular pressure acts as stimulus for mesangial matrix production and glomerulosclerosis (fibrosis). Reduction of this high pressure via ACEi (-prils) or ARBs (-sartans) blocks this process.
268
Q

What does proteinuria tell you is happening in the kidney?

A
  • Marker for intraglomerular HTN

- Severity related to likelihood of progression of underlying renal dz

269
Q

Indications for percutaneous renal biopsy

A
  1. Cause cannot be predicted with reasonable accuracy by less invasive procedure
  2. SSx suggest dz that can be diagnosed by pathologic evaluation
  3. DDx included diseases that have different tx or prognoses
270
Q

Gold standard for diagnosing glomerular renal dz

A
  • Percutaneous renal biopsy
271
Q

See L31 case studies

A

See L31 case studies

272
Q

T/F. You won’t have CKD if you have normal Cr and UA

A
  • False. You can.
273
Q

There will be an exam question about identifying the class of kidney dz that someone is in.

A

There will be an exam question about identifying the class of kidney dz that someone is in.

274
Q

Define CKD

A
  • Presence of kidney damage OR decreased kidney function for three or more months
  • Kidney damage: albuminuria, urinary sediment abnormalities (RBC or WBC casts), electrolyte abnormalities d/t tubular disorders, imaging abnormalities (polycystic kidneys, hydronephrosis, echogenic kidneys), kidney biopsy (glomerular, vascular tubulointerstitial dz), kidney transplantation
  • Decreased kidney function: GFR
275
Q

Why do we care about identifying CKD patients early?

A
  • Increased risk for all-cause and CV mortality
276
Q

Prevalence of CKD

A
  • 1/10 Americans. Kidney dz = 9th leading cause of death in US.
277
Q

In what age, sex and race groups does CKD have higher prevalence/incidence?

A
  • Age: 65+
  • Sex: males
  • Race: blacks/AA (ESRD > 3 times higher in AA than Caucasians) – may be d/t APOL1 gene.
278
Q

Risk factors for susceptibility to CKD

A
  • Most common: DM and HTN
279
Q

Which GFR estimation is most accurate and why?

A
  • CKD epi. It analyzed a healthier population base. MDRD and C-Gault derived from population with kidney problems.
280
Q

Stages of CKD

A
  • Two components: GFR and albuminuria

GFR:
**value here = GFR in ml/min

  1. Stage 1 (G1): > = 90
  2. Stage 2 (G2): 89 – 60
  3. Stage 3 (G3): 59 – 30
    a. G3a: 59 – 45
    b. G3b: 44 – 30
  4. Stage 4 (G4): 29 – 15
  5. Stage 5 (G5): 300. Very high
281
Q

Describe compensatory changes in renal hemodynamics as CKD progresses. How can you retard this change to slow progression?

A
  • Increased intraglom. pressure (d/t systemic pressures or via glomerular afferent dilation/efferent constriction) = Compensatory increase in filtration in preserved nephrons
  • Later = decline in GFR d/t direct endothelial damage, formation of hyaline deposits that narrow lumen and increased strain on mesangial cells leading to inflammation and mesangial proliferation. This results in decreased perfusion and filtration.
  • How to retard progression: blockade of RAAS through ACEi and ARBs. These reduce intraglomerular pressure.
282
Q

How does proteinuria contribute to CKD disease progression? Why do I care?

A
  • Mesangial toxicity, tubular overload/hyperplasia, toxicity from specific filtered compounds (transferrin/iron and albumin-bound FAs), induction of pro-inflammatory molecules.
  • Care: Can have a patient with better GFR w/ proteinuria compared to a patient with worse GFR w/o proteinuria do worse.
283
Q

Secondary factors that affect progression of CKD

A
  • Intraglomerular HTN and hypertrophy, phosphate retention and interstitial CaPO4 deposition, increased PG synthesis, hyperlipidemia esp in nephrotic syndrome, metabolic acidosis, proteinuria, tubulointerstitial dz, retained uremic toxins, filtered iron in nephrotic syndrome
284
Q

How often should GFR and albuminuria be checked in CKD patients?

A
  • At least once q year.
285
Q

1 cause of death in CKD patients?

A
  • CV death (MI, CVA, CHF). Must tx CVD risk factors aggressively to prevent this.
286
Q

Risk factors for CVD in CKD patients

A
  • Traditional: HTN, dyslipidemia, DM, metabolic syndrome, smoking
  • Non-traditional: anemia, disordered mineral metabolism, endothelial dysfunction, inflammatory state, hyperhomocysteinemia
287
Q

Complications/SSx of CKD

A
  1. Azotemia (presence of nitrogenous waste products BUN and Cr)
  2. Uremia (azotemia + ssx that result from renal failure)
  3. Neurologic: encephalopathy, confusion / decrease mental acuity, seizures, fatigue
  4. Endocrine/metabolic: mineral bone disease (hypocalcemia, hyperphosphatemia, high PTH, low vit D), anemia, calciphylaxis, volume depletion
  5. CV: HTN
288
Q

What is calciphylaxis?

A
  • Type of extraosseous calcification characterized by systemic calcification of arterioles that lead to ischemia and subcutaneous necrosis. Can occur in CKD.
289
Q

General mgmt. plan for CKD

A
  1. Tx reversible causes of renal failure
  2. Prevent / slow progression of renal dz
  3. Tx of complications of renal failure
  4. Adjust drug doses appropriate for level of GFR
  5. Identification and adequate prep of patient in whom renal replacement therapy will be required.
290
Q

Reversible factors that can cause CKD

A
  • Meds (NSAIDs, ACEi, ARBs, radiocontrast), volume depletion, infection, obstruction of urinary flow, CHF/pericardial tamponade, hypercalcemia
291
Q

Tx to slow rate of progression of CKD

A
  • In general, want to interrupt maladaptive hyperfiltrative process
    1. ACEi/ARB/aldosterone antagonist/renin inhibitor **primary
    2. Reduce proteinuria (meds/diet)
    3. Control BP
    4. Diet: Low protein/low phosphorus
    5. Tx dyslipidemia and smoking
    6. Tx metabolic acidosis
292
Q

Target BP in CKD

A
  1. Diabetic/non-DM with AER 30 mg/day:
293
Q

What is normal A1C?

A

-

294
Q

Recommended salt intake for CKD patients

A

-

295
Q

Lifestyle recommendations in CKD patients

A
  • Physical activity of at least 30 mins 5 times per week
  • BMI 20 to 25
  • Stop smoking
296
Q

How to tx volume overload in CKD patients?

A
  • Tx with salt and water restriction. Give diuretics (loop)
297
Q

Cause of anemia in CKD patients

A
  • Renal production of EPO/bleeding/decreased RBC survival/nutritional
298
Q

Anemia in CKD defined as?

A
  • Hb
299
Q

When should anemia be identified in CKD patients?

A
  • Clinically indicated in people with GFR > 60 (grade 1)
  • Annually in people with GFR 30-59 (grade 3a and 3b)
  • Twice per year in people with GFR
300
Q

Goal Hb in CKD patients? How to tx anemia?

A
  • 10-11 g/dl. Don’t increase it to normal! Why? No change in all-cause or CV mortality.
  • Tx with EPO and nutritional supplements
301
Q

Tx of hyperkalemia in CKD patients

A
  • Low K diet, diuretics and alkali (citrate or NaHCO3)
302
Q

Tx goal of metabolic acidosis

A
  • 20-24 meq/L.

- Use alkali

303
Q

Cause of hyperkalemia in CKD patients

A
  • Certain meds, hypoaldosteronism, metabolic acidosis
304
Q

Cause of metabolic acidosis in CKD patients

A
  • Inability to excrete H+ based on CKD and / or hypoaldosteronism
305
Q

Causes of malnutrition in CKD patients

A
  • Anorexia, dietary restriction, catabolic state
306
Q

2 cause of death in CKD

A
  • Immune suppression/infection
307
Q

When does hyperphosphatemia occur in CKD patients? Result?

A
  • Early in CKD. Leads to secondary hyperparathyroidism. PTH is uremic toxin??!
308
Q

Tx of hyperphosphatemia in CKD

A
  • Dietary restriction of phosphate, phosphorus binders (CaCO3), calcimimetics (lowers PTH). Goal: keep Ca x P product
309
Q

Why should caution be taken with imaging CKD patients?

A
  • Radiocontrast: iodine-based contrast is used in CT. Patients
310
Q

CKD tx options

A
  1. Maintenance hemodialysis
  2. Peritoneal dialysis
  3. Kidney transplantation
  4. Palliative care
311
Q

Who survives longer – CKD patients undergoing dialysis or transplant?

A
  • Transplant
312
Q

Review L34 case

A

Review L34 case

313
Q

What happens to fluid compartments with intake of Na? Which fluid compartment expands?

A
  • ECF expands
314
Q

Effect of decreased effective arterial volume on GFR and FF (filtration fraction)?

A
  • FF = GFR/RPF. Answer = increased filtration fraction. I’m unsure of reason why this occurs. GFR decreases with higher decrease in RPF.
315
Q

Causes of volume (Na) expansion

A
  1. Primary renal Na retention: hyperaldosteronism (Na retained by aldosterone), renal failure, Cushing, inherited HTN (d/t various genetic diseases)
  2. Secondary renal Na retention: nephrotic syndrome (decreased oncotic pressure = edema), liver cirrhosis (decreased oncotic pressure), CHF, pregnancy, ARDS, drugs, sequestration (third spacing)
316
Q

Clinical signs of volume (sodium) expansion

A
  • Edema, pulmonary crackles, ascites, JVD, hepatojugular reflux, HTN (late finding)
317
Q

Describe tx of volume (Na) expansion

A
  • Tx of underlying disorder
  • Reduction of dietary Na intake
  • Diuretic therapy
318
Q

Side effects with diuretics

A
  1. CAI: metabolic acidosis
  2. Loop: electrolyte disorders (hypokalemia/natremia), ototoxicity (usually associated with IV), hypersensitivity rxn (sulfonamide groups)
  3. Thiazide: electrolyte disorders (hypokalemia/natremia), gout, lipid disorders
  4. Aldosterone antagonist: hyperkalemia, gynecomastia, amenorrhea
  5. Epithelial Na channel blockers: hyperkalemia
319
Q

Causes of volume (Na) depletion (hyponatremia)

A
  1. Extrarenal losses: GI, skin, pulmonary
  2. Renal losses
    a. Extrinsic: solute diuresis, diuretics, adrenal insufficiency (no aldosterone for example)
    b. Intrinsic: ARF (diuretic phase, non-oliguric), post-obstructive diuresis, salt-wasting nephropathy (renal insufficiency, interstitial nephropathy, medullary cystic dz, polycystic kidney dz, urinary obstruction)
320
Q

How to tell the difference between extrarenal and renal losses of Na that lead to volume (Na) depletion?

A
  • Urine Na []
  • Extrarenal: low urine Na []
  • Renal: normal or elevated urine Na []
321
Q

Clinical ssx of volume (Na) depletion

A
  • Orthostatic Hypotension with increase HR
  • Decrease pulse volume
  • Decrease venous pressure
  • Loss of axillary sweating
  • Decreased skin turgor
  • Dry MM
322
Q

Normal physiologic serum osmolality

A
  • 285 – 290 mOsm/kg
323
Q

Major determinant of water excretion in body

A
  • ADH
324
Q

Lab findings in SIADH

A
  • Decreased ECF osmolality ( 100 mOsm/kg)

- Note: this is euvolemic state

325
Q

Causes of SIADH

A
  • CNS disorders
  • Carcinomas
  • Pulmonary disorders
326
Q

Tx of chronic hyponatremia

A
  1. Fluid restriction
  2. ADH antagonists: lithium, demeclocycline, V2-receptor antagonists
  3. Increased solute intake: NaCl with furosemide.
327
Q

Central vs nephrogenic DI

A
  • Central: defect in ADH production or release

- Nephrogenic: failure of collecting duct to respond to ADH

328
Q

Normal urine osmolality

A
  • > 800
  • Higher = concentrated urine
  • Lower = dilute urine
329
Q

Tx of central DI

A
  • ADH
330
Q

Tx of nephrogenic DI

A
  • Correct Ca and K
  • Remove offending drugs (commonly lithium)
  • Low Na diet (hypernatremic)
  • Thiazide diuretic
  • Amiloride (if lithium-induced)
331
Q

How to calculate free water deficit?

A
  • 0.6 x (total body weight) x ([serum Na – 140] / 140)
332
Q

Tx of severe hypernatremia

A
  • Replace half of total water deficit over 12-24 hrs
  • Replace the remaining half over next 24-26 hrs
  • Rate at 2mmol/hour
  • Perform serial neurologic examinations
  • Monitor serum and urine electrolytes q 1-2 hours
333
Q

Disorders of Na concentration are most often related to what?

A
  • Abnormal water balance
334
Q

Review L35 cases

A

Review L35 cases

335
Q

Cystic diseases of renal medulla specifically

A
  • Medullary cystic dz (AR or AD)

- Medullary sponge kidney

336
Q

Types of hereditary polycystic kidney disorders? Hereditary cystic kidney disorders?

A
  • Polycystic: AR PKD, AD PKD

- Cystic: tuberous sclerosis, VHL

337
Q

Genes responsible for ADPKD

A
  • PKD1 and 2

- Code for polycystin protein

338
Q

How is AD PKD diagnosed?

A
  • Renal US, IVP (intravenous pyelogram), CT/MRI

- Criteria: at least two cysts in one kidney under age 30. As age increases, need more cysts.

339
Q

Conditions associated with AD PKD

A
  • Intracranial aneurysms (most deadly)**know. 60% of patients with SAH die before hospital admission. Ruptured higher in AD PKD. Note: -ve screening study is valuable. Must screen!
  • Polycystic liver dz, HTN, cardiac complications (LVH, valve abnormalities), renal complications
340
Q

What is the most common AD polycystic kidney dz next to ADPKD?

A
  • Tuberous sclerosis
341
Q

What is tuberous sclerosis?

A
  • Systemic disease characterized by multiple hamartomas around the body
342
Q

Pathognomonic findings for tuberous sclerosis

A
  • Cortical brain tubers
343
Q

Most common renal finding in tuberous sclerosis

A
  • Multiple renal angiomyolipomas +/- renal cysts
344
Q

What is VHL disease?

A
  • Rare disorder d/t mutation in tumor suppressor gene. Results in retinal angioma and cerebral hemangiomas as the most frequent initial clinical manifestations. Renal cysts occur in ¾. RCC is common and presenting manifestation in 10% of patients.
345
Q

Which cancer is common in VHL disease patients?

A
  • RCC
346
Q

Manifestations and diagnosis of medullary cystic disease

A
  • I suspect this is low yield
  • Manifestations: sodium wasting, anemia, renal insufficiency. Clinical presentation in 1st / 2nd decades of life
  • Diagnosis: excretory urography (inhomogenous streaking confined to medulla d/t accumulation of contrast), sonography, CT, open renal biopsy
347
Q

What is MSK?

A
  • Enlargement of medullary and inner papillary portions of collecting ducts
348
Q

T/F. MSK (medullary sponge kidney) causes ESRD

A
  • Not typically. Nuisance dz.
349
Q

What GU disorder is common in MSK?

A
  • Nephrolithiasis (d/t defective urinary solute concentrating ability, inability to reduce urinary pH to 5.5 and RTA)
350
Q

Presentation of MSK (medullary sponge kidney)

A
  • Gross/microscopic hematuria
  • UTIs
  • Nephrolithiasis
351
Q

How is MSK diagnosed?

A
  • IVP, renal US or CT
352
Q

Types of tubulointerstitial injury

A
  1. ATN: acute tubular necrosis
  2. Acute interstitial nephritis
  3. Chronic interstitial nephritis
353
Q

Clinical presentation of acute interstitial nephritis

A
  • Non-specific sx: oliguria, malaise, anorexia, nausea, vomiting
  • Classic triad: low-grade fever, skin rash, arthralgias
354
Q

Lab abnormalities seen in acute interstitial nephritis

A
  • Elevation of BUN/Cr
  • UA: eosinophiluria
  • CBC: eosinophilia
355
Q

Gold standard to diagnose acute interstitial nephritis

A
  • Renal biopsy. Features: infiltration with lymphocytes and PMNs usually eosinophils, edema. Sparing of glomeruli and BVs.
356
Q

Causes of acute interstitial nephritis

A
  • Drug-induced (abx, NSAIDs, diuretics, misc drugs including PPIs), infection-associated, autoimmune idiopathic (anti-tubule BM ab, which presents with uveitis)
357
Q

Clinical presentation of chronic interstitial nephritis

A
  • Slow progressive chronic renal insufficiency
  • UA: normal or sterile pyuria (WBCs)
  • Mild proteinuria (
358
Q

Biopsy findings in chronic interstitial nephritis

A
  • Atrophy of tubular cells with flattened epithelium and tubular dilatation, interstitial fibrosis and areas of cellular infiltration (lymphocytes, macrophages)
359
Q

Causes of chronic interstitial nephritis

A
  • Drugs, toxins, metabolic disorders, immune mediated, infection, hematologic disorders
360
Q

SSx of uremia

A
  • GI (anorexia, nausea), CNS (seizures, sleep disturbances, coma), reduced body temp, bone disease, pericarditis, itching (d/t phosphorus retention), hiccups, anemia, bleeding.
361
Q

When is renal replacement therapy indicated?

A

** Mnemonic = AEIOU

  • A: acidosis
  • E: electolytes (hyperkalemia for example)
  • Ingestion (drugs, toxins)
  • Overload (refractory fluid overload)
  • Uremia ssx
  • Note: corresponds to GFR
362
Q

Types of hemodialysis

A
  1. Diffusion: [] gradient

2. Convection: removal of water plus solutes by “solvent drag” (shooting fluid through filter – think making espresso)

363
Q

Define clearance

A
  • Volume of plasma cleared completely of given substance per unit time
364
Q

Types of access for dialysis. What is preferred and why?

A
  • AV fistula, PTFE graft and cuffed tunneled catheter. Want fistula or graft. Catheter imposes high risk for infection.
365
Q

Most common causes of death in dialysis patients?

A
  • CV disease = #1

- Infection = #2

366
Q

Components of a dialysis order

A
  • How long, blood flow rate, dialysate flow rate, ultrafiltration rate (ie. how much fluid to take off), dialysate composition, intradialytic meds, anticoags
367
Q

What determines the efficiency of dialysis

A
  • Membrane characteristics and surface area
  • Blood flow rate
  • Dialysate flow rate/characteristics
  • Duration of tx
  • Ultrafiltration
368
Q

Complications of dialysis procedure

A
  • Hypotension, cardiac arrhythmias, muscle cramps, nausea/vomiting, disequilibrium syndrome, hypoxemia, anaphylactoid reactions, vascular access issues
369
Q

Two types of peritoneal dialysis

A
  1. CAPD: continuous ambulatory peritoneal dialysis (
  2. APD: automated peritoneal dialysis
    - In either case, peritoneal membrane acts as endogenous dialyzing membrane
370
Q

What is the osmotic agent for fluid removal with peritoneal dialysis (PD)?

A
  • Dextrose (glucose) or icodextrin in various concentrations
371
Q

Complications of PD

A
  • Biggest = peritonitis (suspect if cloudy fluid with WBC count > 100 with more than 50% PMNs or SSx)
  • Other = catheter malfunction, hernia, fluid leaks, peritoneal membrane changes and loss of ultrafiltration, hyperglycemia/weight gain, malnutrition
372
Q

See L36 Case

A

See L36 Case

373
Q

Most effective therapy for end-stage renal disease

A
  • Kidney transplantation
374
Q

Most common primary diagnoses that lead to kidney transplants

A
  1. Malignant HTN
  2. Polycystic kidneys
  3. DM
  4. Hypertensive nephrosclerosis
375
Q

Standard vs extended criteria donor

A
  • SCD: age 60 or age 50-59 w/ 2 out of 3: HTN, death from CVA, serum Cr > 1.5
376
Q

Survival benefit with renal transplantation from ECD vs SCD

A
  • Risk of death immediately after surgery with ECD > SCD. Long term about the same.
377
Q

Benefits of kidney transplantation

A
  • Life expectancy increases, CV benefits, QOL, socioeconomic benefits
378
Q

Absolute contraindications for donor to receive kidney transplant

A
  • Active malignancy (except skin cancer), acute infection (osteomyelitis, line sepsis), clinically active SLE or vasculitis, active substance abuse, pos T cell crossmatch
379
Q

Immunologic barriers to kidney transplantation

A
  • ABO blood groups, MHC, presence of pre-formed circulating abs in host to HLA antigens (PRA – panel reactive antibodies)
380
Q

Targets of immunosuppressants

A
  • Based on three signal model
  • Signal 1: MHC w/peptide(s) binds to TCR/CD3 propagating signal transduction
  • Signal 2: Co-stimulation
  • Signal 3: IL-2
381
Q

Induction and maintenance immunosuppressant classes

A
  1. Induction (perioperative period): corticosteroids, anti-thymocyte globulin (ATG) and IL-2 R antagonist
  2. Maintenance: corticosteroids, calcineurin inhibitors, mTOR inhibitors, antimetabolites. Most common maintenance regimen in kidney transplants = TMP combo = tacrolimus, mycophenolate and prednisone
382
Q

Common complications of transplantation

A
  1. Early complications = surgical (graft thrombosis, urine leak – imaging shows renal extravasation), delayed/slow graft function (requiring dialysis in first week), lymphocele (collection of lymph caused by leakage from iliac lymphatics)
  2. Acute rejection: cellular or antibody mediated
  3. Infectious: CMV, BK, others
  4. Malignancy
  5. Chronic allograft dysfunction
  6. Medical complications: HTN, anemia, hyperkalemia, hypercalcemia, hypophosphatemia, DM (NODAT), dyslipidemia, calcineurin toxicity, recurrent disease, bone disease, drug interactions
383
Q

Define hyperacute rejection. What immunologic substance mediates this process? Tx?

A
  • Rejection within hours
  • Mediated by preformed antibodies to HLA antigens in donor organ.
  • Tx: plasmapharesis or pulse steroids
384
Q

What mediates acute allograft rejection? Time frame? Tx?

A
  • T-lymphocytes (or antibodies per lecturer). During first 6 months.
  • Histology: blue = bad (infiltrative cells)
  • Tx:
    a. Cellular: steroids or anti-T cell antibody (thymoglobulin)
    b. Humoral: plasma exchange, IVIG, rituximab (anti-CD20), 26S proteasome inhibitor (bortezomib)
385
Q

Time frame chronic allograft rejection

A
  • > 6 months typically (in slide says weeks to years)

- Nothing much you can do to treat

386
Q

Most common viral infection after kidney transplant

A
  • CMV.
387
Q

Risk factors for CMV infection post-transplant

A
  • Max risk = donor seropositive and recipient seronegative

- Use of antibody induction

388
Q

Clinical presentation of CMV infection after transplant

A
  • Asymptomatic, neutropenia, malaise & constitutional, GI CMV (gastritis, colitis, esophagitis), clinical hepatitis, pneumonitis
389
Q

Tx for CMV

A
  • Valganciclovir
390
Q

Most common malignancy after kidney transplant

A
  • Skin cancer. Mandatory for patients to use sun protection.

- Other specifics: KS, PTLD (post-transplant lymphoproliferative disorder)

391
Q

HTN agents of choice in kidney transplantation patients

A
  • DHP type (cardiac and vasodilatory specific effects): nifedipine and amlodipine. Want vaso specific effects d/t vasoconstrictor effect of immunosuppressants.
  • Avoid non-DHP: diltiazem, nicardipine, verapamil
392
Q

Read over other complications following kidney transplant

A

Read over other complications following kidney transplant

393
Q

Biggest causes of death following transplant

A
  1. CV death
  2. Infection = malignancy
  3. Liver dz (hep B and C)
394
Q

T/F. Kidney transplant recipients can become pregnant.

A

True

395
Q

What immunosuppressants are safe during pregnancy?

A
  • Tacrolimus, cyclosporine, azathioprine, prednisone at lowest dose. Mycophenolate is absolutely contraindicated.

Renal (2 decks)

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