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CPRII Exam 2 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What are the most common causes of hyporeninemic hypoaldosteronism

A

CKD or DM; leads to RTA IV

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2
Q

What are predisposing factors in women for UTI

A

Use of spermicide, frequent sex, recurrrence in post menopausal, diabetes

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3
Q

What should you include in your ddx of a women with dysuria

A

Cystitis or cervicitis

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4
Q

What can UTIs cause in pregnant females

A

Premature labor, low birth weight babies *untreated asymptomatic bacteriuria in pregnant female more likely to result in pyelonephritis and sepsis.

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5
Q

What can cause complicated UTIs

A
  • anatomical variant (ie: polycystic kidneys)
  • foreign body
  • extrinsic compression (tumors, profound constipation)
  • immune suppression (DM, drug induced, HIV)
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6
Q

What is important about the abx tx for prostatitis

A

Requires prolonged ab course (4-6wks)

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7
Q

Which bacteria can cause hematogenous spread to kidneys

A

Candida, salmonella, staph aureus

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8
Q

What are the 3 main complications of pyelonephritis

A
  • Papillary necrosis
  • Emphysematous pyelonephritis
  • Xanthogranulomatous pyelonephritis
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9
Q

What can cause papillary necrosis

A

Obstruction, DM, sickle cell, analgesic nephropathy

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10
Q

What patients does emphysematous pyelonephritis usually occur in

A

Diabetic

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11
Q

What are the causes of xanthogranulomatous pyelonephritis

A

Chronic obstruction, chronic infections

-cause suppurative destruction of renal tissue and can lead to abscess formation

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12
Q

What are the features of septic shock

A

Subset of sepsis; vasopressor therapy needed to maintain arterial pressure at 65 or greater; serum lactate greater than 2 mil/L *hypotension that cannot be reversed with infusion of fluids

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13
Q

What causes the tubular damage in acute ischemia

A

Endotoxins and inflammatory cytokines

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14
Q

What is the initiating treatment for sepsis/septic shock

A

Volume resuscitation (IV fluids), cultures, initiate broad spectrum abx, pressors (NE, vasopressin), correct acid/base imbalance, monitor electrolytes

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15
Q

What does increased BUN:Cr ratio indicate

A

Pre-renal azotemia

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16
Q

What labs would you we with sepsis and ischemic AKI

A

Decreased urine concentration, FeNA <1%, minor proteinuria, hematuria, muddy brown casts on micro (sloughing of renal tubular epithelial cells)

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17
Q

What are preventive strategies for UTI

A

Wipe front to back, empty bladder after sex, showers not baths, lactobacillus probiotics, cranberry products, vitamin C, increased fluid intake

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18
Q

What level of albumin will show up on a dipstick

A

300 mg

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19
Q

What do you do after a dipstick reveals protein

A

Quantify the protein

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20
Q

When is the preferable time to test the albumin/creatinine (ACR)

A

First morning void

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21
Q

What does 24 hr urine collection provide testing for

A

Protein, albumin, Cr clearance; sample to do electrophoresis to determine which types of protein

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22
Q

What are the components of nephrotic syndrome

A

Nephrotic range proteinuria, hyperlipidemia, hypoalbuminemia, edema

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23
Q

What tests should T2DM patients get annually

A

ACR

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24
Q

How do you slow progression of proteinuria

A

ACEI and ARBs

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25
Q

What drugs can cause nephrotic syndrome

A

NSAIDs, Lithium, IV heroin abuse

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26
Q

What can cause hematuria in athletes

A

Heavy exercise; can be accompanied by proteinuria; likely related to decreased RBF; also NSAID use
*evaluation: r/o infection, rest 48-72 hrs and recheck

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27
Q

What does ibuprofen do to GFR

A

Decreases it

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28
Q

What does indomethacin and celecoxib do to the kidney

A

Decrease free water clearance

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29
Q

What can give you false positives for blood on UA

A

Myoglobinuria, hemoglobinuria, high alkaline pH, ascorbic acid; confirm with micro

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30
Q

What is considered negative for hematuria on micro

A

Less than 3 RB/hpf

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31
Q

When do you do radiogaphic evaluations on someone with kidney trauma

A

Only if they are hemodynamically unstable

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32
Q

What can sickle cell trait cause

A

Impaired urinary concentration, renal papillary necrosis, hyperfiltration leas to albuminuria, interstitial fibrosis, decrease # of nephrons (FSGN), renal medullary carcinoma (actually more of an increased risk than SCD)

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33
Q

What are the risk factors for transitional cell and bladder CA

A

Male, >35 yo, smoking, analgesic abuse, exposure to chemical or dyes, exposure to chemo or carcinogens, chronic UTI, chronic foreign body

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34
Q

What is US good for

A

Tumors >3cm, cysts and hydronephrosis; may miss urothelial cancers

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35
Q

What can cystoscopy test for

A

Urethral stricture, benign hyperplasia and bladder masses *requires sedation, risk of post procedural UTI

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36
Q

What does activation of RAAS do

A

Vasoconstriction of afferent and efferent arterioles; increases glomerular pressures (hyperfiltration), causes direct glomerular damage; activates inflammatory system and leads to interstitial and tubular fibrosis

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37
Q

What would be your plan for someone with cardiomyopathy in terms of their kidney

A

U/S; daily BP checks, send US for micro evaluation, BUN, Cr, Na, 24 hr urine for albumin and microalbumin/Cr ration

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38
Q

What does RBC casts or dysmorphic RBCs in the urine indicate

A

Glomerulonephritis

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39
Q

What diseases does gross hematuria usuallly appear in

A

IgA nephropathy and sickle cell

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40
Q

What can pyuria be seen in

A

Inflammatory glomerulonephritis or UTI

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41
Q

What is sustained proteinuria

A

> -2 g/24 hr; sx include edema and foamy urine

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42
Q

What is benign proteinuria

A

<1-2 g/24 hrs; aka functional or transient; fever, exercise, obesity, sleep apnea, emotional stress, and CHF; orthostatic proteinuria

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43
Q

What is the normal Albumin: Cr ratio

A

<30

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44
Q

What gene puts ppl at an increased risk for HTN nephroslcerosis

A

APOL1

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45
Q

What are risk factors for HTN nephrosclerosis

A

Smoking, male, hyper cholesterolemia , duration of HTN, low birth weight and preexisting renal injury

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46
Q

What are the signs of HTN nephrosclerosis

A

HTN, microhematuria, moderate proteinuria

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47
Q

What is damaged in diabetic nephropathy

A
  • ECM; imbalance btw synthesis and degredation of ECM causes expansion of mesangium; GFR surface decreased
  • Type I: glomerular, tubular, interstitial and vascular lesions progress in parallel and independent of albuminuria
  • Type II: variable in progression and can develop albuminuria without change to the nephron
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48
Q

What are the change in flow seen in unilateral ureteral obstruction

A
  • initial phase: urine backflow (increases hydrostatic pressure), increase in glomerular capillary pressure induced by afferent vasodilation which maintains GFR
  • activation of RAAS; 6 hours; decrease glomerular blood flow due to vasoconstriction
  • decreased luminal hydrostatic pressure and RBF; reduced GFR
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49
Q

What are the changes in flow from a bilateral ureteral obstruction

A
  • urine backflow (same as unilateral)

- RAAS activated; decreased RBF; but maintains GFR; ANP may play a role in maintaining GFR

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50
Q

What is the difference in salt reabsorption in Unilteral vs bilateral tubular dysfunction

A

Unilateral: inability to reabsorb salt (salt wasting); downregulation of receptor and enzyme activity
Bilateral: presence of volume expansion; ANP blocks effects of renin -> decreased Angio II, diuresis and natiuresis

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51
Q

What does high urinary K+ delivery to the collecting duct result in (low flow luminal state)

A

Hyperkalemia b/c no gradient for it to be pumped across

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52
Q

What is the pathophysiology that occurs as a result of b/l ureteral obstruction

A

Acute: increase in RBF, decrease in GFR, increase in prostaglandins and NO increased tubule pressure and increased reabsorption of Na, urea, and water *oliguria
Chronic: decreased RBF, decreased GFR, vasoconstrictor prostaglandins, increased RAAS; decreased concentration ability; decreased transport function *polyuria, hyperkalemia, hyperchorlemic acidosis

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53
Q

What should you always consider in someone who presents with azotemia, hyperkalemia, and metabolic acidosis

A

Urinary tract obstruction

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54
Q

How do you evaluate for residual volume in the bladder after voiding

A

US; >100 ml indicates incomplete emptying

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55
Q

What can cause neurogenic bladder

A

Spinal cord trauma, spinal myelomeningocele, spinal stenosis, herniated disc

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56
Q

What imaging is preferred for dx of kidney stones

A

CT

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57
Q

What do you do for hydronephrosis caused by pregnancy

A

Just monitor unless becomes symptomatic (then relieve with a stent)

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58
Q

When does postobstructive diuresis occur

A

After bilateral obstruction; combo of fluid overload, urea accumulation, and electrolyte imbalance; results from downregulation of sodium transporters during obstruction; ANP released in response to cardiac preload during obstruction

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59
Q

What factors can alter serum Cr

A

Age, sex, muscle mass, race, catabolic rate

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60
Q

What are some intrarenal causes of AKI

A

Glomerular injury, tubules, vascular injury (Vasculitis, rheumatologic, malignant HTN, TTP-HUS)

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61
Q

What are some exogenous nephrotoxins that can cause tubulointerstitial injury

A

Iodinated contrast, aminoglycosides, amphotericin B, cisplatin, PPIs, NSAIDs

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62
Q

What are some endogenous nephrotoxins that cause tubulointerstitial injury

A

Hemolysis, rhabdomyolysis, myeloma, intratubular crystals

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63
Q

How do you treat pre renal AKI

A

Remove/treat underlying cause; stop med offenders: NSAIDs, cyclosporine, ACEI/ARB

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64
Q

How do you treat post renal AKI

A

Drain bladder; eliminate obstruction

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65
Q

How do you treat intrinsic AKI

A

Improve renal perfusion; optimize CO, minimize 3rrd spacing, fluids

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66
Q

What is distinct about the pathogenesis of candida in UTI

A

Hematogenous route

67
Q

What is the diagnostic gold standard for cystitis

A

Bacteria in the urine culture.

68
Q

What are the 4 C’s of control of STIs

A
  • contact tracing
  • ensuring compliance
  • counseling on risk reduction
  • condom promotion
69
Q

What are the sx of urethritis in men

A

Urethral discharge, dysuria, but no frequency

70
Q

How can you dx an STI in males

A

Smear of anterior urethra

Centrifuged sediment of first 20-30 mL of urine

71
Q

What is a possible harmful systemic response

A

Two or more of:
Fever or hypothermia
Tachypnea
Leukocytosis

72
Q

What is septic shock

A

Sepsis with hypotension (<90 or 40 below patients normal BP for at least. Hr despite fluid resuscitation or need for pressors

73
Q

What are the cardiopulmonary manifestations of shock

A
  • Ventilation perfusion mismatch, increased alveolar capillary permeability, leads to ARDS
  • hypotension, normal or increased CO, decreased PVR; normal stroke volume
74
Q

What lab findings would you see with someone in septic shock

A

Leukocytosis, thrombocytopenia, prolonged PT, decreased fibrinogen, HAGMA, elevated lactate, hypoalbuminemia

75
Q

What should you give if your septic patient doesn’t respond to fluid therapy

A

Hydrocortisone

76
Q

What is an important tool for dx diabetic nephropathy

A

Miccroalbuminuria (urin albumin: Cr >30)

77
Q

What are detection of RBC casts specific for

A

Glomerulonephritis

78
Q

What is post renal failure more common in

A

Ambulatory ppl vs hospitalized patients

79
Q

What are the clinical features of pre renal azotemia

A

Orthostatic hypotension, tachycardia, low JVP, dry mucous membranes; high BUN:Cr (>20:1); low sodium urine (<10-20) and FeNa<1% ; renal US usually normal; UA shows hyaline and few granular casts

80
Q

What are the lab findings of intrinsic renal azotemia

A

FeNa >1; urine sodium >20, urine Cr:plasma Cr >20; urine urea:plasma urea <3; low urine specific gravity; plasma BUN:Cr <10-15; muddy brown granular casts

81
Q

What are the lab values for prerenal azotemia.

A

FeNa <1, urine sodium <10; urine Cr:plasma Cr >40; urine urea: plasma urea >8; plasma BUN:Cr >20; hyaline casts

82
Q

What is the main dif in the presentation of interstitial disease vs GN

A

Interstitial dont normally have HTN or proteinuria (except NSAID induced interstitial nephritis)

83
Q

What are the absolute indications for dialysis

A

Severe volume overload refractory to diuretic agents, severe hyperkalemia and/or acidosis, encephalopaathy and pericarditis or serositis

84
Q

What are the complications of dialysis

A

Hypotension, acccelerated vascular dz, rapid loss of residual renal function, access thrombosis, access or catheter sepsis, dialysis related amyloidosis, protein energy malnutrition, hemorrhage, anaphylactic reaction, thrombocytopenia

85
Q

What is peritoneal dialysis

A

Catheter that infuses dialysate solution into the abdomen; allows for transfer of solutes across peritoneal membrane

86
Q

What does hyperfiltration result in

A

Sclerosis and decrease number of nephrons

87
Q

How do you define acute renal injury/disease vs chronic kidney dz

A

Acute: rise in serum Cr
Chronic: GFR

88
Q

What are the ranges for each of the stages of CKD

A 
G1: >90
G2: 60-89
G3a: 45-59
G3b: 30-44
G4: 15-29
G5: <15
89
Q

What are the categories for albuminuria

A

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

90
Q

What pathologies do you see at each stage of CKD

A 
Stage 1:nothing
Stage : HTN
Stage 3: increased PTH, anemia 
Stage 4: hyperphosphatemia, acidosis and hyperkalemia 
Stage 5: uremic syndrome
91
Q

What sodium levels do you get on serum labs for CKD

A

Fictitious normal levels b/c of fluid overload

92
Q

What causes the metabolic acidosis seen in CKD

A

Reduce ammonia production *initially Hyperchloremic metabolic acidosis but as functional worsens becomes HAGMA b/c of retain organic acids;; presence of acidosis induces protein catabolic state

93
Q

What does uremia lead to

A

Accumulation of multiple toxins, loss of fluid and electrolyte homeostasis and hormone regulation, progressive increase in systemic inflammation

94
Q

What happens to the bones in CKD

A

Decreased phosphate excretion from the kidney leads to stimulation of PTH and growth of parathyroid gland -> decreased D3; leads to m weakness, osteitis fibrosis cystica (high turnover bone dz - cysts w/in bones), osteomlcia (defective mineralization), adynamic bone dz (decreased rate of bone turnover w/o mineralization defect; worse in DM)

95
Q

What is the effect of acidosis on the bone

A

Dissolution of bone buffers leads to bone decalcification and osteoporosis

96
Q

What is the effect of PTH on the heart

A

Causes cardiac m fibrosis; elevated phosphorus/calcium complex increases vascular calcification and atherosclerosis; *tx with supplemental calcitriol to suppress PTH

97
Q

What is the number one cause of mortality in patients with CKD

A

CV dz

98
Q

What causes anemia seen in CKD

A

Decreased EPO; *normochromic, normocytic until late in renal failure; neocytolysis (hemolysis of youngest RBCs in circulation); bone marrow fibrosis *leads to Left ventricular hypertrophy (chronic low O2 to the kidney activates sympathetic to increase HR and stroke volume)

99
Q

What stage of CKD displays neuromuscular problems

A

3; causes twitching, hiccups, cramps; *peripheral neuropathy seen in stage 4 (sensory >motor and LE>UE)

100
Q

What are the effects of uremia on GI

A

uremic fetor: urine like odor on breath associated with unpleasant metallic taste
Gastritis, peptic dz, mucosal ulceration, anorexia, N/V, constipation

101
Q

What is the effect of CKD on the endocrine system

A

Increased plasma insulin, decreased estrogen in women, decreased testosterone in men

102
Q

What does CKD do to the skin

A

Hyperpigmentation (decreased excretion of pigments), pruritus (worse with hyperphosphatemia)

103
Q

What is the tx for CKD

A
  • control BP: 130/80; ACEI and ARB first line
  • monitor for edema
  • Na restriction, protein restriction (but monitor for malnutrition)
  • avoid nephrotoxic drugs
104
Q

When should you refer someone with CKD to nephrology

A

GFR <30

105
Q

When are renal transplants considered

A

CKD stage 4

106
Q

What is peritoneal dialysis

A

Infusion of hyperosmolar solution which creates osmotic gradient and removes low molecular weight substances (Cr, urea, potassium and albumin)

107
Q

What considerations need to be made with peritoneal dialysis

A

Nutritional changes (based on needs), diabetics need additional insulin, *can cause sclerosing encapsulating peritonitis (entrap loops of bowel), infection

108
Q

What are contraindications to renal transplant

A

Malignancy, active infection, significant cardiopulmonary dz

109
Q

What percentile is normal BP for a kid

A

<90th percentile

110
Q

When should BP be checked in kids

A

Annually if over 3; if are obese, taking meds known to increase BP, have renal dz or aortic arch obstruction or DM - at every visit

111
Q

When should kids have their BP measured < 3 y/o

A

History of prematurity, congenital heart dz, recurrent UTI, renal dz, solid organ transplant, malignancy,

112
Q

How many readings do you need to classify a kid as hypertensive

A

3

113
Q

When do you refer a child to emergency care for high BP

A

If symptomatic or BP is >30 mm Hg above 95th percentile

114
Q

What is usually more elevated in primary vs secondary HTN

A

Primary: systolic
Secondary: diastolic

115
Q

When would you not do a further investigation for a secondary cause of HTN in a child

A

If >6, have a fhx of HTN, or are overweight

116
Q

What is pulse pressure

A

systolic-diastolic

117
Q

What is the highest acceptable systolic BP for kids 1-10

A

70 + (2 x age)

118
Q

What is masked HTN

A

Normal in clinic but HTN outside

119
Q

What is the most targeted organ abnormality seen in kids with HTN

A

LVH **use ECHO

120
Q

What is the definition of hematuria

A

Presence of 5 or more RBCs/hpf on 3 consecutive specimens obtains in the span of a few weeks

121
Q

When will hemoglobin be seen in urine

A

HUS, burns, acute nephritis, hemolysis

122
Q

What can color the urine

A

Rifampin, nitrofurantoin, pyridium, sulfa drugs, beets, rhubarb, fruit juices
*in newborns, uric acid crystals

123
Q

When is a urinalysis done in a kid

A

5 year old check up and part of a pre-participation physical

124
Q

What is the difference in glomerular vs extra glomerular hematuria

A
  • glomerular: RBC casts present, dysmorphic RBCs, proteinuria may be present, no clots, red or brown color
  • extra glomerular: no RBC casts, uniform RBCs, absent proteinuria, clots may be present, red
125
Q

What findings are seen in kids with post strep glomerulonephritis

A

Gross hematuria, HTN, swelling, elevated ASO titer, low serum complement

126
Q

What can hypercalciuria cause in kids

A

Asymptomatic hematuria *urine Ca:Cr ration of > 0.2 is indicative of excess calcium excretion

127
Q

What do you do with a kid who has asymptomatic hematuria and proteinuria

A

Refer to nephrologist

128
Q

How can you obtain a urine sample from a child

A

Catheter or suprapubic aspiration

129
Q

What is the criteria for dx of UTI

A
  • if clean catch: presence of pyuria and at least 50,000 colonies/mL of a single organism
  • if catheter: pyuria and colony
  • If suprapubic aspiration any growth on culture
130
Q

Which organisms convert nitrate to nitrite

A

E. coli, klebsiella, proteus, pseudomonas, enterobacter, citrobacter

131
Q

What can you use to tx a child with a UTI

A
  • if can tolerate PO, cephalosporin or fluoroquinolones
  • if cant tolerate PO, parenteral 3rd gen cephalosporin; add ampicillin if enterococcus suspected
  • length of tx: afebrile 3-4 days; febrile 10-14
132
Q

When do you image a child’s urinary tract

A
  • after first UTI in boys, do renal and bladder US and VCUG
  • in girls, after 2nd UTI o renal and bladder US, include VCUG if anomaly’s identified or temp >39 and a pathogen other than E. coli or poor growth and HTN part o clinical presentation
133
Q

What are the complications of renal scarring

A

HTN, decrease renal function, proteinuria, ESRD

134
Q

What should be included in your PE for a child with suspected UTI

A

Documentation of BP, temp, ab exam, documentation of growth, CVA tenderness, external genitalia, lower back, examine for other sources of fever

135
Q

When should the primary care pediatrician refer to a specialist for renal cases

A

-dilating VUR grades III-V, if obstructive uropathy present, when renal abnormalities identified, when kidney function impaired, if HTN, if bladder and bowel dysfunction refractory to primary care measures

136
Q

How do you calculate the urine anion gap

A

Sodium + potassium - chloride

137
Q

What does a negative urine anion gap indicate

A

Non renal cause for acidosis

138
Q

What do you look at if the urine pH is > 5.5

A

Urine anion gap; if negative -> extrarenal loss of base; if positive -> look at serum K -> if decreased, Type 1 RTA; if increased -> generalized tubular defect or ureteral obstruction

139
Q

What drugs can cause RTA I

A

Lithium, toluene, amphotericin

140
Q

What does RTA type I do to NH4 levels

A

Decreased in urine; causes urine pH >5.5

141
Q

What are ppl with RTA I prone to

A

Hypocitraturia and hypercalcuria -> nephrolithiasis, nephrocalcinosis and bone dz

142
Q

What makes RTA IV worse

A

Any drug that affects RAAS, increase potassium intake and potassium sparing diuretics

143
Q

How do you prove RTA IV

A

Low renin and aldosterone levels

144
Q

Which RTA do you use the bicarbonate challenge for

A

II

145
Q

What can cause RTA II

A

Carbonic anhydrase deficiency, fanconi, Wilson, hyperparathyroidism, vitamin D deficiency lead, drugs

146
Q

What is a generalized tubular defect

A

Both H and K secretion are impaired; elevated serum K; urine pH >5.5 associated with interstitial kidney dz (SLE, sickle cell, obstructive uropathy)

147
Q

What is the urinary pH in someone with diarrhea

A

Increased; hypokalemia increases renal production of NH4

148
Q

What is chronic tubulointerstitial disease characterized by.

A

Isothenuria with polyuria, moderate proteinuria, Type I, II, or IV RTA; broad waxy casts, small kidneys
CAUSES: prostate obstruction, analgesics, VU reflux, lead, gout, myeloma

149
Q

where are the deposits found in MPGN I and II

A

I: subendothelial
II: intramembranous

150
Q

What kind of cancers are associated with MPGN vs membranous nephropathy

A

MPGN: leukemia/lymphoma
Membraneous: solid

151
Q

What do cystine crystals look like

A

Hexagon shape

152
Q

What do tyrosine crystals look like

A

Spiny

153
Q

What are the complications of mucinous adenocarcinoma

A

Thrombotic

154
Q

In someone who has polycystic kidneys, what needs to be done in terms of tx for pyelonephritis

A

Prolonged abx

155
Q

If you have a very alkaline urine, what organism should you suspect

A

Proteus

156
Q

Is irritative voiding usually a sign of cancer

A

No

157
Q

What is the MOA of damage in HTN nephropathy

A

RAAS and hyperfiltration leading to inflammation and fibrosis

158
Q

What ranges of GFR do you usually get NAGMA vs HAGMA in CKD

A

NAGMA: 40
HAGMA: 20

159
Q

How do you calculate water deficit

A

.6 x body weight x (1-(140/Na))

160
Q

How do you calculate GFR

A

(140-age)x weight/Pcr x 72 (x.85 for female) = RPF x .2

161
Q

How do you calculate half life

A

(.693 x Vd)/Cl

162
Q

How do you calculate clearance

A

Ux x V/Px

163
Q

How do you calculate filtration fraction

A

GFR/eRPF

164
Q

How do you calculate fractional excretion

A

Ux x Pcr/Px x Ucr

CPRII Exam 2 (17 decks)

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