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Renal-Pulm > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

Where is Tamm-Horstfall protein made?

A

Thick ascending limb

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2
Q

Role of virulence determinants

  • fimbriae
  • flagellum
  • siderophore
  • cytotoxic necrotizing factor I
  • hemolysin
  • Lipopolysaccharide
A
  • fimbriae -> bind to bladder epithelial cell receptors via glycosphinolipid ix
  • flagellum -> movement
  • siderophore -> assist in acquiring iron
  • cytotoxic necrotizing factor I -> tissue damage
  • hemolysin -> tissue damage
  • Lipopolysaccharide -> antiphagocytic
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3
Q

List the inhibitors of bacterial adherence

A 
–  Tamm-Horstfall protein
 –  Mucopolysaccharide
–  Oligosaccharides
–  sIgA
–  Lactoferrin
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4
Q

Dx for cystitis

A

Pyuria

  1. > 5 WBCs per HPF
  2. leukocyte esterase positive
  3. nitrite positive - not all
    - gm + NOT nitrite positive
  4. urine culture
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5
Q

Sxs used to distinguish cystitis from pyelonephritis

A

Fevers, chills, flank pain

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6
Q

Only oral antibiotic approved for tx of pyelonephritis?

A

Fluoroquinolones

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7
Q

How to distinguish b/w relapse and reinfection recurrent infections?

A

– Relapse
• Same organism-may mean uneradicated focus
• Symptoms return < 2 weeks; one has to consider antibiotic resistant organism

– Reinfection
• Same organism but > 2 weeks after last infection
• Most recurrences are reinfection
• Original risk factors still exist

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8
Q

Young men getting UTIs think?

A

– Strictures
– Neurogenic bladder
– Incomplete voiding for any reason
– Vesicoureteral reflux

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9
Q

Old man w/ UTI?

A

prostatic hypertrophy

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10
Q

Sexually active male w/ prostatitis -> evaluate for?

A

Neisseria gonorrohoeae and Chlamydia trachamotis

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11
Q

Chronic prostatitis

  • time frame
  • organism
  • presentation
  • tx
A

• Infection persisting for > 3 months
• E. coli is the most common, but also Pseudomonas aeruginosa, Proteus, and Klebsiella
• Enterococcus is in fact the second most commonly isolated organism
• Often present with recurrent UTI symptoms
• Or perineal or back pain
-tender boggy prostate

TX w/ fluoroquinolones

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12
Q

Define primary vs 2ndary TIN

A

Primary
-glomeruli and vasculature normal

2ndary
-consequence of primary changes in glomeruli or vasculature

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13
Q

Out of the 3, which one correlates best w/ renal fx?

  • Tubulointerstitial changes
  • glomerular changes
  • vascular changes
A

TI changes

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14
Q

Hallmark of analgesic nephropathy is

A

Papillary necrosis

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15
Q

Acute TIN + MCGN is the classic lesion associated with?

A

ARF due to NSAIDs

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16
Q

What effect does NSAID use have in patients w/ CRF or hemodynamic instability

A

Dec GFR: prerenal azotemia -> dec prostaglandins -> dec RBF/GFR

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17
Q

Mech for hyperkalemia with NSAID use

Hyponatremia?

A

Hyperkalemia: dec in PGE -> dec in renin -> inc in K

Hyponatremia: removal of inhibitory effect of PGE on ADH

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18
Q

Mech for Na retention with TIN due to NSAIDs

A

dec RBF and GFR

-if HTN -> gets worse

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19
Q

Where in the kidney does lithium accumulate?

Mechanism of toxicity

A

Accumulates in collecting duct
Enters cells via ENaC
Down regulates APQ-2: dec regulation of cAMP -> Nephrogenic DI (can tx w/ HCTZ)

Dec activity of H+-ATPase pump -> RTA

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20
Q

3 major renal conditions due to lithium

-also describe recovery from each

A

RTA -> resolves if d/c’d

Nephrogenic DI -> resolves if d/c’d EARLY

Chronic TIN -> may continue to progress even w/ d/c
-creeping Cr

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21
Q

Which type of RTA can cause nephrocalcinosis?

A

Distal RTA - problem w/ maintaining proton gradient

  • needed to excrete proton and reabsorb bicarb
  • also get hypokalemia

NOT proximal RTA

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22
Q

Define nephrocalcinosis

  • where does it occur?

- associated w/ conditions causing?

A 
Calcium deposition (commonly oxalate) in renal parenchyma
-mostly in medulla

Associated w/ conditions causing:

  • hypercalcemia
  • hypercalciuria
  • hyperphosphaturia
  • hyperoxalosis
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23
Q

Causes of nephrocalcinosis (6)

A 
Distal RTA
Primary HyperPTH
Milk Alkali syndrome -> Calcium carbonate 
-CKD and on Ca supplements 
Sarcoidosis
Vit D intoxication
Vit C abuse  -> contains oxalate
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24
Q

Renal effects of hypercalcemia

MUST KNOW SLIDE

A
  1. DI – down regulation of AQP-2 ARF
  2. Pre-renal
    - Dehydration & renal vasoconstriction
  3. TIN/Nephrocalcinosis – if sustained
  4. Nephrolithiasis – if sustained
  5. Hypertension (vasoconstriction)
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25
Q

Exception to the following rule - Na and Ca excretion go in the same direction

A

HCTZ use

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26
Q

Tx for hypercalcemia

MUST KNOW SLIDE

A
  1. Normal saline
    - To repair volume
    - Na and Ca excretions go in same direction (exception – HCTZ)
  2. Furosemide
    - To increase calcium excretion (via NKCC blockade)
    - Replace K, Mg as needed
  3. Bisphosphonates – Pamidronate, Alendronate
    - To reduce osteoclastic activity
    - Alendronate IV a good choice
  4. Steroids
    - To decrease intestinal absorption
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27
Q

Tubulo-interstitial disease

  • Urinalysis
  • Quantitative proteinuria

MUST KNOW SLIDE

A

Urinalysis

  • minimal proteinuria
  • benign sediment

Quantitative proteinuira
-typically =/< 500mg/day

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28
Q

2 ways to get pylo

A
  1. Ascending UTI
    - E. coli
    - MOST COMMON
  2. Hematogenous
    - Staphylococcal
    - minority
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29
Q

Light chain cast nephropathy

  • associated with?
  • leads to?
  • clues to ID on histopath (3)
A

Multiple myeloma

ARF w/ proteinuria
-Bence jones proteins = Ig light chains (kappa or lambda)

Histopath
-tubule filled w/ protein cast
-inflammatory rxn w/ giant cells (macrophages) -> unique quality in light chain gammopathies
-another clue -> light chain doesn’t react with PAS
last clue -> cracks seen in the protein cast

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30
Q

MCC of nephropathy

A

Diabetic nephropathy in T2DM

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31
Q

Microalbuminemia in HTN w/out diabetes is a sign of?

A

Inc CV risk

  • endothelial association w/ GBM
  • start tx
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32
Q

90% of essential HTN onset occurs in which age group? Which race does it occur earlier in?

A

35-55 - Caucasians
-earlier in A.A.

If earlier age -> 2ndary cause

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33
Q

1st? MCC of ESRD

2nd MCC of ESRD?

A 
1 = diabetes 
2 = HTN nephrosclerosis
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34
Q

Classical lesion for onset of essential HTN in kidney is?

A

Glomerular ischemia

  • due to chronic afferent arteriole constriction -> neointimal hyperplasia
  • wrinkling of GBM
  • eventually get global sclerosis
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35
Q

Which mutation associated w/ earlier onset and more rapid progression of diabetic nephropathy, HTN nephrosclerosis, HIV nephropathy, and focal glomerulosclerosis

  • which race?
  • where expressed?
  • evolutionary advantage?
A
  • Apol 1
  • AA
  • podocytes and renal arterioles
  • protective against trypanosomes -> sleeping sickness
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36
Q

List the proven tx for slowing progression of diabetic nephropathy (5)

A 
diabetic control
BP control 
Smoking cessation 
weight loss in obesity 
reducing proteinuria to <1g/24 hrs
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37
Q

In what instances is kidney bx in diabetic nephropathy indicated?

A

Rapid decline in renal fx

active urine sediment

other findings suggestive of alternative disease

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38
Q

Classic sign on EM in diabetic nephropathy w/ regards to GBM

A

Uniform thickening of the lamina densa
-abnormally glycosylated proteins accumulate

Also see mesangial sclerosis

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39
Q

At what stage of pathological classification of diabetic kidney disease is nodular sclerosis seen?

Global glomerular sclerosis?

A

Stage III

Stage IV (last stage)

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40
Q

List stage of CKD

A

Stage 1
>90

Stage 2
60-89

Stage 3
30-59

Stage 4
15-29

Stage 5
<15 or dialysis

Most people fall under stages 1-3
-more likely to die due to CV events in these stages rather than progress to IV and V

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41
Q

What 2 prognostic tests are good for CV and renal disease?

A

eGFR + albuminuria

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42
Q

Proteinuria followed by HTN suggestive of?

A

Primary renal disease

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43
Q

Final common pathway pathogenesis

A

loss of nephrons -> hypertrophy of remaining nephrons to maintain GFR -> glomerular hypertrophy -> inc capillary radius and increased hydrostatic pressure -> HYPERFILTRATION DAMAGE

-2ndary glomerular sclerosis = component adaptive nephron

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44
Q

Examples of disease that lead to final common pathway

A

HTN nephrosclerosis
Reflux nephropathy
Lupus nephritis
nephrectomy -> single kidney in patient w/ renal disease (RCC)

-all these cause SCATTERED LESIONS (not all glomeruli are involved)

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45
Q

Final common pathway accompanied by? (5)

-which stage?

A

STAGE 3

HTN
Anemia
Metabolic acidosis
phosphate retention 
renal osteodystrophy
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46
Q

If not HTN by stage IV or V of CRF think?

A

diminished EF or renal salt wasting

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47
Q 
Renal diet
CRF stages 3-5
-protein 
-Na
-K
A

Protein
-0.8g/kg -> reduces H+, PO4 intake; avoids protein malnutrition and delays uremia

Na
-2-2.5 gNa = 5G NaCl = 100mEq Na

K

  • avoid high K food especially if tendency (e.g. diabetes)
  • dec renin release w/ diabetes -> inc risk of hyperkalemia due to dec aldo
  • also insulin pushes K into cells
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48
Q

Metabolic acidosis in CRF due to?
contributes to?
how much NaHCO3 needed?

A

Diminished NH4 production
-contributes to CRF progression and catabolism of protein and bone; bone is a buffer system for protons

-shift hyperkalemia

  • 20-30mEq of NaHCO3 adequate to restore HCO3 > 22 mEq/L
  • CaCO3 also useful
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49
Q

Describe the osteoid to mineralized bone ratio in osteomalacia

A

Too much osteoid and not enough mineralized bone -> weak bones
-due to inc Ca resorption

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50
Q

Cholesterol clefts seen with?

A

atheroembolic renal disease

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51
Q

What is the gene involved with ARPKD? what does it code for?

A

PKHD1 - fibrocystin

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52
Q

What is the proposed pathogenesis for PKD?

A

Improper connection b/w nephron and collecting system OR squeezing of the connection -> cysts = swollen nephrons that can’t drain

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53
Q

What does the cloaca form

A

Rectum

Primitive UG sinus -> bladder + pelvic urethra + definitive UG sinus

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54
Q

Tourneux vs Rathke folds

A

Tourneux fold -> superior portion of urorectal septum

  • b/w rectum and bladder
  • T = top

Rathke -> inferior portion of urorectal septum

  • b/w rectum and urethra
  • right and left
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55
Q

What happens when both Tourneux and Rathke folds fail to form

A

Rectovesical fistula - connection b/w rectum and bladder

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56
Q

ureteric buds (urethra) become directly attached to?

Mesonephric ducts become attached to

A

Bladder

urethra (prostatic)

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57
Q

Ectopic ureter occurs when

Describe the drainage

consideration for females

consideration for males

A

2 ureteric buds sprout from same mesonephric duct

  • gets pulled down inferiorly w/ mesonephric duct
  • ectopic ureter drains inferior to the bladder

URETERS CROSS
Ectopic ureter -> drains the superior pole
Normal ureter -> drains inferior pole

In females -> ectopic ureter may drain into vestibule, vagina or uterus

  • all are BELOW the sphincter urethrae muscle -> incontinence
  • urinate normal w/ dribbling in b/w
  • apparent during potty training

In males -> drains into prostatic urethra, ejaculatory duct, vas def, or seminal vesicles

  • all are ABOVE the sphincter urethrae muscle -> NO incontinence
  • but inc risk for infection
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58
Q

most common inherited autosomal dominant kidney disease

A

ADPKD

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59
Q

Characteristics of Frasier Syndrome

A 
46, XY w/ female phenotype 
kidney disease
pubic hair 
mullerian structures
mutation in WT1
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60
Q

PKD1

  • codes for?
  • linked to?
A

polycystin -> large membrane bound protein

linked to TSC2 -> tuberous sclerosis

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61
Q

PKD1 vs PKD2

  • chromsome
  • avg age for renal failure
A

PKD1 - 53
-chromosome 16

PKD2 - 69
-chromosome 4

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62
Q

Mutation in ARPKD

  • chromosome?
  • death from
  • which part of nephron gets the cysts?
A

PKHD1

  • chromosome 6
  • pulmonary hypoplasia -> respiratory insufficiency
  • Cysts = DILATED COLLECTING DUCTS
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63
Q

We have no reliable testing for mutations in

A

regulatory elements

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64
Q

MCC of palpable mass in newborn is

A

cystic kidney disease

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65
Q

90% of multicystic dysplastic kidney disease associated with? (renal dysplasia)

Path?

A

obstruction (urinary tract malformations)

Path

  • disruption of pre-renal mesenchyme coming together w/ ureteral bud
  • ureteric bud and metanephric blastema
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66
Q

Wilms tumor

  • sporadic and unilateral vs congenital syndrome/family hx percentages
  • genes
A
  • sporadic and unilateral = 90%
  • congenital syndrome/family hx = 10%
  • chromosome 11 - deletion of short arm
  • WT1 gene
  • WT2 gene

Loss of heterozygosity

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67
Q

WAGR

A
  • wilms tumor
  • aniridia
  • genitourinary anomalies
  • mental retardation
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68
Q

Denys-Drash

A
  • wilms
  • dysgenetic disorders
  • glomerular disease
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69
Q

Beckwith-Wiedemann syndrome

A

-Wilms
-hemihypertrophy visceromegaly
macroglossia

70
Q

Nephrogenic rests

  • define
  • precursor for
  • risk of
A

small foci of persistent primitive blastemal cells

precursor lesion for wilms tumor

risk of bilateral wilms

71
Q

MC renal tumor in neonate?

  • presents as
  • uni or bilateral
  • risk of mets
  • tx
  • histology
  • gross comparison to wilms
A

Mesoblastic nephroma

  • less than 3 months of age
  • 1/3 to 1/2 noted w/in 1st week of life
  • abdominal mass
  • ALWAYS unilateral
  • low risk of mets
  • nephrectomy

histo -> spindles cell tumor
-no primitive appearance

Unlike Wilms -> no sharp distinction b/w normal kidney and tumor

72
Q

Subgroups w/ HTN at inc risk

A 
African american 
hispanic 
elderly 
metabolic syndrome
DM2
CKD
73
Q

ACEI don’t work well in which population?

A

African Americans

74
Q

Minimum eval of HTN patient

A 
urinalysis, microalbumin test
Hct
renal profile
fasting glucose
lipid profile
EKG
75
Q

Describe the rule of tens with regards to HTN tx

A

1 additional drug for every additional 10-mmHg reduction in BP

76
Q

JNC-8 guidelines for HTN drugs

  • General population
  • AA
  • CKD
A
  1. general (including diabetics) -> initiate tx w/ a thiazide, Ca channel blocker, ACE inhibitor or ARB
  2. Black population -> include a thiazide or a CCB
  3. In patients w/ CKD -> include ACE-I or ARB until age 75
    - use clinical judgement to tx > 75
77
Q

Chronic proteinuria is predictive of

78
Q

Why is proteinuria harmful to kidney?

A
  1. Podocyte damage
  2. fibrosis and tubulointerstitial disease
    AGII, endothelin and TGF-beta play role
79
Q

What is an acceptable inc in Cr following ACEI tx?

80
Q

What occurs in adynamic bone disease?

A

Bone doesn’t respond normally to PTH

81
Q

Cinacalcet

  • class
  • action
  • indication
  • side effects
  • other
A
  1. class -> calcimimetic agent
  2. Action
    - reduces PTH production at same Ca level -> sensitizes Ca-sensitive receptor to serum Ca
  3. Indication -> 2ndary hyperPTH
  4. Side effects -> hypocalcemia
82
Q

Sevelamer Carbonate

  • class
  • action
  • indication
  • side effects
  • other
A

Sevelamer Carbonate

Class
-Phosphate - Blocker

Action
-Chelates PO4 in gut

Indication
-CRF with elevated serum PO4

Side effects

(a) hypophosphatemia ((a) = action of drug)
(b) constipation – may interfere with absorption of other drugs * ((b) = other side effects)

Other
-Reduces serum LDL also

  • Take other drugs at least 1 hour before Sevelamer
83
Q

Calcitriol

  • class
  • action
  • indication
  • side effects
  • other
A

Class
-Calcitriol (1-25 (OH)2Vit D)

Action

  • Most active effect on vitamin D receptors (VDR)
  • stimulates bone Ca++ mobilization and gut Ca++ reabsorption
  • directly lowers PTH levels

Indication
-Hypocalcemia due to low levels of 1-25(OH)2VitD in presence of normal levels of 25(OH)VitD

Side effects
(a) Hypercalcemia

Other

(a) Beneficial effects in CV disease, immune function, cancer?
(b) Paricalcitol in CRF may have reduced effects on absorption of calcium and phosphate in the gut and thus cause less hypercalcemia while reducing PTH levels

84
Q

Starting drug tx for HTN vs renal disease

A

HTN -> amlodipine + ACE

renal disease -> ACE or ARB

85
Q

Malignant HTN

  • hallmark
  • characterized by
A
  • papilledema

- fibrinoid and necrotizing arteriolitis

86
Q

3 toxic effects of aldosterone

A
  • fibrosis
  • hyperplasia
  • inflammation
87
Q

Typical presentation for unilateral renal artery stenosis txed with ACEI

A

Dec in BP and slight dec in GFR (inc Cr)

88
Q

When should a loop be used over thiazide for HTN management?

A

If filtered low is too low (i.e. low GFR)

<30??

89
Q

If K is high in urine with high serum K ->

If K low in urine with high serum K ->

A

If K is high in urine with high serum K -> diet problem

If K low in urine with high serum K -> renal problem

90
Q

Simplified henderson-hasselbalch eq

A

log (P/U) = pKa - pH

91
Q

Weakly basic drugs are concentrated/trapped in?
-can be eliminated more quickly by?

How about weak acids

A
  1. Acidic fluid; acidify urine

2. Opposite for weak acids

92
Q

Given a fixed pH, the higher the pKa of a weak acid, the more will be in the (charged/uncharged) form?

93
Q

Relationship b/w elimination rate constant and half life of drug

A

INVERSELY PROPORTIONAL

94
Q

Vol distribution =

A

Vd = dose/[drug in plasma] at t=0

95
Q

Cl=

96
Q

Css (steady state) =

A

Css = k0/Cl

steady state plasma [drug] = influx (infusion rate)/efflux (CI

97
Q

Inc risk for getting what with glyburide or metformin in patients with DM and renal insufficiency

A

LACTIC ACIDOSIS

98
Q

Dose levels in CRF

  • Stage 3
  • Stages 4 and 5
A

3 -> 50% decrease

4+5 -> 75%

99
Q

DOC for txing volume overload in AKI or low GFR

100
Q

Drugs that can cause pre-renal AKI

A

ACEI and ARB -> inhibit efferent arteriole vasoconstriction

NSAIDs -> inhibit afferent arteriole vasodilation

Cyclosporin + Tacrolimus
-calcineurin inhibitors and potent renal vasoconstrictors

101
Q

Intra-renal injury by drugs

  • ATN -> 3
  • AIN -> 8
A

Acute tubular necrosis

  • Aminoglycoside antibiotics (e.g., Gentamicin) – bind to and uptake by proximal tubule cells in renal cortex—cell death
  • Amphotericin B (anti-fungal) – renal arterial vasoconstriction and distal renal tubule cell toxicity (minimize with liposomal drug formulations)
  • Cisplatin (and to a lesser degree, carboplatin - antineoplastics)

Acute interstitial nephritis (only main drug examples listed)

  • Beta-lactam antibiotics (penicillins and cephalosporins) Fluoroquinolones (e.g., ciprofloxacin)
  • Thiazide diuretics (HCTZ, chlorthalidone) – rare, but heavily used
  • Loop diuretics (furosemide) – rare, but heavily used
  • Allopurinol (xanthine oxidase inhibitor used to treat gout)
  • Sulfonamides (including sulfonylureas for diabetes (e.g., glipizide))
  • Rifampin (anti-mycobacterial used to treat tuberculosis, CYP450 inducer)
  • NSAIDS
102
Q

Post-renal AKI

-drugs

A
  1. Acyclovir (a nucleoside analogue HSV antiviral drug used for genital herpes, cold sores, shingles)
  2. Methotrexate (anti-folate anti-metabolite used for cancer and autoimmune diseases)
  3. Indinavir (antiviral protease inhibitor used to treat AIDS)
  4. diuretics -> excess Ca in urine -> inc risk of stones
103
Q

Probenecid competes w/ which 2 drugs

  • for what?
  • transporter?
  • effect?
A
  • penicillins and MTX
  • secretion via organic anion transporter
  • dec secretion -> inc plasma concentration of penicillins or MTX
104
Q

Half life of Li+?

what happens when give thiazide to chronic Li patient

A

24 hours

inc concentration of Li

105
Q

What metabolizing enzyme is found in kidney?

A

CYP450

UDP-glucuronyltransferase (Phase II) -> furosemide metabolized here
-inc half life in AKI patients

106
Q

Which drug can make inc risk of euvolemic hyponatremia with thiazides? how?

A

NSAIDS

  • PGE2 is an ADH antagonist
  • blocking PGE2 with NSAIDs will lead to inc water reabsorption
  • combine that with Na loss -> euvolemic hyponatremia

MCC of of EH in old people is thiazides

107
Q

Match up the drugs associated w/ the following:
-from luke 2-24 lecture

ATN
AIN
HUS
RTA

A

ATN -> gentamycin (aminoglycosides)
AIN -> amoxicillin
HUS -> clopidogrel
RTA -> amphotericin B

108
Q

Which type of RTA does amphotericin B cause? What’s the mech?

A

Type ! RTA

  • alpha intercalated cells can’t secrete H+ -> new HCO3- can’t be generated -> met acid with hypokalemia
  • also inc risk of of CaPO4 kidney stones due to inc urine pH and inc bone turnover

Amphotericin B pokes holes in walls of collecting duct
-also vasoconstricts kidneys

109
Q

Should a patient stop taking ACEI, ARB and/or diuretics d/c if GI loss or high fever? If so why?

A

YES!!!

Inc risk of Pre-renal AKI

110
Q

ATN risk factors for aminoglycosides (like gentamycin) are (list 4)

A
  • high trough levels
  • prolonged administration
  • older age
  • concomitant use of loops (also for 8th nerve damage)
111
Q

Which endogenous chemical is both naturetic (salt wasting) and aquaretic? What is an inhibitor of this chemical? What effect does the inhibitor have on response to antiHTNs and diuretics

A

PGE2; inhibited by NSAIDs

-dec response; always ask about NSAID use!

112
Q

NSAIDs

  • effect on Na
  • effect on K
  • effect on kidneys
A

Hyponatremia: inhibit PGE2 = an ADH antagonist

Hyperkalemia: less renin release -> diminished aldosterone production

Renal: AIN; nephrotic syndrome and ATN by inhibiting autoregulation of GFR

113
Q

Signs/sxs of AIN

-difference with NSAID?

A

Rash
fevers
eosinophiluria
hematuria

W/ NSAIDs -> no rash or fever!!!

114
Q

Rxing in ARF and CRF
-which adjustment to the drug dose is better if patient needs high blood levels quickly? (e.g. sepsis)

-what about for ppl in stage 3 CRF? Stage 4 and 5?

A

reduce dosing interval for 1st question

If stage 3 CRF -> reduce dose level by 50%
If stage 4 and 5 -> reduce dose level by 75%

115
Q

Give 2 reasons why there is an inc risk of hypoglycemia w/ glyburide in diabetics w/ renal failure

A
  1. Renally excreted
    - Drug will be higher in blood
  2. Half life of insulin is longer in patients w/ chronic renal failure
    - Insulin will stay around longer
  3. Use glipizide instead -> handled by liver
116
Q

Salicylate poisoning

  • toxicity at what level?
  • signs and sxs (list 4)
  • how to promote excretion
  • tx for severe poisoning
  • kids vs adults w/ regard to acid-base presentation
  • can mimic?
A

Toxicity when >40 mg/dL

  • hyperventilation and respiratory alkalosis
  • tinnitus
  • fever
  • vomiting and GI bleeding
  • mental status change
  • lactic acidosis - anion gap, mixed acid base disturbance

alkalinizing urine increase renal excretion

  • target = 6.5 - 7
  • don’t go too high

Hemodialysis effective tx for severe poisoning

adults - alkalotic side

kids - acidemic side

can mimic sepsis

117
Q

how to calc ratio of charged over uncharged salicylate

A

pH - 3 = Log SALc/SALus

118
Q

Acids responsible for causing inc anion gap acidemia for the following poisons:

  • methanol
  • ethylene glycol
  • what effects can they cause?
A

methanol -> formic acid
-blindness

ethylene glycol -> oxalic acid
-renal failure -> death

119
Q

How to calc osmolar gap

-MCC of osmolar gap?

A

osmolar gap = MEASURED serum

Osm - calculated Osm
Calculated Osm = (Na x 2) + [glucose] + [urea] = 280 + 18 mOsm + 2.8 mOsm

If > 10 mOsm then osmolar gap

MCC = ethyl alcohol
(mg/dL) / 5 = mOsm due to alcohol

120
Q

Fomipezole

  • MoA
  • indications
A

MoA -> competitive antagonist of alcohol dehydrogenase which converts toxic alcohols to their anionic metabolites

For methanol and ethylene glycol toxicity

121
Q

Which toxic alcohol cause osmolar gap and CNS toxicity but NOT metabolic acidosis?

A

Isopropyl alcohol

122
Q

Alcoholic ketoacidosis

  • main ketonacid
  • is it detected by acetest (nitroprusside) tabs?
  • tx w?
  • watch out for?
A

Beta hydroxybutyrate

NOT DETECTED

tx w/ glucose and saline and refeeding

watch out for refeeding syndrome
-K, phosphate and Mg replacement requirements

123
Q

Lithium

  • CNS side effects in acute vs chronic toxicity
  • Renal effect?
  • tx?
  • watch out for what with tx?
A
  • CNS side effects come on later with acute
  • nephrogenic DI: Li = ADH antagononist
  • tx by restoring ECF volume and produce natriuresis by saline infusion
  • hemodialysis w/ severe toxicity and renal impairment

-avoid hypernatremia in those w/ polyuria especially if isotonic saline being infused

124
Q

3 major criteria for a single simple cyst on US?

A
  • mass is round and sharply demarcated w/ smooth walls
  • no echoes w/in mass
  • strong posterior wall echo indicating good sound transmission through the cyst

Can’t be seen on plain film radiography

125
Q

RCC imaging

  • dxic procedure of choice
  • screening test to dx renal cyst
  • vascular invasion
A
  1. CT
    - peri-renal extension
    - vascular invasion
    - liver involvement
  2. US
  3. MR
126
Q

Nephrogenic phase of CT

  • time?
  • good for?
A

90-100 sec after contrast injection

Renal masses

127
Q

What can mimic RCC on CT?

A

renal abscess

128
Q

Is MRI good for renal calculi

129
Q

Clear cell RCC on T1 vs T2 MR

A

T1 - low signal

T2 - high signal

130
Q

Rxns to contrast
Minor
Moderate
Major

A

Minor
-hives/flushing

Moderate
-bronchospasm

Major

  • laryngeal edema
  • hypoTN ->aggressive IV fluids
  • arrhythmia -> atropine for brady if no response to fluid
131
Q

Risk factors for rxn to contrast

  • dose and rate
  • elderly patients
  • allergy hx
  • hx of previous rxn
A
  • not predictive
  • higher risk of arrythmias and MI
  • doubles risk
  • high risk -> pretreat

drugs -> can give steroids and benadryl

132
Q

Indications for RRT?

A
  1. ARF or CRF
    -uremic syndrome
    -pericarditis
    Failed conservative management for
    -hyperkalemia
    -acidosis
    -fluid overload
  2. Drug overdose:
    - lithium
    - ethylene glycol
    - methanol
    - salicylate
  3. Electrolyte disorders
    - hypercalcemia
    - hyperkalemia
  4. Metabolic disorders
    - severe hyperuricemia - tumor lysis
133
Q

CRRT vs IHD -> when is CRRT preferred

A

CRRT only used in ICU

  • high fluid removal needed (4L+)
  • hemodynamically unstable
134
Q

Absolute indications for RRT w/ acute or chronic renal failure

MUST KNOW SLIDE

A 
ARF or CRF
-uremic syndrome
-pericarditis 
Failed conservative management for 
-hyperkalemia
-acidosis
-fluid overload
135
Q

2 key fxs of dialysis
-how are they accomplished

MUST KNOW SLIDE

A
  1. Solute removal
    a) diffusion -> 85% (size dependent)
    b) convective transport -> 15%
    - solvent drag effect
    - for middle molecules
  2. Fluid removal
    - by hydrostatic pressure (ultrafiltration) -> HD
    - by osmotic pressure -> PD
136
Q

Best vascular access for hemodialysis
-why?

MUST KNOW SLIDE

A

AV fistula

  • long life
  • effective
  • least prone to infection

Catheter is worst

137
Q

PD vs HD - which one is better?

A

PD - better for 1st 3 years

HD - takes over after that

138
Q

What are 2 fxs of the kidney that dialysis can’t replace?

MUST KNOW SLIDE

A

endocrine and erythropoiesis

139
Q

Complete sentence:

After 1 year, 50% of grafts are lost due to?

A

NON-ADHERENCE

140
Q

What are the top 2 reasons for exclusion from transplant eligibility?

A

1 -> medical CI = ~50%

2 -> patient declined = 25%

141
Q

CI for kidney donation w/ regards to:

  • age
  • BP
  • proteinuria
  • GFR
A

AGE
- 65-70

BP
> 140/90

PROTEINURIA
>250 mg/24 hrs

GFR
<80 ml/min

142
Q

3 factors involved in tissue matching and Ab production

A
  1. HLA
  2. Crossmatch
  3. Panel-reactive Ab
143
Q

drugs used for induction immunosuppression

A

Corticosteroids

  • high dose and then tapered off
  • efficacy due to immunosuppressive and anit-inflammatory effects

Anti-lymphocyte Abs
-poly and monoclonal

144
Q

Adverse effects of corticosteroids include

A 
METABOLIC
l  Obesity
l  Hyperlipidemia
l  Diabetes mellitus
l  Osteopenia/Osteoporosis
l  Growth retardation (children)

COSMETIC

OTHER
l  HTN
l  Poor wound healing 
l  Mood changes
l  Proximal myopathy
145
Q

UC induction prototype for immunosuppression (3 drugs)

A

thymoglobulin
MMF
Solumedrol

146
Q

List 4 lymphocyte proliferation inhibitors

A

azathioprine

mycophenolate mofetil

Mycophenolate sodium

Sirolimus

147
Q

List 2 calcineurin inhibitor

A

cyclosporine

tacrolimus

148
Q

List a CNI sparing T-cell inhibitor

A

Belatacept

149
Q

Adverse effects of azathioprine

A

Myelosuppression - dose dependent

Hepatotoxicity

acute pancreatitis

skin cancer

150
Q

MMF adverse effects

A

diarrhea

leukopenia

anemia

tissue invasive CMV disease

151
Q

Cyclosporine adverse effects

-include cosmetic effects

A 
l  Nephrotoxicity
l  Hypertension
l  Cosmetic side effects – gingival
hyperplasia, hirsutism
l  Hyperlipidemia
l  Neurotoxicity – headache, tremor,
seizures
l  Hepatoxicity – transaminitis
152
Q

Tacrolimus adverse effects

-include race dependent effects

A

l Nephrotoxicity
l Neurotoxicity – tremor, paraesthesias
l Diabetes mellitus – more common in African-Americans & Hispanics
l Alopecia
l Hypertension
l Hyperlipidemia

153
Q

Cyclosporine and tacrolimus are metabolized by?

implication?

A

CYP-450 3A4

LOTS OF DRUG-DRUG IX

154
Q

Belatacept

  • MoA
  • black box warning
A

MoA -> selective T-cell costimulation blocker

BLACK BOX

  • Inc risk of post-transplant lymphproliferative disorder
  • mostly in the CNS
  • esp in patients who are EBV seronegative
155
Q

Sirolimus

  • class
  • indications
  • adverse effects
A

class -> macrolide anitbiotics

indication -> CNI sparing tx

Adverse effects
l  Thrombocytopenia
l  Hyperlipidemia – predominantly hypertriglyceridemia
l  Oral ulceration
l  Impaired wound healing
l  Proteinuria
156
Q

CER

A

-proportion of people not exposed who experienced the event

c/(c+d)

157
Q

EER

A

-proportion of people exposed who experience the event

a/(a+b)

158
Q

RR

A

-relative risk

EER/CER

159
Q

RRR

A

-relative risk reduction

(CER - EER) / CER

160
Q

ARR

161
Q

Best interest Standard

A
  • acting to promote maximally the good of the individual
  • legal standard
  • medical standard

Parents ALWAYS need to make decision most favorable to the child

162
Q

Medical reasoning in kids parallels

A

Piaget Stages

Age 2-6 -> preoperational stage

Age 7-10 -> concrete operational stage

Age 11-16+ -> formal operation stages

  • developmental milestone
  • can start making their own decision
163
Q

Acutely sick vs chronically sick kids with regards to maturity of explanation

A

Acutely sick -> less mature

Chronically sick -> more mature

164
Q

3 exceptions when minors can CONSENT for themselves

A
  • emancipated minor laws
  • mature minor laws
  • public health/awkward topic laws
165
Q

What are the NEWEST guidelines for when to start tx for HTN (JNC-8)
-break down by age

A

60+ -> tx to goal BP less that 150 over 90

less than 60 -> tx to goal BP less than 140 over 90

Over 18 w/ CKD and/or diabetes -> tx to goal less than 140 over 90

166
Q

Compare unilateral stenosis w/ bilateral RAS

A

Unilateral

  • sensitive to ACE inhibition:
    1. drop in BP
    2. can cause drop in GFR

Bilateral

  • more severe hypertension
  • small effect of ACEI
  • drop in BP ONLY after volume depletion
167
Q

List foods high in K

A
  1. Fruits – bananas, oranges, melons, etc.
  2. Vegetables – potatoes, tomatoes, greens, mushrooms, vegetable juices, pumpkin, etc.
  3. Dried beans, nuts, seeds
  4. Salt substitutes
  5. Milk
  6. Chewing tobacco
168
Q

List foods high in phosphate

A
  1. Dairy products
  2. Dried beans, peas, nuts, seeds
  3. Bran and whole grain breads
  4. Beer and dark sodas
  5. Processed meats
169
Q

Renal multivitamins contain?

A

i. Renal multivitamin contains B vitamins (B6, B12, etc.), folate, vitamin C, zinc (sometimes)

170
Q

IDWG should be (blank %) of dry body weight

171
Q

Fluid MNT for AKI

For CKD on HD?

A

AKI
-replace output from previous session + 500ml

CKD
-1000 + urine out

Renal-Pulm (9 decks)

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