Renal Flashcards

1
Q

Define serum anion gap

A

Accounts for unmeasured anions in metabolic acidosis
Na - (Cl + HCO3)
*normal 10-12
*over 12 means high gap

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2
Q

CUTE DIMPLES (AG metabolic acidosis)

A
cyanide
uremia
toluene
ethanol
DKA
isoniazid 
methanol
propylene glycol
lactic acidosis 
ethylene glycol
salicylates
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3
Q

Clinical features metabolic alkalosis

A

High pH + CO2

  • muscle cramping, tetany, parathesia
  • confusion, obtundation, seizures
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4
Q

Metabolic alkalosis ddx

A

caused by:

  • lose acid from vomiting, NG suction, diarrhea, diuretic
  • post-hypercapnia (lag for excretion)
  • pee out low bicarb fluid, bicarb concentrated
  • mineralcorticoid excess
  • hypercalcemia
  • citrate 2nd to blood transfusion
  • refeed (insulin ^ makes H+ go intracellular)
  • hypokalemia (K goes out of cells; H+ goes in)
  • hypovolemia causes prolonged met alk
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5
Q

Metabolic alkalosis tx

A
Cl responsive (urine Cl <25): give NaCl, K
Cl resistant (urine Cl >40): tx disease 

Cl resistant

  • low urine K: laxative abuse/sev. K depletion
  • HTN: check renin/cortisol
  • high cortisol = Cushing
  • high renin, NL cortisol = RAS, malg HTN, renin tumor
  • NL renin+cortisol = licorice, aldosteronism
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6
Q

HARDUPS (non-AG metabolic acidosis)

A
hyperalimentation (tube feed)
acetozolamide
rental tubular acidosis
diarrhea
uretero-pelvic shunt
post-hypocapnia
spironolactone
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7
Q

Causes of metabolic alkalosis

A
  • lose acid from vomiting, NG suction, diarrhea, diuretic
  • post-hypercapnia (lag for excretion)
  • pee out low bicarb fluid, bicarb concentrated
  • mineralcorticoid excess
  • hypercalcemia
  • hypochloremia
  • citrate 2nd to blood transfusion
  • refeed (insulin ^ makes H+ go intracellular)
  • hypokalemia (K goes out of cells; H+ goes in)
  • volume depletion causes prolonged met alk
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8
Q

Kidney normal response to acid load

A

Excrete as NH4

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9
Q

Clinical features metabolic acidosis

A

hyperventilation
decreased myocardial contractility, arrthymia
decreased vasc R (dec response to catecholamine)
N/V/D/abdominal pain
muscle weakness
osteomalacia/osteopenia…hypercalcemia
ostetitis fibrosa
lethargy, coma
kids: imp bone growth, listless, anorexia

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10
Q
Winters formula 
(metabolic acidosis)
A

expected pCO2 = (1.5 x HCO3) + 8 +/- 2

lower: + resp alk
wnl: hyperventilating approps
high: +resp acid

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11
Q

Delta gap

when the anion gap >12

A

(AG-12) / (24-HCO3)
between 1-2 means AG metab acid alone
less than 1 means + non AG metab acid
over 2 means + metabolic alkalosis

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12
Q

“Winters” but for

metabolic alkalosis

A

pCO2 = 0.7(24-HCO3) + 40 +/-2
low: uncomp
WNL: comp
high: + resp acidosis

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13
Q

Glomerular hematuria - what does the urine look like?

A

Dysmorphic RBC
RBC cast
Red-brown urine
No clots

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14
Q

Nonglomerular hematuria - what does the urine look like?

A

Scant normally shaped RBC
WBC cast, muddy brown casts
Pink-red
Clots

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15
Q

Asymptomatic hematuria

A

think of Ca risk
low = CT urography + urine cytology
high = CT urography + cystoscopy + cytology

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16
Q

Bladder Ca risk

A
smoking
occupational
gross hematuria
>40 yo
voiding sx 
cyclophosphomide
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17
Q

MCC hematuria F>60

A

UTI, then bladder Ca

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18
Q

MCC hematuria M>60

A

BPH, then bladder Ca

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19
Q

MCC hematuria 40-60

A

UTI, bladder Ca, calculi

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20
Q

MCC hematuria 20-40

A

UTI, calculi, bladder Ca

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21
Q

MCC hematuria <20

A

glomerulonephritis, UTI, congenital

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22
Q

Way to tell if pre-renal, intra-renal, post-renal

A

Labs
BUN/Creat > 20 pre-renal
BUN/Creat <10 post-renal
BUN/Creat 10-20 intra-renal

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23
Q

Urethritis, orchititis, prostatitis MCC

A

STI

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24
Q

Why nosociomal UTI more deadly?

A

Bugs themselves

Immunocompromised hosts

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25
Q

Most common type of nosocomial infection

A

UTI

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26
Q

Why do elderly people get more UTIs

A

Decreased elasticity of bladder

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27
Q

Structural UTI cause

A

Female (short urethra), BPH, stones, tumors

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28
Q

Functional UTI cause

A
Neurogenic bladder (nerve damage from DM, Parkinson, MS)
Sex/honeymood cystitis
Pregnancy (hormone changes)
Foley catheters
Tampons
Diaphragms
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29
Q

Tam-Horsfall protein

A

Immunodefensive protein that bind to protein and prevents epithelial attachment

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30
Q

Common UTI pathogen

A

E. coli, Staph, Proteus, Klebsiella, Psuedomonas, Enterobacter

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31
Q

S. epidermidis UTI pt

coagulase negative

A

No sex preference, >50
90% asymptomatic!
hospitalized
MDR

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32
Q

S. saphrophyticus UTI pt

A

95% female, 16-35
90% sypmtomatic
sensitive to abx

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33
Q

Elderly pt presentation of UTI

A

Mental status change, fever

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34
Q

<2 UTI presentation

A

fever, vomiting, FTT

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35
Q

Cystitis presentation

A

dysuria, suprapubic pain

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36
Q

Pyelonephritis sx?

How do you treat it?

A

fever, dysuria, flank pain
culture (try cipro while results pending)
7-14d abx (cipro)
hospitalize: fever, tachypnea, tachycardia, hypotension, debilitated (sepsis!)

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37
Q

UTI UA findings

A

WBC casts - upper tract infection

> 10 WBC/hpf

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38
Q

Women w/ UTI and no vaginal discharge have >90% chance of?

How do you treat it?

A

Acute cystitis

3d of abx

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39
Q

Complicated UTI means what?

How do you treat it?

A

Function, anatomic, or metabolic abnormality
Hx MDR
Hx pyelonephritis

Culture and start empiric abx

40
Q

Uncomplicated UTI tx

A

1) nitrofurantoin (100mg x 5d)
2) TMP/SMX (160/800mg bid x 3d)
If MDR…
fluroquinolones

41
Q

Uncomplicated UTI tx

A

1) nitrofurantoin (100mg x 5d)
2) TMP/SMX (160/800mg bid x 3d)
If MDR…
fluroquinolones

42
Q

Pregnant UTI

A

1) nitro (same as uncomplicated)

2) amoxicillin or amox-clauv

43
Q

Treat asymptomatic bacturia in these people

A

Pregnant, before urologic procedure, young kids

44
Q

Prostatitis sx and tx

A

Sx: back pain, pooping pain, high fever, UTI-like sx; VERY tender on PE
Tx: SMX/TMP x 6 weeks or…
if STI ceftraxone + azithromycin

45
Q

Nephrotic distinguishing features

A

Lipiduria and lipidemia
Proteinuria >3.5 f/d
Hypoalbumenimia
Lotsa edema

46
Q

Nephritic distinguishing features

A
Hematuria w/ dysmorphic RBC
RBC casts, granular casts
Oliguria
Pyruia
HTN, renal insufficiency
47
Q

Minimal change glomerularpathy

A

Nephrotic kids, 2-3week onset, corticosteriods

onset may have to do w/ allergens, Hodgkins

48
Q

Membranous glomerulonephropathy

A

Nephrotic adults, corticosteriods/immune suppressor depending on cause

“rule of 1/3” prognosis

49
Q

Focal segmental glomerulosclerosis

A

Nephrotic adults

HIV/hep, obesity, sickle cell, pamidronate are risk factors

50
Q

Membranous proliferative glomerulonephritis

A

Nephrotic, immune-mediated, thick BM but no inflammation

No tx

51
Q

Diabetic nephropathy

A

Nephrotic

ACEI, glycemic control BP control

52
Q

Post-streptococcal glomerulonephritis

A

Brown urine + casts; infiltrative lymphocytes in glomerular tuft

  • Na HTN d/t ^ENaC
  • Low C3

Tx: supportive/antimicrob

53
Q

Lupus nephritis

A

Rash, joint pains
Class 1-2: no tx
Class 3-4: steroid+immunosup

54
Q

IGA nephropathy

A

Hematuria

Chronic, no tx, no inflammation

55
Q

Rapidly progress glomerulonephritis

A
Macrophages go from glomerular capillaries to Bowmans space, compress capillaries, GFR ceases
"crescenteric"
==anuria==
==hemoptysis==
Tx: transplant, dialysis
56
Q

Defense against hypernatremia

A

Thirst (osmoreceptors)
Baroreceptor > RAAS > ENaC
ADH release (aquaporins reabsorb water)

57
Q

Hypernatremia ddx

A
  • gfr diminished (age, renal dz)
  • NaCl reabsorption in TALH diminished (loops, osmotic, interstitial dz)
  • dec ADH (diabetes insipidus)
  • urea (diuresis, low pro diet)
58
Q

Hypernatremia tx

A

Hypovolemic

  • isotonic saline
  • tx cause of loss (obstruction, insulin, remove osmotic diuretic)
  • fix water deficit (0.45% saline, D5, or oral water)

Euvolemic

  • fix water deficit as above
  • monitor serum Na to avoid water intox
  • may need SC ADH

Hypervolemic

  • remove sodium
  • furosemide
  • HD
59
Q

Clinical approach to hyponatremia

A

Symptomatic
- chronic >48h v acute

Asymptomatic
- no immediate tx needed

60
Q

Diabetes insipidus

A

hypernatremia d/t ADH not being released and not concentrating urine

central: damage to pituatary prevents ADH release
- sarcoid, aneurysm, GBS, meningitis, idiopathic

nephrogenic: kidney tubules can’t respond to ADH
- PCKD, amyloid, multiple myeloma, hypercalcemia, hypokalemia, lithium)

61
Q

SIADH causes

A
Inc. hypothalamic production:
CNS infection, neoplasms
Drugs
- cyclophosphamide
- haloperidol
- amytriptline, MAOI
Pulmonary dz (TB, pneumo)
Postop

Inc. ectopic production
- oat cell carcinoma

Potentiated affect of ADH

  • carbamazine
  • cyclophosphamide
62
Q

CKD definition

A

GFR <60ml/min for 3+ mo

63
Q

GFR level when sx begin

A

<30 ml/min

64
Q

CKD UA

A
  • elevated Cr
  • hematuria
  • proteinuria
  • imaging abnormality
65
Q

CKD nephrotoxic

A

Metformin
NSAID
aminoglycoside
IV contrast

66
Q

Indications for dialysis (AEIOU)

A
Acid/base (metabolic acidosis)
Electrolyte abn (hyperK)
Intoxication (remove poison)
Overload volume (CHF)
Uremia (Cr clearance <15, pericarditis, neuropathy, encephalopathy)
67
Q

Recurrent calcium stones tx

A
  • 24h urine collection
  • thiazide (dec urine Ca)
  • citrate supps
  • allopurinol if uric acid
68
Q

Urinary incontinence types

A

urge: MCC elderly, women w/ atrophic vaginitis and irritation of urethra; also diuretics
stress: 2nd MCC women, intra-abdominal pressure
dribbling: 2nd MCC men, overly full bladder
functional: cognitive/physical impairments

Mixed: typically stress+urge, stress+functional

69
Q

Urinary incontinence types (urge, stress, dribbling, functional, mixed) - who gets them most frequently?

A

urge: MCC elderly, women w/ atrophic vaginitis and irritation of urethra; also diuretics
stress: 2nd MCC women, intra-abdominal pressure
dribbling: 2nd MCC men, overly full bladder
functional: cognitive/physical impairments

Mixed: typically stress+urge, stress+functional

70
Q

Interstitial cystitis sx and dx

A

Pain w/ full bladder, women
Foods w/ K, tobacco, EtOH, spicy make it worse
Cystoscopy to dx

71
Q

How to dx urinary obstruction

A

Sx: pain, hydronephrosis causing palpable mass, voiding issues, urine volume decreased if b/l

  • urethral: voiding cystourethrography (VCUG)
  • proximal: abd US (1st choice, detects hydronephrosis); CT 2nd choice
72
Q

Wilms

  • who gets it
  • what is it
  • treatment?
A

Kidney tumor in kids <10

  • palpable mass+/- hematuria
  • well circumscribed
  • 90% cure rate
  • anaplastic unfavorable

Tx: nephrectomy +/- chemo (depends on stage)

73
Q

PKD

  • who gets it
  • what is it
  • treatment?
A

dominant: MCC, b/l (40s)
recessive: early death
acquired: blacks

cysts in epithealial cells of CD and tubules; back/flank pain, huge kidneys, nocturia

  • anemia
  • HA (anuerysm risk)
  • recurrent UTI

dx: US
tx: supportive (ACE/ARB, tx infections

74
Q

Wilms

  • who gets it
  • what is it
  • treatment?
A

Kidney tumor in kids <10

  • palpable mass+/- hematuria
  • well circumscribed
  • 90% cure rate
  • anaplastic unfavorable

Tx: nephrectomy +/- chemo (depends on stage)

75
Q

Bladder ca

  • who gets it
  • MC cell type involved?
  • sx
  • tx
A

M:F is 3:1, 60s-80s

  • smoking, aryl amines, long term analgesic, schisto, prev. radiation,
  • urothelial transitional cells MC
  • painless hematuria+irritative sx, hydronephrosis (if obstructive)
  • tx: resect via urethra, BCG; radical cystectomy/chemo (only if muscle involvement/mets)
76
Q

Renal cell carcinoma

  • who gets it
  • risk factors
  • sx including “classic triad”
  • tx
A

M:F is 2:1; 60s-70s
MCC renal Ca adult
Not usually inherited

Risk: tobacco, obesity (W), HTN, HRT (W), absestos, petroleum, ESRD, cystic kidney dzs

Classic triad: flank pain, palpable flank mass, hematuria (but mostly asymptomatic)

Common mets upon dx (lung/bone MC)

Tx: partial/full nephrectomy

77
Q

AKI - prerenal

A
hypovolemia
setpic shock
CHF
renal artery occlusion
small vasculitis 
anesthesia (low BV+low BP)
78
Q

AKI - intrinsic

A
  • sm. vessel (atheroembolism, vasculuitis)
  • glomerular diseases
  • acute tubular necrosis (toxins, rhabdo)
  • acute interstitial nephritis (drugs, infection, systemic dz)
  • tubular obstruction (casts, crystals)
79
Q

AKI - post-renal

A
  • tumor
  • papillary necrosis
  • calculi
  • bladder outlet obs
  • BPH
80
Q

AKI - most common intrinsic

A

acute tubular necrosis (ischemia, toxins)

drugs are MCC

81
Q

AKI - tx

A

Optimize hemodynamic
Fix volume if needed
Remove toxin/stone
RRT if needed

82
Q

AKI - staging (urine output)

A
  1. <0.5ml/kg/hr >6h
  2. same for >12h
  3. anuria for 12h OR
    <0.3 ml/kg/h for 24h
83
Q

4 factors modulating K excretion

A
  • GFR (minor unless <20)
  • Mcorticoid (ENaC resorb sodium, push K to lumen)
  • Dietary intake; eat more, pee more
  • TALH (Na/K/Cl) - can be inhibited by loops, losing K
84
Q

Role of diet in potassium d/o.. what happens when

  • starved + refeed
  • eat too much K when you have kidney disease
A

anorexic then refeed = hypokalemic leading to arrthymia, death

lots of potassium + CKD = hyperkalemia

85
Q

Hyperkalemia complications

A

Bradycardia
Weakness
Conspitation

86
Q

Hypokalemia complications

A
SVT + vtach
Weakness, flaccidity
Poor GI motility 
Low RBF, GFR
Rhabdomyolysis
Nephrogenic DI
^ ammonia
87
Q

Tx severe hypokalemia

A

KCl po or IV + magnesium

88
Q

Potassium d/o first step

A
Transcellular shift
vs
Renal ability to excrete K
vs 
Spurious
89
Q

CKD epi/risk factors

A

Older age, M=F
minorities, low income, unedu
DM, HTN, autoimmune dz
hx UTI, stones

90
Q

CKD staging

A
Dependent on GFR + level of albuminuria 
GFR > 90 normal
GFR 30-89 moderate
GFR 15-29 severe
GFR <15 dialysis

Asymptomatic til <30 ml/min

91
Q

CKD - how to slow progression to ESRD

A
treat BP
reduce hyperfiltration via RAAS inhibition
low protein diet
statin, ACEI to reduce proteinuria
avoid NSAID
92
Q

CKD - how does it progress

A
hyperfiltration
proteinuria
hypotension/HTN
nephrotoxins
- NSAIDS
- herbal supplements
- aminoglycosides
- IV contrast
93
Q

Cardiovascular dz + CKD connection

A

anemia: low oxygen to heart
high renin: high BP
high HCy (can’t excrete): CAD
high phosphate: CAD

94
Q

CKD complications

A
high or low volume
"" Na
"" Ka
hypocalcemia
hyperphosphatemia
hypermagnesemia
metabolic acidosis>alkalosis
95
Q

How does CKD cause anemia?

A
  • Decreased EPO production
  • Shortened RBC 1/2 life
  • gastrin/mucosa disturbances
  • platelet dysfunction
96
Q

CKD - mineral disturbances?

  • what are they?
  • prevention?
A

Serum

  • low bicarb (dec. acid excretion)
  • low K
  • low Ca
  • high phosphate (dec GFR)
  • high Mg (dec GFR)