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Kidney Week 1 > Kidney Week 2 > Flashcards

Kidney Week 2 Flashcards

1
Q

Anion Gap definition

A

normal= 12+/-4

anion gap= cations - anions&raquo_space; [Na=] -([Cl-]+[HCO3-])

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2
Q

Sources of H+ gain and loss

A 
GAIN=
* CO2 ventalation
*non-volatile acids from protein metabolism
* loss of HCO3- in GI
* loss of HCO3 in urine
LOSS=
*metabolism of anions (that use H+)
*in urine
*in vomit
*Hyperventalation
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3
Q

How are non-volatile acids buffered?

A
  • HALF amount of fixed acids buffered with HCO3-
  • so they always REDUCE the HCO3-
  • other half by intracelluar buffers (organic stuff, proteins, etc)
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4
Q

What acids/bases does the GI system contribute?

A

GI system

  • metabolism of proteins and organic molecules makes fixed acids
  • stomach makes H+ (in form of HCL, stomach acid)
  • lower bowel makes HCO3-, excretes in feces
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5
Q

How is CO2 (volatile) acid buffered?

A
  • CO2 buffered almost entirely by intracellular buffers

* hemoglobin

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6
Q

Name extracellular and intracellular buffers

A 
Extracellular= HCO3-
Intracellular = hemoglobin, protein, organic PO4, bone
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7
Q

name the 2 rules of compensation

A

1) opposite system

2) same direction

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8
Q

Describe respiratory compensation

A
  • happens quickly in minutes
  • change in [H+] sensed by chemoreceptors in medulla, carotid/ aortic
  • reflexively adjust ventilation
  • to breath off acidic CO2
  • or slow breaths to retain CO2 and H+
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9
Q

Describe renal compensation

A
  • regulate plasma HCO3-
  • makes NEW bicarb to: 1)compensate respiratory acidosis, 2) correct metabolic acidosis
  • reabsorbs bicarb 1)keeps all filtered bicarb in normal to acidic conditions, 2) does not reabsorb bicarb in alkalosis, just dumps it
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10
Q

Reabsorbing bicarb in Proximal tubule: describe process and changes w/ pH

A
  • normal or acidic conditions= all bicarb reabsorbed
    *alkaline conditions = bicarb is dumped
    Process=
  • in proximal epi cell, H20+CO2 combine, HCO3- diffuses into interstium, then blood. The H+ secreted to lumen, where it combines with HCO3-, makes H20/CO2 which can be brought back into cell. Cycle repeats
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11
Q

Describe renal response to acidic conditions

A

1) make new bicarb
2) excrete H+
PROCESS to make new bicarb
*2 ways to make new bicarb
*distal tubule – H2O/CO2 – HCO3- diffuses into blood, H+ combines with organic base filtrate and is excreted
*proximal tubule – glumamine - broken into HCO3 (which goes into blood) and NH4+, exhanced for Na+ and then excreted

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12
Q

describe step by step approach to acid/base disorder

A

1) check for internal validity
2) determine pH– acidic or alkaline
3) determine primary cause
4) calculate anion gap
5) is compensation appropriate? mixed disorder?
6) does patient’s exam match analysis

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13
Q

Respiratory Alkalosis (hypocapnia) : etiology/ s/s / labs/ mgmt

A 
ETIOLOGY= hyperventilation
S/S= dizziness, perioral numbness, parasthesias, tenany
LABS= ↑pH ↓HCO3 ↓↓PaCO2
COMPENSATION= kidneys dump HCO3-
Expected Comp:
Acute: △HCO3 = 0.2 x △Pco2
HCO3 cannot go
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14
Q

Respiratory Alkalosis causes:

A 
hypoxemia, pulmonary disease, stimulation of medullary respiratory center, mechanical venatlation. OR:
CHAMPS: 
CNS disease
Hypoxia
Anxiety
Mechanical ventalation
Progesterone (prego, cirrhosis)
Salycilates/ sepsis
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15
Q

Respiratory Acidosis (hypocapnia): etiology/ s/s/ labs/ mgmt

A 
ETIOLOGY= hypoventalation
S/S= somnolence, altered LOC, asterixis, myoclunus (acute)
↑ cerebral blood flow, cerebrospinal fluid pressure, and intracranial pressure; papilledema and pseudotumor cerebri (chronic)
LABs= ↓pH ↑HCO3 ↑↑PaCO2
If chronic: ↓CL-
COMPENSATION= kidney make more bicarb
Expected Comp: 
Acute: △HCO3 = 0.2 x △pCO2
HCO3 cannot go > 30 mmHg
Chronic: △HCO3 = 0.4 x △pCO2
HCO3 cannot go > 45 mmHg
MGMT= treat underlying condition
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16
Q

Respiratory acidosis causes:

A

acute respiratory failure, COPD, opiate overdose, upper airway obstruction, inhibition of medullary center, any disorder that prevents chest wall/ respiratory muscle movement

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17
Q

Describe and discuss the following conditions associated with a normal anion-gap acidosis

A

1) gastrointestinal HCO3- loss
- - GI tract secretes bicarb at multiple sites. Small bowel and pancreatic secretions contain large amounts of bicarb
- - massive diarrhea or pancreatic drainage can result in bicarb loss.
- -This will result in hyperchloremia because bicarb is secreted in exchange for Cll- by countertransport.
- - Volume loss results in the kidneys holding onto Cl-.
- -Tx: Stop cause of diarrhea; administration of alkali (HCO3- or citrate) to correct acidosis

2) renal tubular acidosis (RTA)
- - defined as hyperchloremic acidosis with a normal anion gap and normal GFR in the absence of diarrhea.
- - due to an inability to excrete H+ or inappropriate reabsorption of HCO3-.
- -3 major types distinguished by the clinical setting, urinary pH, urinary anion gap, and serum K+ level.

Classic distal RTA (type I) - Deficiency of H+ secretion in the collecting tubule - so despite acidosis, urinary pH cannot be acidified. Urinary excretion of NH4+Cl- is decreased, and urinary anion gap is positive. K+ excretion increases due to less competition for H+ and due to hyperaldosteronism in response to renal salt wasting.
Causes: consequence of paraproteinemias, autoimmune disease, and drugs and toxins such as amphotericin
Tx: Alkali (either as bicarbonate or citrate) 1-3 mEq/kg/d

Proximal RTA (type II) - selective defect in the PCT’s ability to reabsorb filtered HCO3- . This will overwhelm the DCT’s ability to absorb HCO3- initially causing bicarbonaturia. Distal delivery will decline as plasma HCO3- levels drop to a point where the DCT can keep up - approx 15-18 mEq/L - bicarbonaturia will resolve and the urine will become acidic. Increase in HCO3- flow to DCT will increase K+secretion resulting in hypokalemia.
Causes: Carbonic anhydrase inhibitors; Fanconi syndrome; multiple myeloma; nephrotoxic drugs
Tx: Alkali 10-15 mEq/kg/day; Thiazides - induce volume contraction and enhance proximal HCO3- reabsorption. Also K+ supp.

Hyporeninemic hypoaldosteronemic RTA (type IV) -
-The most common RTA.
-The defect is aldosterone deficiency or antagonism, which impairs distal nephron Na+ reabsorption and K+ and H+ excretion. Renal salt wasting and hyperkalemia are frequently present.
Causes: Diabetic nephropathy, tubulointerstitial renal disease, hypertensive nephrosclerosis, and AIDS.
Note: ACE inhibitors, spironolactone, and NSAIDs can exacerbate the hyperkalemia
Tx: Dietary potassium restriction; Fludrocortisone; sometimes oral alkali substitution

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18
Q

causes of normal anion gap acidosis –acronymn

A

H - hyperalimentation (increased acid load from over feeding of amino acids)
A - Acetazolamide, Amphotericin (bicarb loss in urine)
R - RTA (bicarb loss in urine)
D - Diarrhea (bicarb loss in stool)
U - Ureteral diversion (bicarb loss in stool)
P - Pancreatic fistula (bicarb loss in stool)
S - Spironolactone (bicarb loss in urine)

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19
Q

causes of Anion Gap acidosis– acronymn

A

G Glycols (ethylene & propylene)
O Oxoproline (metabolite of acetaminophen)
L L-lactate (anaerobic respiration)
D D-lactate (comes from bacteria, such as in the case of proliferation of bacteria in your gut post gastric bypass)
M Methanol
A Aspirin
R Renal Failure
K Ketoacidosis (diabetic, alcoholic, starvation)

Special Cases: Clues to Intoxications Causing High AG Acidosis
• Aspirin ‐ high salicylate level; also primary respiratory alkalosis
• Methanol ‐ blindness ‐ optic papillitis
• Ethylene Glycol ‐ renal failure ‐ calcium oxalate crystals
• Additionally a number of intoxicants cause a high osmolar gap

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20
Q

Causes of Metabolic Alkalosis

A 
CLEVER PD 
Contraction (renal)
Licorice (renal)
Endo: Conn’s, Cushing’s, Bartter’s (renal)
Vomiting (GI)
Excess Alkali (GI)
Refeeding alkalosis (GI)
Post‐hypercapnia (renal)
Diuretics (renal)
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21
Q

Metabolic Acidosis-

A

ETIOLOGY– depends on anion gap (see those cards)
S/S: depends on underlying cause
LABS: ↓pH ↓↓HCO3 ↓pCO2, sometimes hyperkalemia
COMPENSATION: respiratory hyperventatlation
Expected comp:
pCO2 = last 2 digits of pH
△pCO2 = 1.2 x △HCO3
pCO2 cannot go

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22
Q

Metabolic Alkalosis

A

ETIOLOGY: requires both excess HCO-/loss of H+, AND impaired HCO3- dumping, so kidney dysfunction
CAUSES: (loss of H+, retention of HCO3-, contraction/ volume depletion) AND (decreased GFR, increased HCO3 resporbtion, increased aldosterone activity)
S/S= Hypotension, orthostasis Concomitant hypokalemia may cause weakness and hyporeflexia. Tetany and neuromuscular irritability occur rarely.
LABS= hypokalemia maybe, urine
MGMT=

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23
Q

most common kind of metabolic alkalosis

A

saline responsive (volume loss)

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24
Q

lactic acidosis : etiology, s/s/, labs/ mgmt

A

ETIOLOGY= too much lactic acid, tissue hypoxia (more common), poor removal ability from bad liver, kidneys
–in cardiac and septic patients – lack of perfusion
S/S= hyperventilation, can have normal BP, acyanotic
LABS= Anion gap >15, Low plasma bicarb 5mmol/L, NEGATIVE ketones
MGMT= Ensure adequate oxygenation and tissue perfusion. **Alkalinization with IV sodium bicarb to keep pH >7.2 is controversial

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25
Q

DKA– etiology, s/s, labs, mgmt

A 
ETIOLOGY= poorly controlled diabetes, can be initial presentation of diabetes.  hyperglycemia+metabolic acidosis+high anion gap
S/S= hyperglycemia, starts w/ polyuria, polydysia, fatigue, n/v.  progresses to descreased LOC, tachycardia, hypotension, hyperventalation
LABS= Hyperglycemia >250mg/dL (13.9mmol/L), Blood pH
26
Q

Alcoholic ketoacidosis

A

ETIOLOGY= alcoholism
3 types
1) ketoacidosis
2) lactic acidosis -excessive alcohol -too much lactic acid
3) hyperchloremic acidosis – too much bicarb loss in urine
metabolic acidosis – from vomiting and dehydration
often mixed w/ respiratory alkalosis

27
Q

Pyelonephritis

A

WHAT IS IT?
– infectious inflammation of kidney parenchyma, pelvis
–usually Gram NEG bacteria: e.coli, proteus, klebsiella, enterobacter
–usually ascending spread from lower GU, can be hematogenous though (gram +)
RISK FACTORS=
- previous UTI, especially untreated
–geriatric population
S/S
– fever, CVA tenderness, tachycardia, flank pain, n/v, irritative voiding symptoms
LABS
– culture for bacteria
–increased WBC w/ left shift
– pyuria, WBC casts, bactiuria, sometimes hematuria
COMPLICATION
can progress to hydronephrosis, sepsis
MGMT
-inpatient= empiric IV Ampicillin+aminoglycoside
-outpaitnet = quinolone
adjust when culture comes back
treat obstruction if applicable

28
Q

Urethritis

A 
WHAT IS IT?  inflammation of ureter
CAUSE?  usually STI: gonnohrea, clamydia, or Reactive arthritis
S/S= urethral discharge, painful urination, pruritis
LABS= 
--first catch UA-- leukocytes
--swab 
--NAAT-- to test for pathogen
MGMT?  
-gonoccocal= ceftriaxone,
-clamydia= zpak or doxy
-treat both partners
29
Q

Cystitis/ UTI

A

WHAT IS IT? infection of bladder, UTI.
usually females, rare in males.
usually gram NEG bacteria– E.Coli most common
CAUSES?
catheters, genetics, sexual activity
S/S? irritative voiding symptoms, suprapubic pain, NO systemic toxicity, +/- hematuria
LABS
–UA clean catch – bactermeia, pyuria, +/- hematuria, get culture
MGMT= Short term Abx course: 1 dose or 1-9 days therapy. Cephalexin, nitrofurantoin, and fluoroquinolones. Bactrim not ideal because of bacterial resistance.
Hot sitz baths or urinary analgesics (phenAZOpyridine) may provide symptomatic relief

30
Q

Interstitial Cystitis

A

WHAT IS IT? painful bladder syndrome.
CAUSES? unknown. dx of exclusion. F>M.
S/S?
pain w/ full bladder, goes away when you pee, urgency, frequency
LABS? UA, culture, cytology – all negative, hydrodistention
MGMT? symptom mgmt via
-hydrodistention
- acupuncture
-amitriptyline, nefedipine, elmiron

31
Q

Significant Bacteriurea vs insignificant

A

significant = >10*5 colony forming units

asymtomatic – no symptoms, only treat before procedures, pregnancy

32
Q

Normal lab values: pH, PCO2, PO2, bicarb

A 
pH= 7.35-7.45
PCO2=  35-45
PO2= 80-100
bicarb= 22-26
33
Q

Sulfa drugs/ Bactrim – MOA, when to choose it,

A 
MOA:  folic acid synthesis inhibitor
**FIRST LINE Therapy for uncomplicated cystitis
DON'T USE: 
--in pregnant women, nursing
--empirically d/t resistance
-- known sulfa drug allergies
-- infants
34
Q

Quinolones– Cipro, norfloxacin

A 
MOA:  DNA synthesis inhibitor
DON't USE
-- arrthymias
-- pregnant women
--
35
Q

Penicillins

A

MOA:

36
Q

Nitrofurantoin

A

**FIRST LINE therapy for uncomplicated Cystitis
MOA: Ribosomal protein inhibitor
DON’T use

37
Q

Macro UA – pH

A
    • avg 5- 6.5
    • range can be 4.5 – 8
    • > 8 means bacteria
    • proteus, pseudomonas UTI >7
    • uric acid stones 7.5
  • -acid UTI – Ecoli,
38
Q

Macro UA – specific gravity

A

definition– how much stuff is in urine
lower = dilute, higher = concentrated
normal = 1.005– 1.030

39
Q

Macro UA – Protein

A

normal = 0-trace
2+ requires follow up
3+ = 95% renal deficiency

40
Q

Macro UA – Hemoglobin

A

normal = none
can be myoglobin or beets
macro can’t tell if there are whole red blood cells or broken
whole RBC will be “stipled” in appearance

41
Q

Macro UA – color

A 
cherry red -- myoglobin
normal color-- straw color, yellow, amber
darker -- more concentrated
clarity -- should be clear
turbid -- means solutes in uring
42
Q

Macro – glucose

A

normal – none
can’t dx diabetes
serum glucose >160 – will spill into urine
possible to have trace in pregnancy

43
Q

Macro UA – Keytones

A

normal– none
Dx – diabetes, starvation
fat metabolism

44
Q

Macro UA – bilirubin

A 
normal -- none
dx-- liver disease, biliary obstruction
unconjugated = INdirect = INsoluble water= free floating
conjugated = direct = water soluble
dipstick measures conjugated/direct
45
Q

Macro UA – Urobilinogen

A 
normal = small amounts
none = obstruction of bile ducts
elevated = hemolytic anemias,
46
Q

Macro UA – Leukocyte esterase

A

normal = none
presence means infx or inflammation
if nitrites are also present = gram neg bacteria
5-15 WBC per high powered field if leukocytes

47
Q

Macro UA – nitrites

A 
normal= none 
if present -- means gram neg bacteria
urine must be in bladder for 4 hours --false negative
get first catch
vitamin c -- false negative
phenazoperidine -- false positive
48
Q

Micro UA – leukocytes

A

> 5/ high powered field = pyuria
WBC can vary d/t state of hydration
must be tested w/in 1 hr of collection

49
Q

Micro UA – erythrocytes

A

> 3 RBC/ high power field = hematuria
whole RBC = lower GU
dysmorphic = upper GU
most likely cause in men = BPH

50
Q

Micro UA – epithelial cells

A

squamous cells = 2 contamination,
transitional cells can indicate cancer
studded epithelial cells == bacteria vaginosis

51
Q

what is #1 presenting symptom of bladder cancer?

what is biggest risk factor for bladder cancer?

A

painless hematuria

smoking

52
Q

how is bacteria reported from lab?

A

rare, few, moderate, many, TNTC

53
Q

Micro UA – bacteria

A

several/few per high powered field indicated infx

gram stain, culture?

54
Q

Micro UA – yeast

A

candida albicans most common species for yeast infx

Colony counts don’t correlate to infx

55
Q

Micro UA – casts

A

casts formed in tubules, indicates renal disease. always look on low power first

  • Hyaline casts: can be normal or not, mucoproteins, jelly stuff
  • RBC: glomerular nephritis
  • WBC: Infx, (pyelo), inflammation of kidney, (SLE, interstitial nephritis)
  • Epithelial: papillary necrosis, ATN
  • Granular: epithelia becomes granular: not intact cells: brown muddy casts: ATN, renal disease, vigourous exercise
  • Waxy: granular and hyaline degrade and becomes waxy, brittle, irregular shaped.
  • broad casts– the worst – waxy becomes broad – means renal failure
56
Q

Micro UA – crystals

A

these particular crystals are usually precipitated in acidic urine

  • Calcium oxalate crystals are the more commonly found chemical constituents in renal stones, and less commonly identified are urate and cystine
  • presence of uric acid and oxalate: can be seen in normal patients as well as stone formers
  • cystine crystals (characteristic hexagonal benzene ring shape) are seen in pts with cystinuria and are pathologic
57
Q

cystourethroscopy– cysto – cystoscopy

A

puts camera up urethra, bladder
low risk
low infx rate, very safe
staging for cervical cancer, verify placement of suprapubic catheters

58
Q

renal biopsy

A

only for dx of systemic, diffuse renal dx

lots of blood and pain

59
Q

renal ultrasound

A

hydronephrosis – best dx method
doppler – renal perfusion
maybe stone location

60
Q

most common place for kidney stone to land?

worst place for kidney stone in terms of treatment?

A

distal ureter

lower pole

61
Q

urinary anion gap

A

good for differentiating between 2 types of non-anion gap metabolic acidosis (RTA vs gastro bicarb loss)
no urinary anion gap = GI bicarb loss
urinary anion gap = RTA

62
Q

RTA

A

renal tubular acidosis (RTA)

    • defined as hyperchloremic acidosis with a normal anion gap and normal GFR in the absence of diarrhea.
    • due to an inability to excrete H+ or inappropriate reabsorption of HCO3-.
  • -3 major types distinguished by the clinical setting, urinary pH, urinary anion gap, and serum K+ level.
    • hypoaldosterone type 4 most common type

Kidney Week 1 (3 decks)

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