Kidney Week 2 Flashcards
Anion Gap definition
normal= 12+/-4
anion gap= cations - anions»_space; [Na=] -([Cl-]+[HCO3-])
Sources of H+ gain and loss
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
How are non-volatile acids buffered?
- HALF amount of fixed acids buffered with HCO3-
- so they always REDUCE the HCO3-
- other half by intracelluar buffers (organic stuff, proteins, etc)
What acids/bases does the GI system contribute?
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
How is CO2 (volatile) acid buffered?
- CO2 buffered almost entirely by intracellular buffers
* hemoglobin
Name extracellular and intracellular buffers
Extracellular= HCO3- Intracellular = hemoglobin, protein, organic PO4, bone
name the 2 rules of compensation
1) opposite system
2) same direction
Describe respiratory compensation
- 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+
Describe renal compensation
- 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
Reabsorbing bicarb in Proximal tubule: describe process and changes w/ pH
- 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
Describe renal response to acidic conditions
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
describe step by step approach to acid/base disorder
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
Respiratory Alkalosis (hypocapnia) : etiology/ s/s / labs/ mgmt
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
Respiratory Alkalosis causes:
hypoxemia, pulmonary disease, stimulation of medullary respiratory center, mechanical venatlation. OR: CHAMPS: CNS disease Hypoxia Anxiety Mechanical ventalation Progesterone (prego, cirrhosis) Salycilates/ sepsis
Respiratory Acidosis (hypocapnia): etiology/ s/s/ labs/ mgmt
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
Respiratory acidosis causes:
acute respiratory failure, COPD, opiate overdose, upper airway obstruction, inhibition of medullary center, any disorder that prevents chest wall/ respiratory muscle movement
Describe and discuss the following conditions associated with a normal anion-gap acidosis
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
causes of normal anion gap acidosis –acronymn
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)
causes of Anion Gap acidosis– acronymn
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
Causes of Metabolic Alkalosis
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)
Metabolic Acidosis-
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
Metabolic Alkalosis
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=
most common kind of metabolic alkalosis
saline responsive (volume loss)
lactic acidosis : etiology, s/s/, labs/ mgmt
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
DKA– etiology, s/s, labs, mgmt
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
Alcoholic ketoacidosis
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
Pyelonephritis
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
Urethritis
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
Cystitis/ UTI
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
Interstitial Cystitis
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
Significant Bacteriurea vs insignificant
significant = >10*5 colony forming units
asymtomatic – no symptoms, only treat before procedures, pregnancy
Normal lab values: pH, PCO2, PO2, bicarb
pH= 7.35-7.45 PCO2= 35-45 PO2= 80-100 bicarb= 22-26
Sulfa drugs/ Bactrim – MOA, when to choose it,
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
Quinolones– Cipro, norfloxacin
MOA: DNA synthesis inhibitor DON't USE -- arrthymias -- pregnant women --
Penicillins
MOA:
Nitrofurantoin
**FIRST LINE therapy for uncomplicated Cystitis
MOA: Ribosomal protein inhibitor
DON’T use
Macro UA – pH
- 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,
Macro UA – specific gravity
definition– how much stuff is in urine
lower = dilute, higher = concentrated
normal = 1.005– 1.030
Macro UA – Protein
normal = 0-trace
2+ requires follow up
3+ = 95% renal deficiency
Macro UA – Hemoglobin
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
Macro UA – color
cherry red -- myoglobin normal color-- straw color, yellow, amber darker -- more concentrated clarity -- should be clear turbid -- means solutes in uring
Macro – glucose
normal – none
can’t dx diabetes
serum glucose >160 – will spill into urine
possible to have trace in pregnancy
Macro UA – Keytones
normal– none
Dx – diabetes, starvation
fat metabolism
Macro UA – bilirubin
normal -- none dx-- liver disease, biliary obstruction unconjugated = INdirect = INsoluble water= free floating conjugated = direct = water soluble dipstick measures conjugated/direct
Macro UA – Urobilinogen
normal = small amounts none = obstruction of bile ducts elevated = hemolytic anemias,
Macro UA – Leukocyte esterase
normal = none
presence means infx or inflammation
if nitrites are also present = gram neg bacteria
5-15 WBC per high powered field if leukocytes
Macro UA – nitrites
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
Micro UA – leukocytes
> 5/ high powered field = pyuria
WBC can vary d/t state of hydration
must be tested w/in 1 hr of collection
Micro UA – erythrocytes
> 3 RBC/ high power field = hematuria
whole RBC = lower GU
dysmorphic = upper GU
most likely cause in men = BPH
Micro UA – epithelial cells
squamous cells = 2 contamination,
transitional cells can indicate cancer
studded epithelial cells == bacteria vaginosis
what is #1 presenting symptom of bladder cancer?
what is biggest risk factor for bladder cancer?
painless hematuria
smoking
how is bacteria reported from lab?
rare, few, moderate, many, TNTC
Micro UA – bacteria
several/few per high powered field indicated infx
gram stain, culture?
Micro UA – yeast
candida albicans most common species for yeast infx
Colony counts don’t correlate to infx
Micro UA – casts
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
Micro UA – crystals
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
cystourethroscopy– cysto – cystoscopy
puts camera up urethra, bladder
low risk
low infx rate, very safe
staging for cervical cancer, verify placement of suprapubic catheters
renal biopsy
only for dx of systemic, diffuse renal dx
lots of blood and pain
renal ultrasound
hydronephrosis – best dx method
doppler – renal perfusion
maybe stone location
most common place for kidney stone to land?
worst place for kidney stone in terms of treatment?
distal ureter
lower pole
urinary anion gap
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
RTA
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
