Nephrology 43-46, 55-57 Flashcards
1
Q
Urinary tract infection pathogens
A
E. Coli
other gram-negatives (Klebsiella, Proteus, Enterobacter, Citrobacter)
gram-positives
(staphylococcus saprophyticus, enterococcus, staphylococcus aureus)
adenovirus,
fungi
2
Q
Classification of UTI
A
depending on level of infection
- Upper urinary tract infection: pyelonephritis
- Lower urinary tract infection: cystitis
- Uncomplicated:
*limited to the lower tract
*age >2
*no underlying medical problems or anatomical malformations
*caused by typical microorganism - Complicated: if any of above is false
3
Q
risk factors for UTI
A
- Lack of circumcision
- Boys younger than 1 year, girls older than 4 years
- Female gender (more connected to how bacteria attach to female urethra than its absolute length)
- Urinary obstruction, bladder/bowel dysfunction, vesicles-ureteral reflux, bladder catheterization ◦
Sexual activity
4
Q
symptoms of UTI children below 2
A
fever (may be the only symptom),
irritability,
poor feeding,
weight gain
5
Q
symptoms of UTI children above 2
A
fever,
dysuria,
urgency,
increased frequency,
incontinence,
hematuria, ◦
abdominal pain,
suprapubic tenderness,
costovertebral angle tenderness
6
Q
UTI diagnosis
A
- clinical presentation
- urinary sample (dipstick, culture, microscopic)
- inflammatory marker
- imaging
-US
-voiding cystourethrogram
-renal scintigraphy (DMSA nuclear medicine: renal scarring) - Generally not mandatory during first and uncomplicated UTI
7
Q
UTI - urine sample diagnosis
A
- Children who are not potty-trained —> catherization, suprapubic aspiration, (sterile collection bag - not recommended)
- Dipstick
- Urine culture ‣
- Microscopic evaluation ‣
- Bacteriuria: bacteria in urine ‣
- Pyuria: white blood cells in urine (not specific for UTI though, consider appendicitis, GAS
infection, Kawasaki disease
8
Q
US indication in uti
A
1ST CHOICE
< 2 years with febrile UTI
recurrent febrile UT
no response to AB
family history of renal or urological disease
9
Q
Voiding cystourethrogram indication
A
Best for testing VUR
Indications:
2+ febrile UTIs
abnormalities on US
uncommon pathogen
poor growth
10
Q
complication of UTI
A
Upper UTI —>
renal scarring,
hypertension,
end-stage kidney disease
11
Q
treatment of UTI
A
- Early antibiotic treatment may prevent renal damage ◦
- Empiric therapy - can be initiated immediately after urine collection with a high probability of UTI
- E. Coli antibiotic choice: 3rd generation cephalosporins (cefuroxime, cefotaxime, ceftriaxone)
50% are resistant against amoxicillin and ampicillin
Increasing resistance toward 1st generation cephalosporins
Aminoglycosides can also be given: gentamicin, amikacin
12
Q
- E. Coli antibiotic choice UTI
A
3rd generation cephalosporins (cefuroxime, cefotaxime, ceftriaxone)
50% are resistant against amoxicillin and ampicillin
Aminoglycosides can also be given: gentamicin, amikacin
13
Q
Considerations in neonates with UTI:
A
- Blood culture should also be obtained for diagnosis (but relative high risk of an urosepsis)
- US is recommended to identify structural abnormalities
- Empiric treatment: ampicillin + gentamicin 10-14 days, then amoxicillin until radiologic evaluation is done
14
Q
empiric tratment of neonates with UTI
A
- Empiric treatment: ampicillin + gentamicin 10-14 days, then amoxicillin until radiologic evaluation is done
15
Q
Urinary tract malformations incidence
A
Incidence: 2-3%
16
Q
Urinary tract malformations are associated with
A
Associated with other organ anomalies: VATER/VACTERL
* Vertebral anomalies
* Anal atresia
* Cardiovascular anomalies
* Tracheoesophageal fistula,
* Esophageal atresia
* Renal and/or radial anomalies
* Limb defects
17
Q
Urinary tract malformations suspicion signs
A
hypospadias
3rd nipple
neck cysts + fistulas
coloboma
aniridia
preauricular fibroma
18
Q
Kidney malformations
A
- Renal agenesis
- Renal hypoplasia
- Horseshoe kidney
- Kidney dysplasia
- Multicystic dysplastic kidney
- Ectopic kidney
- Hydronephrosis
- Duplex kidney
19
Q
Renal agenesis
A
Kidneys fail to develop
**Bilateral agenesis **
—> part of Potter syndrome, not compatible with life since oligohydramnion
(decreased amniotic fluid)
—> no normal lung development
—> respiratory failure
-
Unilateral agenesis
—> intact kidney is compensating and becomes larger
20
Q
Renal hypoplasia
A
- Kidney size and number of nephrons are smaller than average —> reduced performance
- Bilateral hypoplasia
—> hypertension (from increased peripheral resistance)
—> chronic RF - Unilateral hypoplasia
—> asymptomatic, sometimes hypertension
21
Q
treatment of renal hypoplasia
A
Treatment:
removal of HTN
+ recurrent pyelonephritis
+ performance < 10%
+ + other kidney is intact
22
Q
Horseshoe kidney
A
- Kidneys are connected
- VACTERL-association
- Important to look for:
*males —> gonadal dysgenesis,
females —> Turner syndrome
Treatment not needed but can be associated with hydronephrosis
23
Q
what can horseshoes kidney be associated with
A
VACTREL
HYDRONEPHROSIS
24
Q
Kidney dysplasia
A
Histological structure shows a significant dysplasia/abnormal structure
- Bilateral dysplasia: decreased renal function, chronic kidney disease
- Unilateral dysplasia: asymptomatic
25
US finding of kidney dysplasia
Ultrasound findings:
increased echogenicity
cortex and medulla cannot be differentiated,
small cortical cysts
26
Multicystic dysplastic kidney
* Intact renal parenchyma does not develop, ureter atresia, kidney is completely dysfunctional
* Bilateral: incompatible with life
27
diagnosis of multicystic dysplastic kidney
intrauterine or neonatal US or physical examination
28
prognosis of Multicystic dysplastic kidney
* In 40% diseased kidney is absorbed
* In 25% intact kidney undergoes ectopia, hypoplasia, VUR, hydronephrosis
* Rarely malignant transformation (Wilms tumor) —> surgical removal should be considered
29
Ectopic kidney
* Kidney migration does not occur by the 8th gestational week —> stays in pelvis (may cross)
Bilateral ectopic kidneys: frequent pyelonephritis
Unilateral ectopic kidney: VUR
It’s size and performance is usually smaller than that of healthy kidney
30
Hydronephrosis
* Dilation of renal cavity
* Most common intrauterine ultrasound abnormality
31
Etiology hydronephrosis
stenosis of the urinary tract
VUR
ureteral or bladder dysfunction
32
pathomechanism of hydronephrosis
elevated renal cavity pressure
—> renal pelvis and calyces dilate + renal
parenchyma may also become thinner
33
prognostic factors for hydronephrosis
renal parenchyma thickness and reflectivity, renal performance
In mild cases —> regress spontaneously in the first months following birth
34
complication of hydronephrosis
Complication: pyelonephritis
35
Duplex kidney
* Separate kidney parts have a separate drainage system
* Usually unilateral
*The separate ureters of the pyelonephritis merge —> common entrance to bladder ‣
*The separate ureters of two pyelonephritis do not merge —> separate entrances to bladder (or one has an entrance to other organ like vagina/cervix/vestibule)
* Associated with ureterocele
36
duplex kidney associated with
Associated with ureterocele
37
symptoms of duplex kidney
usually
* asymptomatic
* dysplasia
* hydronephrosis,
* VUR
* persistent and therapy-resistant UTIs
38
treatment of duplex kidney
depends on severity, if needed
—> ◦
neoimplantation
heminephrecto-ureterectomia
39
Cystic kidney diseases
* Monogenic cystic kidney disease
*AR Polycystic kidney disease
*AD polycystic kidney disease
* acquired forms (very rare)
40
Monogenic cystic kidney disease inheritance
More than 70 gene mutations are known
Inheritance:
autosomal recessive OR autosomal dominant
41
monogenic cystic kidney disease is Responsible for what % of chronic renal failure in childhood
10-20%
42
Monogenic cystic kidney disease
Progressive disease which spends on the severity of the gene involved and the mutation
—> number and size of cysts increase with age
43
Autosomal recessive polycystic kidney disease (ARPKD)
Monogenic cystic kidney disease
* PKHD1 gene mutation
* The kidneys are enlarged and the tubule dilation affects the collecting ducts
44
what is more common ARPKD) or ADPKD
ADPKD
1:400- 1000
45
US finding of ARPKD
hyperreflectivity, tiny cysts
46
US finding of ADPKD
kidneys are not hyperreflective
47
complications of ARPKD
* Severe form of intrauterine oligohydramnios —> pulmonary hypoplasia
—> neonatal respiratory distress
* Early HTN
* 50% develop end-stage renal disease by 18 years
* Urinary sepsis
48
what is ARPKD associated with
liver fibrosis
49
Autosomal dominant polycystic kidney disease (ADPKD) gene mutation
PKD1 (85%) gene mutation —> more severe form
OR
PKD2 (15%) gene mutation
50
Autosomal recessive polycystic kidney disease (ARPKD) gene mutation
PKHD1 gene mutation
51
complications of Autosomal dominant polycystic kidney disease (ADPKD)
Might develop end-stage renal disease by 50-60 years (in PKD1 type)
52
what is Autosomal dominant polycystic kidney disease (ADPKD) associated with
liver cysts,
berry aneurysms in brain
53
Ureter developmental disorders
* Pyelouretral junction (PUJ) stenosis (extrinsic VS instrinsic)
* Ureter-vesicular junction (UVJ) stenosis
* Ureterocele
* Vesico-ureteral reflux (VUR)
54
forms of PUJ stenosis
Forms: intrinsic or extrinsic (vessel strangulation)
◦
Mostly unilateral
55
diagnosis of PUJ stenosis
* US
(cavity dilation, site of stenosis,
renal parenchyma thickness)
* Isotope test of kidney function
56
complication of PUJ Stenosis
hydronephrosis
57
treatment of PUJ stenosis
depends on severity,
nephrectomy if needed
58
treatment of PUJ stenosis
depends on severity,
nephrectomy if needed
59
Ureter-vesicular junction (UVJ) stenosis diagnosis
* US —> dilated kidney calyces/pyelon/ureter
* Isotope test of kidney function
60
Ureter-vesicular junction (UVJ) stenosis complications
ureteral dilation,
hydronephrosis
61
Ureter-vesicular junction (UVJ) stenosis treatment
depends on severity,
ureter neoimplantation if needed
62
Ureterocele
Cystic dilation of the end of the ureter
80% girls
63
Ureterocele symptoms
large cele covering the inner opening of the urethra —>
dysuria
64
Ureterocele diagnosis
US,
cystoscopy
65
treatment ureterocele
* indiction (during cystoscopy) / resection with
neoimplantation/nehroureterectomy
66
Vesico-ureteral reflux (VUR)
UVJ dysfunction —> urine flows back from the bladder to the ureter/renal pelvis
67
Vesico-ureteral reflux (VUR) classification
* Primary: intramural ureter is short/has abnormal junction
* Secondary:
*Unilateral: other diseases at the UVJ (diverticulum, cele, duplication)
*Bilateral: increased pressure in the bladder (obstruction)
68
symptoms of VUR
recurrent upper UTI
—> scarring
—> reflux nephropathy (renal failure)
69
diagnosis VUR
US
70
treatment of VUR
* usually heels spontaneously
* antimicrobial prophylaxis
* surgery
71
Bladder extrophy
* Complex, severe developmental disorder
* Abdominal wall defect in lower abdominal region —> bladder is herniating outside of skin
72
Bladder extrophy diagnosis and treatment
Diagnosis: after birth
Treatment: surgery
73
Bladder diverticulum
Bladder mucosa protrudes btw muscle fibers
Can be caused by subvesicular obstruction
74
Bladder diverticulum symptoms
UTI
obstruction
VUR, stones
75
diagnosis bladder diverticulum
* US
* MCU (Micturating Cysto-Urethrogram )
* exclusion of primary cause (obstruction)
76
treatment bladder diverticulum
resection, treat primary cause
77
bladder congenital malformations
* bladder extrophy
* bladder diverticulum
* urachus persistens
78
Urachus persistens
* The embryonic passage connecting the tip of the bladder to the navel is not absorbed/closed —> remnant structure
* Caused by subvesicular obstruction with high pressure in the bladder
79
symptoms urachus persistens
moist navel (urine)
soft tissue inflammation
80
diagnosis urachus persistens
US
fistulography
MCU
81
treatment urachus persistens
surgery
82
urethra developmental malformation
* Posterior urethral valve
* Hypospadius
* Epispadius
83
Posterior urethral valve what is it
At the distal border of the prostatic urethra, the mucosa membrane/folds remain to form a urinary barrier
84
Posterior urethral valve etiology
* Absorption disorder of the caudal end of the Wolffian duct
* Persistence of the cloacal membrane
85
Posterior urethral valve symptoms
UTI,
increased pressure of the
urinary tract
86
diagnosis posterior urethral valve
* US
(Keyhole sign:
large bladder beneath the dilated prostatic urethra)
* MCU (micturating cystoscopy-urethrogram)
87
treatment posterior urethral valve
* detention of bladder
* extirpation of valve
* renal failure
—> kidney transplantation
(common cause of kidney transplant in children)
88
Keyhole sign:
large bladder beneath the dilated prostatic urethra
in posterior urethral valve
89
Hypospadius
what is it , treatment?
Urethra does not terminate at the apex of the glans but more ventral and proximal
Treatment: reconstruction
90
Epispadius
Open urethral plate in the dorsal side of the penis/in the recess btw the fissured clitoris, which did not form a tube
In severe cases —> cause complete incontinence
Treatment: reconstruction
91
Glomerulonephritis defined as
Hematuria ◦
Oliguria ◦
Edema ◦
Hypertension ◦
Variable proteinuria
92
Glomerulonephritis etiology
* Post-infectious: most common (streptococci)
* Others: less common
*MPGN (membranoproliferative glomerulonephritis)
*IgA nephropathy
*Systemic lupus erythematosus
*Subacute bacterial endocarditis
*Shunt nephritis
93
Post-infectious etiologies of glomerulonephritis
* Bacterial:
*streptococci (most common)
*staphylococci
*mycoplasma
*salmonella
* Viral: herpesvirus (EBV, varicella, CMV)
* Fungi: candida, aspergillus ‣
* Parasites: toxoplasma, malaria, schistosomiasis
94
diagnosis of glomerulonephritis
* Urine
—> urinalysis (hematuria +/- proteinuria), microscopy (RBC casts)
* Throat swab
* Blood
—> CBC, autoantibodies, complement proteins (lupus), albumin
* Renal US
* Chest x-ray —> if fluid overload is suspected
95
lifethreatening complications of glomerulonephritis which have to be treated
Treat life-threatening complications: A.
* Hyperkalemia
* Hypertension
* Acidosis
* Seizures
* Hypocalcemia
96
treatment of glomerulonephritis
Supportive treatment/monitoring:
* Fluid balance: weigh daily, restricted salt diet, if oliguria
—> fluid restriction to insensible
losses, urinary output, furosemide if overload
* HTN:
*alpha-blockers
*calcium channel blocker
*treat fluid overload, do NOT use ACEi
worsen renal function)
* Penicillin: if signs of infection, since most common cause is post-streptococcal GN
97
Nephrosis syndrome defined as
* Proteinuria (urinary protein to creatinine ratio >200 mg/mmol)
* Hypoalbuminemia (albumin < 25 g/l)
* Edema
* Hyperlipidemia
98
etiology of nephrotic syndrome
* Primary: congenital, infantile
* Secondary:
*minimal change disease (85%)
*focal segmental glomerulosclerosis
*membranoproliferative glomerulonephritis,
*membranous glomerulonephritis
99
clinical features of nephrotic syndrome
* Edema (initially preorbital —> become generalized with pitting edema), most noticeable in morning on rising
* foamy urine
* hypercoagulable
* HTN sometimes
100
diagnosis of nephrotic syndrome
* Urinalysis: protein +++
* Microscopy: hematuria/casts (suggests other than MCD)
* Culture
* Protein:creatinine ratio
* Serum albumin
* C3/C4 (if decreased not MCD)
* Lipids
* Immunoglobulins ◦
* Renal biopsy ◦
Indicated if steroids are not helping
101
what tests suggest that the pathology is NOT minimal change disease (mcd)
* Microscopy: hematuria/casts (suggests other than MCD)
* C3/C4 (if decreased not MCD)
102
treatment of nephrotic syndrome
Patients should be admitted, especially if its their first episode or if concerns about complications
* Fluid restriction + prevention of hypovolemia
* Trial of oral steroid therapy to induce remission (MCD responds to steroids)
* Prophylaxis against bacterial infection (esp pneumococci) c.
* Immunosuppressants (cyclophosphamide, levamisole, ciclosporine A)
103
MCD does it respond to steroids
Trial of oral steroid therapy to induce remission
(MCD responds to steroids)
104
what immunosupressant is used in nephrotic syndrome
(cyclophosphamide, levamisole, ciclosporine A)
105
what bacteria do we use for prophylaxis against in nephrotic syndrome
esp pneumococci
106
complication of nephrotic syndrome
* Infection: due to decreased IgG levels
* Thrombosis: hypercoagulable state ◦
* Hypovolemia:
*suggested by development of oliguria
*and/or presence of low BP
*abdominal pain
* Acute renal failure
107
Enuresis define
Repeated involuntary elimination of urine that is inappropriate for developmental age (bed-wetting)
108
enuresis epidemiology
affects 5-10% of 5-year olds, decreases with age
109
enuresis risk factors
positive family history
psychosocial stressors
psychiatric disorders (eg ADHD, autism)
110
enuresis diagnostic criteria
1) occurs 2x/week > 3 months
2) patients developmental age must be 5 or more
3) symptoms NOT caused by medication/other medical condition
111
types of enuresis
* Nocturnal (mostly boys)
* or diurnal (mostly girls)
* Primary (patient never achieved continence)
* or secondary (after patient achieved continence)
112
treatment of enuresis
* First line:
*fluid restriction at night
*behavioral training
*timed voiding
*parent management training,
*psychoeducation
Second line:
* desmopressin
* behavioral training with an enuresis alarm
113
what causes must be ruled out before enuresis diagnosis
**Organic causes **must be ruled out first:
UTIs
urinary tract abnormalities
renal disorders
114
Polyuria vs polydipsia
polyuria: excessive urinary output
Polydipsia: excessive thirst/drinking
115
etiology of polyuria and polydipsia
Diabetes mellitus
Diabetes insipidus
Primary polydipsia
116
diabetes mellitus how does it lead to polyuria, polydipsia
Chronic hyperglycemia cause excess excretion of glucose —> osmotically active glucose
particles draws water with them —>↑urination —>↑fluid loss —>↑thirst
117
Diabetes insipidus- how does it lead to polydipsia, polyuria
Kidneys are not able to concentrate urine —>↑urination —>↑fluid loss —>↑thirst
118
diabetes insipidus types
Central DI: insufficient levels of circulating antidiuretic hormone (ADH)
Nephrogenic DI: defective renal ADH receptors
119
Primary polydipsia - pathology
Excessive oral intake of fluid in the absence of physiological stimulus to drink
—>↑fluid volume
—>↑urination —>↑fluid loss —>↑thirst
May include
psychogenic polydipsia secondary to psychoses or other mental disorders,
or non- psychogenic varieties
120
diagnosis of polyuria, polydipsia
* check blood glucose —> if high: diabetes mellitus, if normal...
* Fluid restriction
—> if improvement: primary polydipsia,
if no improvement...
* Administer desmopressin (ADH analogue) —> if improvement: CDI (central DI)
if no improvement: NDI (Nephrogenic DI)
121
desmopressin (ADH analogue) test used in?
if improvement: CDI (central DI)
if no improvement: NDI (Nephrogenic DI)
122
if fluid restriction caused improvement in polyuria, polydipsia what can be etiology behind it
Fluid restriction —> if improvement: primary polydipsia
123
Edema
Abnormal accumulation of interstitial fluid
124
classification of edema
* Peripheral (edema of extremities)
* Central (edema in organs and body cavities)
* Pitting edema (residual indentation left by pressure on the site of the swelling)
* Non-pitting edema (no residual indentation left by pressure on the site of swelling)
125
Pitting edema etiologies
* Fluid retention
*heart failure
*kidney failure
*DVT
*portal thrombosis
*AV fistula
*SIADH
*pregnancy
*pharmaceutical effect (eg calcium channel blockers)
* Protein deficiency —> decreased oncotic pressure
*Liver failure
*kidney failure
*malnutrition
*enteropathy
* Increased capillary permeability
*inflammation
*sepsis
*burns
*anaphylaxis
*vasculitis
*hereditary angioedema (HAE)
*SJS
*trauma
126
Non-pitting edema etiologies
* **Lymphedema **(lymphatic obstruction —> reduced fluid clearance due to compromised lymphatic vessels or lymph nodes)
*Lymphatic obstruction:
-primary (eg in Turner syndrome)
-or secondary (eg in tumors, operations, radiation therapy)
*** Myxedema** (accumulation of glycosaminoglycans within dermis —> bind water)
*Hypothyroidism (generalized) *hyperthyroidism (typically pretibial)
127
diagnosis of edema
* Medical history
* Physical examination (application of firm pressure to the edematous tissue for 5 seconds )
* Specific tests for underlying disorder
Treatment: management of underlying condition
128
Decrease in ventilation
hypoventilation
—> increase CO2
—> shift equation towards right
—> respiratory acidosis
129
Increase in ventilation
hyperventilation
—> decrease CO2
—> shift equation towards left
—> respiratory alkalosis
CO2 + H2O —> H2CO3 —> H(+) + HCO3(-)
130
Respiratory acidosis values
pH < 7,35
pCO2 > 45 mmHg
131
etiology of respiratory acidosis
respiratory failure (type II = hypercapnic)
132
symptoms of respiratory acidosis
* increased sympathetic activity
* decreased inotropy (critical pH: 7,2 —> decreased affinity of catecholamine receptors)
* arterial vasodilation (critical pH)
* decreased oxy-Hgb binding
* hyperkalemia
* insulin resistance
* free radical formation
* emesis
* hyperventilation
* coma
133
therapy of Respiratory acidosis
Therapy of underlying disease
Mechanical ventilation
134
Respiratory alkalosis *
values
pH > 7,45
pCO2 < 35 mmHg
135
etiology of respiratory alkalosis
* caused by primary or secondary hyperventilation (hypoxic respiratory failure, salicylate intoxication)
* early sepsis
* hepatic failure
* artificial hyperventilation
136
symptoms of respiratory alkalosis
decreased cerebral or coronary blood flow,
neuromuscular excitability
137
therapy of respiratory alkalosis
Therapy of underlying disease ‣
Increasing of the dead space
138
Metabolic acidosis value
pH < 7,35
HCO3- < 21 mmol/l
BE < -3 mmol/l
139
Anion gap:
Na + K] - [Cl + HCO3]
normally 10-15 mmol/l
140
etiology of elevated anion gap metabolic acidosis
increased acids:
* lactic acidosis
* ketoacidosis
* renal failure
exogenous acids too ethylene glycol
141
Non anion gap MA etiology
* loss of HCO3: renal tubular acidosis, gastrointestinal acidosis
* iatrogenic acidosis (admin of Cl), diarrhea
142
symptoms of metabolic acidosis
* increased sympathetic activity
* decreased inotropy (critical pH —> decreased affinity of catecholamine receptors)
* arterial vasodilation (critical pH)
* decreased oxy-Hgb binding (shift curve to right)
* hyperkalemia
* insulin resistance
* free radical formation
* emesis
* hyperventilation
143
metabolic acidosis shift o2 binding curve to
decreased oxy-Hgb binding
(shift curve to right)
144
therapy of metabolic acidosis
* Therapy of underlying disease
* Maximizing respiratory compensation
* Vitamin B1
* Renal replacement therapy
* NaHCO3 (mmol) = -BE x 0,3 x kg
*Only if patient is in need of extra HCO3 *
* Tromethamine :Base to give instead of HCO3
145
NaHCO3 (mmol) equation for calculating amount to be given
NaHCO3 (mmol) = -BE x 0,3 x kg
Only if patient is in need of extra HCO3
146
Metabolic alkalosis value
pH> 7,45
HCO3 > 26 mmol/l
BE > 3 mmol/l
147
etiology of metabolic alkalosis
* Chloride responsive:
vomiting (loose acidic fluids in stomach),
diuretics
* Chloride unresponsive:
mineralocorticoid excess (increase H+ secretion),
Cushing’s syndrome
* Hypokalemia (increase H+ secretion), massive blood transfusion
Na-lactate/Ringers solution (lactate is metabolized in liver —> HCO3 is produced)
148
symptoms of metabolic alkalosis
* hypoventilation
* respiratory depression
* neuromuscular excitability
* seizures
* hypokalemia
* altered coronary blood flow
* increased oxy-Hgb binding,
* vasoconstriction
* decreased cerebral blood flow
149
therapy of metabolic alkalosis- chloride responsive alkalosis
NaCL
150
therapy of metabolic alkalosis- chloride unresponsive alkalosis
HCL
KCL
151
therapy of metabolic alkalosis- MC excess
spironolactone
