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Parm > Nephrology 43-46, 55-57 > Flashcards

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

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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
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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
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4
Q

symptoms of UTI children below 2

A

fever (may be the only symptom),
irritability,
poor feeding,
weight gain

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5
Q

symptoms of UTI children above 2

A

fever,
dysuria,
urgency,
increased frequency,
incontinence,
hematuria, ◦
abdominal pain,
suprapubic tenderness,
costovertebral angle tenderness

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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
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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
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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

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9
Q

Voiding cystourethrogram indication

A

Best for testing VUR

Indications:
2+ febrile UTIs
abnormalities on US
uncommon pathogen
poor growth

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10
Q

complication of UTI

A

Upper UTI —>
renal scarring,
hypertension,
end-stage kidney disease

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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

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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

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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
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14
Q

empiric tratment of neonates with UTI

A
  • Empiric treatment: ampicillin + gentamicin 10-14 days, then amoxicillin until radiologic evaluation is done
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15
Q

Urinary tract malformations incidence

A

Incidence: 2-3%

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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

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17
Q

Urinary tract malformations suspicion signs

A

hypospadias
3rd nipple
neck cysts + fistulas
coloboma
aniridia
preauricular fibroma

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18
Q

Kidney malformations

A
  • Renal agenesis
  • Renal hypoplasia
  • Horseshoe kidney
  • Kidney dysplasia
  • Multicystic dysplastic kidney
  • Ectopic kidney
  • Hydronephrosis
  • Duplex kidney
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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
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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
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21
Q

treatment of renal hypoplasia

A

Treatment:
removal of HTN
+ recurrent pyelonephritis
+ performance < 10%
+ + other kidney is intact

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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

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23
Q

what can horseshoes kidney be associated with

A

VACTREL
HYDRONEPHROSIS

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24
Q

Kidney dysplasia

A

Histological structure shows a significant dysplasia/abnormal structure

  • Bilateral dysplasia: decreased renal function, chronic kidney disease
  • Unilateral dysplasia: asymptomatic
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25
Q

US finding of kidney dysplasia

A

Ultrasound findings:
increased echogenicity
cortex and medulla cannot be differentiated,
small cortical cysts

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26
Q

Multicystic dysplastic kidney

A
  • Intact renal parenchyma does not develop, ureter atresia, kidney is completely dysfunctional
  • Bilateral: incompatible with life
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27
Q

diagnosis of multicystic dysplastic kidney

A

intrauterine or neonatal US or physical examination

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28
Q

prognosis of Multicystic dysplastic kidney

A
  • 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
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29
Q

Ectopic kidney

A
  • 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

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30
Q

Hydronephrosis

A
  • Dilation of renal cavity
  • Most common intrauterine ultrasound abnormality
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31
Q

Etiology hydronephrosis

A

stenosis of the urinary tract
VUR
ureteral or bladder dysfunction

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32
Q

pathomechanism of hydronephrosis

A

elevated renal cavity pressure
—> renal pelvis and calyces dilate + renal
parenchyma may also become thinner

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33
Q

prognostic factors for hydronephrosis

A

renal parenchyma thickness and reflectivity, renal performance

In mild cases —> regress spontaneously in the first months following birth

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34
Q

complication of hydronephrosis

A

Complication: pyelonephritis

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35
Q

Duplex kidney

A
  • 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
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36
Q

duplex kidney associated with

A

Associated with ureterocele

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37
Q

symptoms of duplex kidney

A

usually
* asymptomatic
* dysplasia
* hydronephrosis,
* VUR
* persistent and therapy-resistant UTIs

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38
Q

treatment of duplex kidney

A

depends on severity, if needed
—> ◦
neoimplantation
heminephrecto-ureterectomia

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39
Q

Cystic kidney diseases

A
  • Monogenic cystic kidney disease
    *AR Polycystic kidney disease
    *AD polycystic kidney disease
  • acquired forms (very rare)
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40
Q

Monogenic cystic kidney disease inheritance

A

More than 70 gene mutations are known

Inheritance:
autosomal recessive OR autosomal dominant

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41
Q

monogenic cystic kidney disease is Responsible for what % of chronic renal failure in childhood

A

10-20%

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42
Q

Monogenic cystic kidney disease

A

Progressive disease which spends on the severity of the gene involved and the mutation
—> number and size of cysts increase with age

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43
Q

Autosomal recessive polycystic kidney disease (ARPKD)

A

Monogenic cystic kidney disease
* PKHD1 gene mutation

  • The kidneys are enlarged and the tubule dilation affects the collecting ducts
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44
Q

what is more common ARPKD) or ADPKD

A

ADPKD
1:400- 1000

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45
Q

US finding of ARPKD

A

hyperreflectivity, tiny cysts

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46
Q

US finding of ADPKD

A

kidneys are not hyperreflective

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47
Q

complications of ARPKD

A
  • Severe form of intrauterine oligohydramnios —> pulmonary hypoplasia
    —> neonatal respiratory distress
  • Early HTN
  • 50% develop end-stage renal disease by 18 years
  • Urinary sepsis
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48
Q

what is ARPKD associated with

A

liver fibrosis

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49
Q

Autosomal dominant polycystic kidney disease (ADPKD) gene mutation

A

PKD1 (85%) gene mutation —> more severe form

OR
PKD2 (15%) gene mutation

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50
Q

Autosomal recessive polycystic kidney disease (ARPKD) gene mutation

A

PKHD1 gene mutation

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51
Q

complications of Autosomal dominant polycystic kidney disease (ADPKD)

A

Might develop end-stage renal disease by 50-60 years (in PKD1 type)

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52
Q

what is Autosomal dominant polycystic kidney disease (ADPKD) associated with

A

liver cysts,
berry aneurysms in brain

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53
Q

Ureter developmental disorders

A
  • Pyelouretral junction (PUJ) stenosis (extrinsic VS instrinsic)
  • Ureter-vesicular junction (UVJ) stenosis
  • Ureterocele
  • Vesico-ureteral reflux (VUR)
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54
Q

forms of PUJ stenosis

A

Forms: intrinsic or extrinsic (vessel strangulation)

◦
Mostly unilateral

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55
Q

diagnosis of PUJ stenosis

A
  • US
    (cavity dilation, site of stenosis,
    renal parenchyma thickness)
  • Isotope test of kidney function
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56
Q

complication of PUJ Stenosis

A

hydronephrosis

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57
Q

treatment of PUJ stenosis

A

depends on severity,
nephrectomy if needed

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58
Q

treatment of PUJ stenosis

A

depends on severity,
nephrectomy if needed

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59
Q

Ureter-vesicular junction (UVJ) stenosis diagnosis

A
  • US —> dilated kidney calyces/pyelon/ureter
  • Isotope test of kidney function
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60
Q

Ureter-vesicular junction (UVJ) stenosis complications

A

ureteral dilation,
hydronephrosis

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61
Q

Ureter-vesicular junction (UVJ) stenosis treatment

A

depends on severity,
ureter neoimplantation if needed

62
Q

Ureterocele

A

Cystic dilation of the end of the ureter
80% girls

63
Q

Ureterocele symptoms

A

large cele covering the inner opening of the urethra —>
dysuria

64
Q

Ureterocele diagnosis

A

US,
cystoscopy

65
Q

treatment ureterocele

A
  • indiction (during cystoscopy) / resection with
    neoimplantation/nehroureterectomy
66
Q

Vesico-ureteral reflux (VUR)

A

UVJ dysfunction —> urine flows back from the bladder to the ureter/renal pelvis

67
Q

Vesico-ureteral reflux (VUR) classification

A
  • 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
Q

symptoms of VUR

A

recurrent upper UTI
—> scarring
—> reflux nephropathy (renal failure)

69
Q

diagnosis VUR

A

US

70
Q

treatment of VUR

A
  • usually heels spontaneously
  • antimicrobial prophylaxis
  • surgery
71
Q

Bladder extrophy

A
  • Complex, severe developmental disorder
  • Abdominal wall defect in lower abdominal region —> bladder is herniating outside of skin
72
Q

Bladder extrophy diagnosis and treatment

A

Diagnosis: after birth

Treatment: surgery

73
Q

Bladder diverticulum

A

Bladder mucosa protrudes btw muscle fibers

Can be caused by subvesicular obstruction

74
Q

Bladder diverticulum symptoms

A

UTI
obstruction
VUR, stones

75
Q

diagnosis bladder diverticulum

A
  • US
  • MCU (Micturating Cysto-Urethrogram )
  • exclusion of primary cause (obstruction)
76
Q

treatment bladder diverticulum

A

resection, treat primary cause

77
Q

bladder congenital malformations

A
  • bladder extrophy
  • bladder diverticulum
  • urachus persistens
78
Q

Urachus persistens

A
  • 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
Q

symptoms urachus persistens

A

moist navel (urine)
soft tissue inflammation

80
Q

diagnosis urachus persistens

A

US
fistulography
MCU

81
Q

treatment urachus persistens

A

surgery

82
Q

urethra developmental malformation

A
  • Posterior urethral valve
  • Hypospadius
  • Epispadius
83
Q

Posterior urethral valve what is it

A

At the distal border of the prostatic urethra, the mucosa membrane/folds remain to form a urinary barrier

84
Q

Posterior urethral valve etiology

A
  • Absorption disorder of the caudal end of the Wolffian duct
  • Persistence of the cloacal membrane
85
Q

Posterior urethral valve symptoms

A

UTI,
increased pressure of the
urinary tract

86
Q

diagnosis posterior urethral valve

A
  • US
    (Keyhole sign:
    large bladder beneath the dilated prostatic urethra)
  • MCU (micturating cystoscopy-urethrogram)
87
Q

treatment posterior urethral valve

A
  • detention of bladder
  • extirpation of valve
  • renal failure
    —> kidney transplantation
    (common cause of kidney transplant in children)
88
Q

Keyhole sign:

A

large bladder beneath the dilated prostatic urethra

in posterior urethral valve

89
Q

Hypospadius
what is it , treatment?

A

Urethra does not terminate at the apex of the glans but more ventral and proximal

Treatment: reconstruction

90
Q

Epispadius

A

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
Q

Glomerulonephritis defined as

A

Hematuria ◦
Oliguria ◦
Edema ◦
Hypertension ◦
Variable proteinuria

92
Q

Glomerulonephritis etiology

A
  • Post-infectious: most common (streptococci)
  • Others: less common
    *MPGN (membranoproliferative glomerulonephritis)
    *IgA nephropathy
    *Systemic lupus erythematosus
    *Subacute bacterial endocarditis
    *Shunt nephritis
93
Q

Post-infectious etiologies of glomerulonephritis

A
  • Bacterial:
    *streptococci (most common)
    *staphylococci
    *mycoplasma
    *salmonella
  • Viral: herpesvirus (EBV, varicella, CMV)
  • Fungi: candida, aspergillus ‣
  • Parasites: toxoplasma, malaria, schistosomiasis
94
Q

diagnosis of glomerulonephritis

A
  • 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
Q

lifethreatening complications of glomerulonephritis which have to be treated

A

Treat life-threatening complications: A.
* Hyperkalemia
* Hypertension
* Acidosis
* Seizures
* Hypocalcemia

96
Q

treatment of glomerulonephritis

A

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
Q

Nephrosis syndrome defined as

A
  • Proteinuria (urinary protein to creatinine ratio >200 mg/mmol)
  • Hypoalbuminemia (albumin < 25 g/l)
  • Edema
  • Hyperlipidemia
98
Q

etiology of nephrotic syndrome

A
  • Primary: congenital, infantile
  • Secondary:
    *minimal change disease (85%)
    *focal segmental glomerulosclerosis
    *membranoproliferative glomerulonephritis,
    *membranous glomerulonephritis
99
Q

clinical features of nephrotic syndrome

A
  • Edema (initially preorbital —> become generalized with pitting edema), most noticeable in morning on rising
  • foamy urine
  • hypercoagulable
  • HTN sometimes
100
Q

diagnosis of nephrotic syndrome

A
  • 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
Q

what tests suggest that the pathology is NOT minimal change disease (mcd)

A
  • Microscopy: hematuria/casts (suggests other than MCD)
  • C3/C4 (if decreased not MCD)
102
Q

treatment of nephrotic syndrome

A

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
Q

MCD does it respond to steroids

A

Trial of oral steroid therapy to induce remission
(MCD responds to steroids)

104
Q

what immunosupressant is used in nephrotic syndrome

A

(cyclophosphamide, levamisole, ciclosporine A)

105
Q

what bacteria do we use for prophylaxis against in nephrotic syndrome

A

esp pneumococci

106
Q

complication of nephrotic syndrome

A
  • 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
Q

Enuresis define

A

Repeated involuntary elimination of urine that is inappropriate for developmental age (bed-wetting)

108
Q

enuresis epidemiology

A

affects 5-10% of 5-year olds, decreases with age

109
Q

enuresis risk factors

A

positive family history
psychosocial stressors
psychiatric disorders (eg ADHD, autism)

110
Q

enuresis diagnostic criteria

A

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
Q

types of enuresis

A
  • Nocturnal (mostly boys)
  • or diurnal (mostly girls)
  • Primary (patient never achieved continence)
  • or secondary (after patient achieved continence)
112
Q

treatment of enuresis

A
  • First line:
    *fluid restriction at night
    *behavioral training
    *timed voiding
    *parent management training,
    *psychoeducation

Second line:
* desmopressin
* behavioral training with an enuresis alarm

113
Q

what causes must be ruled out before enuresis diagnosis

A

**Organic causes **must be ruled out first:
UTIs
urinary tract abnormalities
renal disorders

114
Q

Polyuria vs polydipsia

A

polyuria: excessive urinary output

Polydipsia: excessive thirst/drinking

115
Q

etiology of polyuria and polydipsia

A

Diabetes mellitus
Diabetes insipidus
Primary polydipsia

116
Q

diabetes mellitus how does it lead to polyuria, polydipsia

A

Chronic hyperglycemia cause excess excretion of glucose —> osmotically active glucose
particles draws water with them —>↑urination —>↑fluid loss —>↑thirst

117
Q

Diabetes insipidus- how does it lead to polydipsia, polyuria

A

Kidneys are not able to concentrate urine —>↑urination —>↑fluid loss —>↑thirst

118
Q

diabetes insipidus types

A

Central DI: insufficient levels of circulating antidiuretic hormone (ADH)

Nephrogenic DI: defective renal ADH receptors

119
Q

Primary polydipsia - pathology

A

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
Q

diagnosis of polyuria, polydipsia

A
  • 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
Q

desmopressin (ADH analogue) test used in?

A

if improvement: CDI (central DI)

if no improvement: NDI (Nephrogenic DI)

122
Q

if fluid restriction caused improvement in polyuria, polydipsia what can be etiology behind it

A

Fluid restriction —> if improvement: primary polydipsia

123
Q

Edema

A

Abnormal accumulation of interstitial fluid

124
Q

classification of edema

A
  • 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
Q

Pitting edema etiologies

A
  • 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
Q

Non-pitting edema etiologies

A
  • **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
Q

diagnosis of edema

A
  • 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
Q

Decrease in ventilation

A

hypoventilation
—> increase CO2
—> shift equation towards right
—> respiratory acidosis

129
Q

Increase in ventilation

A

hyperventilation
—> decrease CO2
—> shift equation towards left
—> respiratory alkalosis

CO2 + H2O —> H2CO3 —> H(+) + HCO3(-)

130
Q

Respiratory acidosis values

A

pH < 7,35
pCO2 > 45 mmHg

131
Q

etiology of respiratory acidosis

A

respiratory failure (type II = hypercapnic)

132
Q

symptoms of respiratory acidosis

A
  • 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
Q

therapy of Respiratory acidosis

A

Therapy of underlying disease

Mechanical ventilation

134
Q

Respiratory alkalosis *
values

A

pH > 7,45
pCO2 < 35 mmHg

135
Q

etiology of respiratory alkalosis

A
  • caused by primary or secondary hyperventilation (hypoxic respiratory failure, salicylate intoxication)
  • early sepsis
  • hepatic failure
  • artificial hyperventilation
136
Q

symptoms of respiratory alkalosis

A

decreased cerebral or coronary blood flow,
neuromuscular excitability

137
Q

therapy of respiratory alkalosis

A

Therapy of underlying disease ‣
Increasing of the dead space

138
Q

Metabolic acidosis value

A

pH < 7,35
HCO3- < 21 mmol/l
BE < -3 mmol/l

139
Q

Anion gap:

A

Na + K] - [Cl + HCO3]

normally 10-15 mmol/l

140
Q

etiology of elevated anion gap metabolic acidosis

A

increased acids:
* lactic acidosis
* ketoacidosis
* renal failure

exogenous acids too ethylene glycol

141
Q

Non anion gap MA etiology

A
  • loss of HCO3: renal tubular acidosis, gastrointestinal acidosis
  • iatrogenic acidosis (admin of Cl), diarrhea
142
Q

symptoms of metabolic acidosis

A
  • 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
Q

metabolic acidosis shift o2 binding curve to

A

decreased oxy-Hgb binding
(shift curve to right)

144
Q

therapy of metabolic acidosis

A
  • 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
Q

NaHCO3 (mmol) equation for calculating amount to be given

A

NaHCO3 (mmol) = -BE x 0,3 x kg

Only if patient is in need of extra HCO3

146
Q

Metabolic alkalosis value

A

pH> 7,45
HCO3 > 26 mmol/l
BE > 3 mmol/l

147
Q

etiology of metabolic alkalosis

A
  • 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
Q

symptoms of metabolic alkalosis

A
  • hypoventilation
  • respiratory depression
  • neuromuscular excitability
  • seizures
  • hypokalemia
  • altered coronary blood flow
  • increased oxy-Hgb binding,
  • vasoconstriction
  • decreased cerebral blood flow
149
Q

therapy of metabolic alkalosis- chloride responsive alkalosis

A

NaCL

150
Q

therapy of metabolic alkalosis- chloride unresponsive alkalosis

A

HCL
KCL

151
Q

therapy of metabolic alkalosis- MC excess

A

spironolactone

Parm (15 decks)

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