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Primary Care 3 > Renal > Flashcards

Renal Flashcards

1
Q

AKI

A

major side effect of other medical procedures, diverse spectrum of molecular, biochemical and structural processes that characterize the AKI syndrome

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2
Q

The RIFLE Classification of AKI

A

Risk for renal dysfunction –Injury to kidney –Failure of kidney function –Loss of kidney function –End stage renal disease

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3
Q

These classes represent degrees of injury

A

R = Risk for renal dysfunction I = Injury to the kidney F = Failure of kidney function

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4
Q

These classes represent outcome measures

A

L = Loss of kidney function, E = End stage renal disease (ESRD)

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5
Q

R = Risk for renal dysfunction

A

Increase in serum creatinine ≥ 1.5× baseline, Decrease in GFR ≥ 25%, UO < 0.5 mL/kg/h for 6 h

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6
Q

I = Injury to the kidney

A

Increase in serum creatinine ≥ 2.0× baseline, Decrease in GFR ≥ 50% < 0.5 mL/kg/h for 12 h

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7
Q

F = Failure of kidney function

A

Increase in serum creatinine ≥ 3.0× baseline OR serum creatinine ≥ 4.0mg/dL in the setting of an acute rise ≥ 0.5 mg/dL, Decrease in GFR ≥ 75%, < 0.3 mL/kg/h for 24 h or anuria for 12 h

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8
Q

L = Loss of kidney function

A

Persistent failure > 4 weeks

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9
Q

E = End stage renal disease (ESRD)

A

Persistent failure > 3 months

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10
Q

AKIN criteria

A

• To further refine the definition of AKI • Proposed a modified version of the RIFLE classification, known as the AKIN• An abrupt (within 48 h) reduction in kidney function as measured by an absolute increase in serum creatinine ≥ 0.3 mg/dL, • A percentage increase in serum creatinine ≥ 50%, • Or documented oliguria (

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11
Q

AKIN with RIFLE

A

AKIN replaces the three levels of severity R, I and F with stages 1, 2 and 3.

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12
Q

Besides Establishing the Early Diagnosis Biomarkers are needed to determine:

A
  1. Location of injury
  2. Duration of AKI
  3. AKI subtypes
  4. AKI etiologies
  5. Differentiate from other forms of acute kidney disease
  6. Risk stratification and prognostication
  7. Defining course of AKI
  8. Monitoring interventions
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13
Q

Biomarkers also used for

A

Also- desperately needed for use as surrogate endpoints in clinical trials evaluating potential therapeutics for AKI

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14
Q

validation

A

This linking of the surrogate endpoint to the clinical endpoint is referred to as validation and is an essential step in the biomarker discovery process

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15
Q

the most important AKI biomarkers remain

A

those that are clinically applicable and can lead to early diagnosis and treatment of AKI

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16
Q

prevalence of CKD in the general population

A

10-13% A complex disease that often affects multiple organ systems and often coexists with numerous associated conditions, such as cardiovascular disease, diabetes mellitus, lupus, & chronic inflammation

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17
Q

The ‘gold standard’ measurement for CKD

A

is the ‘true’ glomerular filtration rate (GFR) as tracked by 24-h urine isotope clearance, Method is quite expensive and not always practical in the clinical
setting

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18
Q

A commonly used clinical surrogate for nuclear GFR

A

serum creatinine clearance, the accuracy of serum creatinine is greatly affected by a number of patient dependent and -independent variables, Serum creatinine may fall to one-third of its normal level in advanced kidney disease, unrelated to its renal clearance, Serial 24-h creatinine measurements fail to determine risk progression in approximately 20% of CKD patients

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19
Q

CKD Definition

A

The presence of kidney damage or a glomerular filtration rate less than 60 mL/min/1.73 for 3 months or greater, regardless of cause However, significant increases in cardiovascular disease risk occur at
more subtle loss of kidney function (75) so it needs to be caught earlier

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20
Q

AKI definition

A

abrupt reduction in GFR –> Acumulation of nitrogenous wastes, disturbed f+e balance, and abnormal volume status. Can be polyuric, nonliguric, anuric - can do AKIN or RIFLE. Increase in sCr by 50% in 7 days, or increase by 0.3 in 2 days or oliguria

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21
Q

AKD

A

Classifies patients who may need intervention to restore kidney function or reverse kidney damage. GFR < 60 for < 3 months

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22
Q

Proteinuria

A

Shown to directly represent kidney damage and higher levels of proteinuria correlate well with a more rapid progression of kidney disease, The earliest known marker of kidney damage in glomerular diseases, diabetes and hypertension, and is the most common marker of kidney damage in the adult population Early diagnosis would entail routinely screening asymptomatic patients

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23
Q

However, proteinuria has limitations

A

May occur long after the renal injury has occurred

• Not always present in many types of renal disease

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24
Q

Stages of chronic kidney disease

A

stages 1-5.

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25
Q

Stage 1

A

Kidney damage with normal or high GFR ≥ 90 mL, increased Cr x 1.5 or > 0.3mg/dL. UO <0.5ml/kg/h x 6 h

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26
Q

Stage 2

A

Kidney damage and mild decrease in GFR 60–89, increase Cr x 2, UO < 0,5ml/kg/h x 12 h

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27
Q

Stage 3

A

Moderate decrease in GFR 30–59, increased Cr x 3 or Cr > 4, U0 < 0.3 X 24 or anuria

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28
Q

Stage 4

A

Severe decrease in GFR 15-29

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29
Q

Stage 5

A

Kidney failure, <15 or dialysis

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30
Q

AKI is broadly defined

A

as a rapid deterioration in kidney function as manifested by a reduction in GFR Comprised of a variety of syndromes that are characterized by kidney
dysfunction that occurs over hours to days it can
occur in previously healthy individuals with completely normal kidneys The most commonly employed markers of AKI are serum creatinine and BUN, both of which rise in this setting

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31
Q

Azotemia

A

A buildup of nitrogenous wastes in blood

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32
Q

Uremia

A

A constellation of symptoms and signs of multipleorgan

dysfunction caused by retention of “uremic toxins” in the setting of renal failure

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33
Q

Oliguric

A

<400 mL/day

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34
Q

Oligoanuric

A

<100 mL/day

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35
Q

Polyuric

A

> 3L/day

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36
Q

Anuric

A

none

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37
Q

Does AKI need specific urine output

A

the presence of urine output does not exclude the possibility of AKI

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38
Q

Most common cause of AKI

A

Pre Renal

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39
Q

Does creatitine concentration reflect a true GFR?

A

Because changes in serum creatinine concentration do not precisely correlate with changes in GFR, it actually
is a poor reflection of true GFR because changes in Cr does not correlate with GFR — Why: Cr is cleared through GFR and tubular secretion, drugs can compete w tubular secretion, can be falsely elevated by lab techniques, muscle is the primary source of creatine which is coverted to Cr in the liver females w low muscle mass will have a decrease

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40
Q

Pre Renal AKI

A

A decrease in GFR that occurs as a consequence of reduced renal bloodflow

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41
Q

Intrinsic AKI

A

A decrease in GFR due to direct parenchymal injury in the kidney, subdivided by various compartments (vascular, glomerular, interstitial, tubular)

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42
Q

Post renal AKI

A

a decrease in GFR from obstruction to urine flow from the pelvis to the urethra

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43
Q

ARF

A

Acute renal failure, renal impairment is sustained.

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44
Q

RIFLE v AKIN

A

Rigle is based on serum Cr, AKIN is based on serum Cr, estimated GFR and UO

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45
Q

AKI functional criteria

A

Increase in SCr by 50% within 7 days OR increase in Cr by 0.3 within 2 days OR oliguria, no structural criteria

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46
Q

CKD functional criteria

A

GFR < 60 for > 3 months, structural criteria - kidney damage for > 3 months

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47
Q

AKD

A

AKI or GFR < 60 for < 3 months or a decrease in GFR by > 35% or an increase in SCr by > 50% for < 3 months. Structural critera - kidney damage for < 3 months

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48
Q

NKD

A

GFR > 60, Stable Cr, no damage

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49
Q

Lab tests to identify AKI

A

BUN, GFR/Cr most commonly used

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50
Q

A abrupt increase in Serum Cr usually reflects a decline in ____, signalling the development of AKI

A

GFR

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51
Q

BUN influenced by

A

level of underlying renal function, slow urine flow rates, GI bleeding, protein intake, catabolic states, protein malnutrition, cirrhosis

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52
Q

Prerenal causes of AKI

A

Volume depletion, n/v, diarrhea, overdiuresis, renal salt wasting, DI, sepsis, cardiomyopathy, cirrhosis (hepatorenal syndrome), RAS, ACE, ARB, NSAIDS,

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53
Q

Intrarenal causes of AKI

A

Glomerular diseases – glomerulonephritis. acute tubular necrosis, interstitial nephritis, infection

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54
Q

Post renal causes of AKI

A

Pelvic, ureteral obstructions, kidney stones, fungus balls omg what gross, blood clots, bladder obstruction, BPH, urethral obstruction

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55
Q

Blood tests that can diagnose prerenal specifically

A

FENa (<1%), FEUrea (<35%) , RFI (<1%) DDx use a urine microscopy

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56
Q

Intrinsic renal disease

A

Anatomic compartments that have been acutely injured – vasculature, glomerulus, tubules, insterstitium

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57
Q

Large vessel disease leading to AKI

A

from a thrombosis of RAS or thromboembolism from cardiac thrombus

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58
Q

UTI

A

bacterial infection of the urinary tract, urinary frequency and urgency from spontaneous bladder contraction due to irritation of the trigone

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59
Q

Urinary tract is usually sterile – why

A

Urinary tract is normally sterile due to the fact that bacteria moving upwards are regularly washed out by urination

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60
Q

Types of normal flora in the urinary tract

A

lactobacillus and staphylococcus

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61
Q

Generally speaking –UTI is infections in any components linked to the urinary tract:

A

kidney, bladder, prostate, urethra

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62
Q

To make a diagnosis of UTI you must

A

know and start with the site –and then the nature of the infection

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63
Q

Normal Mechanisms that Maintain Sterility of Urine

A

adequate urine volume, free flow from kidneys through the urinary meatus, complete bladder emptying, normal acidity of the urine, peristalsis of ureters and competent junction, Increased intravesicularpressure preventing reflux, In males, antibacterial effect of zinc in prostatic fluid

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64
Q

Risk Factors of UTI - aging

A

Aging – increased risk of DM, urinary stasis and impaired immune response. In females:

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65
Q

Risk factor of UTI – females

A

short urethra, having sexual intercourse, use of contraceptives that alter normal bacteria flora of vagina and perineal tissues; with age increased incidence of cystocele, rectocele (incomplete emptying)

66
Q

Risk factors of UTI – males

A

prostatic hypertrophy, bacterial prostatitis, anal intercourse

67
Q

Risk factors for UTI - UTI

A

tumor or calculi, strictures. Another risk: bladder innervation

68
Q

Lower UTI

A

Urethritis (often is sexually transmitted), prostatitis, cystitis (traditional UTI)

69
Q

Upper tract infection

A

pyelonephritis, perinephric abscess

70
Q

Bladder patho

A

smooth triangular region of the internal urinary bladderformed by the two ureteral orifices and the internal urethral orifice

71
Q

Trigone

A

Sensitive to expansion and once stretched to a certain degree, the urinary bladder signals the brain of its need to empty
The signals become stronger as the bladder

72
Q

The normal bladder is capable of clearing itself of organisms within X days of their introduction.

A

2 to 3

73
Q

Defense mechanisms of UTIs

A

(1) the elimination of bacteria by voiding
(2) the antibacterial properties of urine and its constituents
(3) the intrinsic mucosal bladder defense mechanisms
(4) an acid vaginal environment (female)
(5) prostatic secretions (male)

74
Q

Dysuria-

A

inflammation of the urethra

75
Q

Symptoms of Urinary Tract Infection

A

Dysuria, increased frequency, hematuria, fever – now systemic, N/V (pyelo) and increased vagal activity, flank pain (pyelo) from stretching of the capsule, pain with defacation from irritation of the trigone or an inflammed prostate

76
Q

Findings on Exam in UTI

A

Physical Exam:
CVA tenderness (pyelonephritis)
Urethral discharge (urethritis)
Tender prostate on DRE (prostatitis)

77
Q

UA Labs

A 
\+ leukocyte esterase
\+ nitrites
More likely gram-negative rods
\+ WBCs
\+ RBCs
78
Q

most valuable laboratory diagnostic test for UTI

A

Urinalysis for evaluation of pyuria

79
Q

This makes the diagnosis of UTI

A

presence of pyuria and bacteria

80
Q

Pyuria is present in almost all men with

A

acute cystitis or pyelonephritis

81
Q

The absence of X strongly suggests an alternative diagnosis or, in a patient with pyelonephritis, the presence of an obstructing lesion

A

Pyuria

82
Q

The gold standard to diagnose a UTI

A

Urine culture

83
Q

Positive Urine Culture

A

Bacterial colony >10^2CFU/mL (Symptomatic Patient)
•
Or, 10^5CFU/mL (Asymptomatic) + leukocytes

84
Q

Colony count is most beneficial in the

A

asymptomatic patient, or pregnant patient

85
Q

Most common pathogen for cystitis, prostatitis, pyelonephritis:

A

Escherichia coli-80%

Staphylococcus saprophyticus-15%The rest made up of Gram –negative rods

86
Q

Most common pathogen for urethritis

A

Chlamydia trachomatis, Neisseria Gonorrhea

87
Q

Lower Urinary Tract Infection -Cystitis

A

Most common symptomatic bladder infection

88
Q

Uncomplicated (Simple) cystitis

A

In healthy woman, with no signs of

systemic disease

89
Q

Complicated cystitis

A

In men, or woman with comorbid medical problems.

90
Q

Uncomplicated simple cystitis symptoms

A

Urinary bacteria, dysuria, lower abdominal cramping, frequency, urgency. Typical for the healthy outpatient, non pregnant, no fever nausea, vomiting flank pain. (if fever look for renal parenchyma pyelonephritis. Diagnose with dipstick UA (no culture, no lab testing)

91
Q

present in almost all patients with complicated UTI

A

Pyuria (absense suggests an alternative dx) White cell casts – pyuria from renal origin. Can have absent pyuria if infection does not communicate with the collecting system or the system is obstructed

92
Q

Tx uncomplicated simple cystitis

A

Bactrim for THREE DAYS. One double strength tablet (160/800) twice daily.

93
Q

Tx uncomplicated simple cystitis with a sulfa allergy

A

May use fluoroquinolone(ciprofoxacinor levofloxacin) in patient with sulfa allergy, areas with high rates of bactrim-resistance

94
Q

optimal duration of antibiotic therapy in men

A

Few studies have evaluated the optimal duration of antibiotic therapy in men, although treatment has traditionally been given for 7 to 14 days.

95
Q

Risk factors for simple cystitis

A

sex, may recommend post coital voiding or prophylactic abx use

96
Q

recent TMP-SMX resistance is increasing and approached x%

A

20%

97
Q

Complicated Cystitis

A

Females with comorbid medical conditions (DM. Immunosuppressed. Renal failure. Renal transplant. UTI in childhood)
All male patients
Indwelling foleycatheters
Urosepsis/hospitalization

98
Q

Diagnosis of Complicated Cystitis

A

Urinalysis, Urine culture

Further labs, if appropriate.

99
Q

Treatment of Complicated Cystitis

A

Fluoroquinolone (or other broad spectrum antibiotic) 7-14 daysof treatment (depending on severity)
May treat even longer (2-4 weeks) in males with UTI

100
Q

Indwelling catheter complicated cystitis

A

Try to get rid of the foley. Only treat with symptomatic (fever, dysuria). WBC in UA, they are frquently colonized with great number of bacteria. Should change foley before obtaining culture.

101
Q

Recurrent Cystitis

A

Want to make sure urine culture and sensitivity obtained. May consider urologic work-up to evaluate for anatomical abnormality. Treat for 7-14 days.

102
Q

Pyelonephritis

A

Infection of the kidney, Associated with constitutional symptoms –fever, nausea, vomiting, headache

103
Q

Dx pyelo

A

Urinalysis, urine culture, CBC, chemistry

104
Q

Pyelonephritis Treatment:

A

2-weeksof Trimethroprim/sulfamethoxazoleor fluoroquinolone, Hospitalization and IV antibiotics if patient unable to take po.

105
Q

Pyelonephritis Complications:

A

Perinephric/Renal abscess, Nephrolithiasis with UTI

106
Q

Perinephric/Renal abscess:

A

Suspect in patient who is not improving on antibiotic therapy.
• Diagnosis: CT with contrast, renal ultrasound
• May need surgical drainage.

107
Q

Nephrolithiasis with UTI

A

Suspect in patient with severe flank pain

• Need urology consult for treatment of kidney stone

108
Q

Prostatitis Symptoms:

A

Pain in the perineum, lower abdomen, testicles, penis, and with ejaculation, bladder irritation, bladder outlet obstruction, and sometimes blood in the semen

109
Q

Diagnosis Prostatitis

A
  • Typical clinical history (fevers, chills, dysuria, malaise, myalgias, pelvic/perinealpain, cloudy urine)
  • The finding of an edematous and tender prostate on physical examination
  • Will have an increased PSA
  • Urinalysis, urine culture
110
Q

Prostatitis tx

A

Trimethoprim/sulfamethoxazole, fluroquinoloneor other broad spectrum antibiotic
• 4-6 weeks of treatment to penetrate

111
Q

Risk Factors Prostatitis:

A

Trauma, dehydration

112
Q

Urethritis Chlamydia trachomatis

A

Frequently asymptomatic in females, but can present with dysuria, discharge or pelvic inflammatory disease. Send UA, urine culture (if pyuriaseen, but no bacteria, suspect Chlamydia)

113
Q

Pelvic exam Urethritis

A

send discharge from cervical or urethral osfor Chlamydia PCR. recc for all females < 25 to be screened

114
Q

Tx Urethritis Chlamydia trachomatis

A

Azithromycin –1 g pox 1 or

Doxycycline –100 mg poBID x 7 days

115
Q

Neisseria gonorrhoeae Urethrtis

A
  • May present with dysuria, discharge, PID
  • Send UA, urine culture
  • Pelvic exam –send discharge samples for gram stain, culture, PCR
116
Q

Treatment Neisseria gonorrhoeae Urethrtis

A 
•Ceftriaxone –125 mg IM x 1
•Cipro–500 mg pox 1
•Levofloxacin –250 mg pox 1
•Ofloxacin–400 mg pox 1
•Spectinomycin–2 g IM x 1
You should always also treat for chlamydia when treating for gonorrhea!
117
Q

Antibiotic choice and duration are determined by

A

classification of UTI.

118
Q

Biggest bugs for UTI are

A

E. coli, S. saprophyticus, Proteus mirabilis, Enterococci and gram-negatives

119
Q

Consider antibiotic resistance in

A

pyelonephritis

120
Q

Among quinolones, don’t use

A

moxifloxacin.

121
Q

Chlamydia screening is now recommended for all women 25 years and under since

A

infection is frequently asymptomatic, and risk for PID/infertility is high!

122
Q

Urinary Incontinence Loss of bladder control due to

A
  • Functional abnormalities of the bladder or urethra
  • Bladder muscle contractions
  • Weak pelvic floor and/or sphincter muscles
  • Blockage in the urethral opening
123
Q

About twice as common in

A

women (men complain about lower quality of life more)

124
Q

Causes of incontinence

A

from localized tumor/cancer, diabetes, neurological disorders and physical changes associated with aging

125
Q

Dual control of urination

A

Autonomic nervous system control and Central nervous system

126
Q

Autonomic nervous system

A
  • Nerve coming from the spinal cord and go directly to the bladder
  • When bladder gets fuller, signals are sent to the brain
127
Q

Central nervous system

A

Voluntary control to choose when to void

128
Q

Voiding Physiology

A
  • Normal voiding requires coordination between multiple structures and nerve pathways
  • Key structures include the brain, brainstem, spinal cord, bladder, and urethral sphincter mechanism
129
Q

The Brain and Social Continence

A 
The brain(cerebral cortex) provides overall control and direction of bladder function.
• The Detrusor area in the cerebral cortex controls bladder function by directing the micturition centers to initiate or delay voiding depending on the social situation.
• This is called social continence
130
Q

Any disruption in the cerebrocorticalfunction can cause or contribute to incontinence like which condition

A

CVA

131
Q

The neural circuitry that controls this process is complex and highly distributed:

A

it involves pathways at many levels of the brain, the spinal cord and the peripheral nervous system is mediated by multiple neurotransmitters.

132
Q

Diseases or injuries of the nervous system →can cause the

A

re-emergence of involuntary or reflex micturition,leading to urinary incontinence

133
Q

pontine micturition center

A

The pontine micturition center in the brainstem provides for automatic coordinated voiding. Meaning the urethra opens before the bladder contracts

134
Q

The pons

A

also holds the micturition ‘reflex’ centerwhich allows the bladder to empty when reaching a certain fullness regardless of social situation.
• Especially important for spinal cord patients.

135
Q

The storage and periodic elimination of urine depends on

A

coordinated activity of smooth and striated muscles in the two functional units of the lower urinary tract: The reservoir (the urinary bladder) And the outlet

136
Q

the outlet consists of

A

the bladder neck,
the urethra
the urethral sphincter

137
Q

Spinal Cord Pathways - Parasympathetic

A

omes off at S2-S4 and cause the bladder to contract and the urethra to relax.
• Parasympathetic stimulation initiates voiding

138
Q

Sympathetic pathways

A

come off at T-10 L2that cause bladder neck to tighten and also contribute to bladder relaxation.
• Sympathetic stimulation contributes to urine storage and promotes continence.

139
Q

Caveat: remember that the bladder has only two modes of operation:

A

storage and elimination

140
Q

Trigone

A

Sensitive to expansion and once stretched to a certain degree, the urinary bladder signals the brainof its need to empty
The signals become stronger as the bladder continues to fill

141
Q

Patients with urge or frequency

A

bladder pressure not greater than urethral pressure

142
Q

Patients with urge incontinence

A

bladder pressure IS greater than urethral pressure

143
Q

Urinary incontinence is Not a natural part of aging

A

It can happen at any age
 Caused by many physical conditions
 Many causes of incontinence are temporary and can be managed with simple treatment

144
Q

Some causes of temporary incontinence are:

A
  • Urinary tract infection
  • Vaginal infection or irritation
  • Constipation
  • Effects of Rx
145
Q

Stress Incontinence

A

urethral hypermobility & intrinsic sphinctericdeficiency People with stress incontinence lose urine when they exercise or move in a certain way. sneeze, cough, or laugh, up from a chair or out of bed, walking, going to the bathroom often to avoid accidents

146
Q

Urge incontinence

A

immediately before involuntary leakagePeople with urge incontinence lose urine as soon as they feel a strong need to go to the bathroom.(AKA Overactive bladder)

147
Q

Mixed stress/urge

A

combined stress & urge

148
Q

Overflow (retention)

A

continuous leakage/ dribbling/un-empty bladder

149
Q

If you have urge incontinence you may leak urine:

A
  • When you can’t get to the bathroom quickly enough
  • When you drink even a small amount of liquid, or when you hear or touch running water
  • You may go to the bathroom very often; for example, every two hours during the day and night
  • You may even wet the bed
150
Q

Causes/Risk Factors of Urge

A 
Aging is a risk factor simply due to:
• reduced bladder capacity
• delayed recognition of bladder filling
• → reduced “response” time.
• Bladder irritants,
• neurological lesions,
• Stones
• cancer
• obstructed flow
• Idiopathic
151
Q

Overflow Incontinence Causes

A

• Do not feel the urge to urinate.
• Incomplete bladder emptying
• Small amounts of urine are leaked on a nearly continuous basis
• Weak bladder muscles:
• caused by nerve damage from diabetes or other diseases
• a blocked urethra can be responsible for overflow incontinence.
Impaired contractibility of the detrusor muscle

152
Q

Overflow Most frequently appears in older men because

A

BPH hinders the flow of urine; urinary stones or tumors also may block the urethra. Women is rare but can be caused by fibroids or ovarian tumors, Spinal cord injuries or nervous system disorders are additional causes

153
Q

s/s Overflow incontience

A
  • Feeling as though the bladder is never completely empty
  • Feeling the urge to urinate, but not being able to
  • Passing a dribbling stream of urine, even after spending a long time at the toilet
  • Nocturia
  • Although some people with overflow incontinence never have the feeling of a full bladder, they may leak urine day and night.
154
Q

Functional Incontinence

A

Diagnosis: Intact urinary storage & emptying –but unable to toilet themselves
• Usually one of elimination.
•Patient voids large amounts at regular intervals.• Incontinence in patient with normal voiding patterns and normal bladder function: • Usually related to cognitive status • Motivation • And/or mobility issues Cortex doesn’t process the signals from the bladder.
• An automatic voiding when bladder is full. No social continence.

155
Q

Tx Functional

A 
prompted or timed voiding. Containment products and skin care. •
Pelvic Muscle Rehabilitation
• Behavioral therapy
• Pharmacological Therapies
• Pessary
• Surgical Therapies
156
Q

Assessment and Evaluation-ONE Idea

A 
D-Delirium
I-Infection
A-Atrophic urethritis/vaginitis
P-Pharmaceuticals
P-Psychological Status
E-Endocrine changes
R-Restricted mobility
S-Stool Impaction
157
Q

Kegel Exercises

A

Pull in the pelvic muscles and hold for a count of 3. Then relax for a count of 3.
• Work up to 3 sets of 10 repeats.
• Start doing your pelvic muscle exercises lying down. This is the easiest position to do them because the muscles do not need to work against gravity.
• When your muscles get stronger, do your exercises sitting or standing. Working against gravity is like adding more weight.

158
Q

Kegels - time frame

A

• It takes just 2-5 minutes a day. You may not feel your bladder control improve for 3 to 6 weeks. Still, most people do notice an improvement after a few weeks

159
Q

Pelvic floor exercise benefits

A
  1. Helps strengthen the muscles of the pelvic floor –improves bladder stability
  2. Helps suppress the feeling of urgency
160
Q

Bladder Training

A
  • Bladder training has many variations but generally consists of three primary components:
  • Education
  • Scheduled voiding
  • Positive reinforcement
161
Q

Pharmacological

A

Work on parasympathetic nervous system-depends on type of incontinence.
Includes:
1.Alpha blockers
2.Antimuscarinics
3.Serotonin norepinephrine reuptake inhibitors

162
Q

Diagnostic Evaluations

A
  • Urodynamics-to determine voiding dysfunction etiology and bladder/urethra function
  • Focused Physical examination and history
  • Dexterity testing
  • Pelvic muscle strength testing
  • Prostate exam
  • Cystoscopy to visualize bladder wall and identify lesions.

Primary Care 3 (29 decks)

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