Disorders Of Renal Function And Urine Elimination

Front 1

Inner mucosal lining of transitional epithelial cells in the bladder is a

Back 1

barrier to prevent the passage of water between the bladder contents & blood

Front 2

Bladder structure

Back 2

-outer serosal layer
-detrusor muscle
-submucosal layer of loss connective tissue
-inner mucosal lining of transitional epithelial cells

Front 3

Motor Control of bladder function

Detrusor Muscle

Back 3

Muscle of micturition
PNS-Contracts >> urine expelled from bladder
SNS relaxes

Front 4

Motor Control of Bladder Function

Abdominal Muscles

Back 4

Contraction >> increase in abdominal pressure >> increase bladder pressure

Front 5

Motor Control of Bladder Function

Internal Sphincter

Back 5

-Circular muscle in neck; cont. of detrusor. Bladder relaxed, fibers are closed, act as sphincter. When detrusor contracts, sphincter is pulled open by change in bladder shape. PNS relaxes. SNS contracts

Front 6

Motor control of Bladder Function

External Spincter

Back 6

Circular muscle surrounds urethra, acts as a reserve mechanism to stop micturition, maintain continence despite increase in bladder pressure
Under voluntary control- somatic NS

Front 7

Micturition

Back 7

As bladder filling occurs, ascending spinal fibers relay info to center, which also receives input from forebrain about behavior cues for bladder emptying.


Coordination of micturition reflex occurs in pontine micturition center, facilitated by input from forebrain & SC reflexes. Center coordinates activity of detrusor & external sphincter.

Descending pathways from center produce coordinated inhibition of somatic systems, relaxation of both sphincters. The onset of urinary flow through the urethra causes reflex contraction of the bladder.

Front 8

Bladder fills >> _________ receptor stimulated >> pelvic nerve carries impulses to _____________ >> ____________ center stimulated >> _______________ motor neurons send impulses to detrusor muscle through the ___________ nerve >> ____________ muscle contracts >> urination

Back 8

bladder fills, stretch receptors stimulated, pelvic nerve carries impulses to sacral region of spinal cord, micturition center stimulated, parasympathetics motor neurons send impulses to detrusor muscle through the pelvic nerve, detrusor muscle contracts, urination

Front 9

At what age does a child become conscious of the urge to urinate

Back 9

2-3

Front 10

As child achieve continence, micturition is

Back 10

voluntary

Front 11

What medications do you give to spastic bladder?

Back 11

-anticholinergics
-sympathetic agonists
-stent, botox

Front 12

Neurogenic Bladder disorders

Back 12

failure to store urine= spastic bladder =decrease in bladder volume

Front 13

Neurogenic bladder results from

Back 13

from neurogenic lesions above the level of the sacral cord that allow neurons in the micturition center in SC to function reflexively without the control of higher CNS centers

Bladder dysfunction that occurs with spinal cord injury, stroke, herniated discs, tumors of the spinal cord

Front 14

Failure to empty bladder =

Back 14

flaccid bladder

Front 15

Flaccid Bladder results from

Back 15

-neurologic disorders affecting motor neurons in DC or peripheral nerves that control detrusor muscle contraction and bladder emptying

-injury to cauda equina, trauma, tumors, MS, spina bifida

Front 16

Flaccid bladder emptying can be achieved by

Back 16

-increase intraabdominal pressure
-manual suprapubic pressure

Front 17

Treat flaccid bladder

Back 17

-catheters or pressure on bladder

Front 18

Stress incontinence

Back 18

Involuntary loss of urine associated with activities (coughing) >> increase IAP

Front 19

Overactive urinary incontinence

Back 19

Urgency, frequency assoc with hyperactivity of detrusor, may/may not involve involuntary loss of urine

Front 20

Overflow urinary incontinence

Back 20

Involuntary loss of urine when bladder pressure > urethral pressure in absence of detrusor activity

Front 21

Stress incontinence in women caused by

Back 21

-loss of posterior urethrovesical angle
-aging, childbirth, surgery
-loss of pelvic floor tonus

Front 22

Stress incontinence in women is caused by the loss of

Back 22

the angle between the bladder and the uretherovesical junction

-angle should be 90 degrees

Front 23

Overactive/urge incontinence is caused by

Back 23

involuntary bladder contractions
-overactive bladder can occur without incontinence

Front 24

Overactive/urge incontinence is clinical syndrome of

Back 24

incontinence, increased frequency, dysuria, nocturia

Front 25

Overflow incontinence

Back 25

retention of urine due to neural disorders or obstruction

-hypertrophy of kidney then dilate >> no muscle >> muscle substitute with fibrotic tissue >> urine in bladder >> badder pressure increases >> high enough >> sphincter, pressure decreases and sphincter closes, urinary retention

Front 26

Overflow incontinence is when the bladder does not

Back 26

contract

Front 27

Treat overactive/urge incontinence

Back 27

-anticholinergics
-beta 2 agonists

Front 28

Overflow incontinence

Back 28

Involuntary loss of urine that occurs when intravesicular pressure exceeds the maximal urethral pressure because of bladder distention in absence of detrusor activity

Front 29

Factors that contribute to incontinence in the elderly

Back 29

-decrease in overall bladder capacity
-urethral closing pressure decreases
-detrusor closing pressure decreases
-detrusor muscle function decreases
-restricted mobility
-medications

Front 30

If damage glomeruli, damage

Back 30

filtration

Front 31

Podocytes form windows that form a fenestrated epithelial cell that allowed for

Back 31

rapid filtration of substances

Front 32

Normal filtration intro bowman's capsule

Back 32

sodium, water, AA, calcium, small molecules, filtered easily, smaller than the pores

Front 33

If albumin in glomerular basement membrane

Back 33

-something is wrong with the membrane

Front 34

Glomerular injury, primary vs secondary

Back 34

1. autoimmune
2. DM, HTN

Front 35

Two immune mechanisms that damage Glomerular basement membrane

Back 35

1.Antiglomerular antibodies leave circulation, react with antigens present in BM of glomerulus.

2. Antigen-antibody complexes circulating in blood become trapped as they are filtered in glomerulus.

Front 36

Acute Nephritic Syndrome

Back 36

-acute glomerular inflammation
-sudden onset with decreased GFR, hematuria, oliguria, fluid and waste accumulation

Front 37

Acute Postinfectious Glomerulonephritis follows infections caused by

Back 37

strains of group A Beta hemolytic streptococi

Front 38

Treatment of Postinfectious glomerulonephritis

Back 38

-antibiotics
-supportive care

Front 39

Acute PostInfectious Glomerulonephritis causes an inflammatory response from circulating complexes that

Back 39

become entrapped in glomerular BM >> oliguria, hematuria, proteinuria > increase cap membrane permeability > increase na and water retention >> edema, HTN

Front 40

Glomerulonephritis is ___ cause of ESRD in the US

Back 40

3rd

Front 41

Nephrotic Syndrome is characterized by

Back 41

massive proteinuria

hypoalbuminemia

salt and water accumulation

edema

HLD

Front 42

Main disease that causes nephrotic syndrome

Back 42

-membranous glomerulonephritis: LUPUS

-deposition of immune complexes, thickening of membrane

Front 43

Test for Lupus

Back 43

check anti DNA antibodies

Front 44

Nephrotic syndrome complications

Back 44

-pulmonary edema
-ascites
-loss of globulins
-thrombotic complications

Front 45

Diabetic Glomerulosclerosis is the major cause of ___________ and ____________ and is caused by

Back 45

-CKD
-ESRD
-type I and type II DM

Front 46

Diabetic glomerulosclerosis damages the membrane by

Back 46

widespread thickening and sclerosis of glomerular basement membrane and mesangial cells

-filter does not work
-mesangial cells become hypertrophic
-form nodules
-destory membrane

Front 47

Manifestations of diabetic glomerulosclerosis

Back 47

microalbuminuria < 300 mg/day

-filter is starting to be malfunctioned

Front 48

In diabetic glomerulosclerosis there is an ______ in GFR and an ______in capillary pressure

Back 48

increase in GFR

increase in capillary pressure

increase in Angiotensin II >> constrict the efferent arteriole (gets blood out from glomeruli) >> open more pores >> albumin and water go into filtrate and cells work harder

Front 49

Can diabetic glomerulosclerosis be reversed?

Back 49

-stop smoking
-control HTN

Front 50

best meds to decrease diabetic nephropathy

Back 50

-ACEI and ARBs
-decrease pressure in efferent arteriole

Front 51

HTN glomerular disease

Back 51

-HTN cause and effect of kidney disease
-change in kidney structure and function
-sclerosis and atrophy of arterioles
-2nd leading cause of ESRD

Front 52

Acute kidney injury

Back 52

kidneys fail to remove metabolic end products from the blood and regulate the fluid, electrolyte, and pH balance of the extracellular fluids

Front 53

Chronic kidney disease

Back 53

end result of irreparable damage to the kidneys, develops over course of years

Front 54

Acute kidney injury

Back 54

abrupt, reversible with early txt

Front 55

Acute kidney injury manifestations

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azotemia

decrease GFR >> decrease urine excretion of wastes >> increase BUN >> increase creatinine

Front 56

Azotemia

Back 56

-accumulation of nitrogenous waste products in blood

-urea, BUN, creatinine

Front 57

Acute Kidney injury BUN and Creat?

Back 57

increase BUn
Increase Creat

Front 58

Acute Kidney injury phases

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1. pre renal
2. intra renal
3. post renal

Front 59

Pre renal injury

Back 59

-decrease in renal blood flow >> increase in GFR >> decrease filtration of substances >> decrease urine output >> increase BUN (urea)/Cr ratio

20/1 (normal) increases to 40/1
-pre RENAL
-GFR low=less fluid in TUBULES-more BUN absorbed

Front 60

MAP < 60

Back 60

no blood flow to the kidneys

Front 61

The kidneys receive approximately ___ of CO to filter blood regulate fluid and electrolyte balance

Back 61

20%

Front 62

Pre renal-quickly restore blood volume

Back 62

kidneys will get better

Front 63

Post renal injury

Back 63

-obstruction of urine outflow from kidneys
-ureters-calculi
-urethra-BPH
-bladder-tumors

Front 64

Intrinsic Renal Injury

Back 64

-damage to structure of kidneys including: glomerular, interstitium, tubular

-injury to tubular structure-ATN : ischemia, toxic insult, intratubular obstruction

Front 65

Ischemic ATN

Back 65

-destruction of tubular cells with acute renal failure

Front 66

Causes of ischemic ATN

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-major sx
-severe hypovolemia
-overwhelming sepsis
-major trauma
-burns

Front 67

Does GFR improve with RBF restoration in ischemic ATN?

Back 67

No

Front 68

Nephrotoxic ATN

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-nephrotoxic drugs or other agents
-main is contrast

Front 69

Tubular Obstruction ATN

Back 69

-myoglobin
-Hgb
-uric acid

Front 70

Myoglobin in tubular obstruction ATN

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-skeletal m breakdown from trauma, exertion, hyperthermia, prolonged sz, sepsis

Front 71

Hgb tubular obstruction ATN

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-blood transfusion reactions

Front 72

Uric acid and myeloma light chains-tubular obstruction ATN

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--chemo and radiation

Front 73

Three phases of ATN

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1. onset/initiating phase
2. maintenance phase
3. recovery phase

Front 74

Onset phase ATN

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hours/days from onset to insul

Front 75

Maintenance phase of ATN

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decrease GFR, retention of metabolites (urea, K, sulfate, Cr), decrease serum Na, generalized edema, pulmonary edema, metabolic acidosis

Front 76

Recovery phase of ATN

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Repair of renal tissues, gradual improvement in U/O, BUN & Cr

Front 77

1st phase of recovery in ATN is

Back 77

hyperuria

Front 78

As glomerular filtration rate decreases chronic kidney disease _____

Back 78

worsens

Front 79

At watch stage of CKD does one require dialysis

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GFR < 15, stage 5

Front 80

Why is CKD not evident until the disease is advanced?

Back 80

-2 kidneys and many nephrons

Front 81

Causes of chronic kidney disease

Back 81

-DM, HTN, glomerulonephritis

Front 82

CKD is ___________, ___________, _____________ of the nephrons

Back 82

progressive, irreversible, destruction

Front 83

CrCl=

Back 83

(140-age) x (wt(kg)) / (72 x serum Cr)

Front 84

What is the best measurement of overall kidney function

Back 84

GFR

Front 85

GFR < 60 =

Back 85

loss of > 1/2 normal kidney function

Front 86

CKD Manifestations

Back 86

-HTN
-HF
-Uremia
-Increase uric acid
-pericarditis
-coagulopathies
-acidosis
-anemia
-low Vit D (give Vit D3-active form)

Front 87

CKD children causes

Back 87

congenital, inherited disorders, metabolic syndromes

Front 88

CKD younger than 5 years old

Back 88

-renal dysplasia
-obstructive uropathy
***congenital MAIN disease

Front 89

CKD greater than 5 years old

Back 89

-acquired, inherited, i.e. STREP

Front 90

CKD children manifestations

Back 90

-problems with growth and development

Front 91

CKD elderly

Back 91

decrease in GFR*
-more susceptible to nephrotoxic drugs
-not associated with increase in Cr (end product of m. metabolism-they do not have m. to begin with)