Pbdii Exam 3

Front 1

definition of renal failure

Back 1

A condition which the kidneys fail to remove the metabolic end products from blood. Also fail to regulate fluid, electrolyte and pH balance.

Front 2

Chronic renal Dx

Back 2

usually involve the glomerulus. In some cases they involve renal tubules or blood perfusion.
NOT REVERSIBLE!

Front 3

Acute renal Dx

Back 3

Inablilty to maintain fluid and elctrolyte homeostasis and a failure to excrete nitrogenous waste. LOW GFR and URINE output. Reversilble.

Front 4

Three types of acute renal dx

Back 4

Pre-renal- affects blood flow
Renal- Acute tubular necrosis
Post-renal- obstruction

Front 5

Common indicators of ARF

Back 5

Azotemia- retention of nitrogenous waste

Uremia-retention of lots of toxins.

Front 6

Azotemia

Back 6

retention of nitrogenous waste either through inability to excrete them or through failure to be delivered to kidney.
INC in Waste!

Front 7

Uremia

Back 7

Complex syndrome that occurs when azotemia becomes symptomatic. All ORGANS involved. Endocrines changes, acid base problems, etc.

Front 8

7 catergories of renal dx

Back 8

Acute Glomerulonephritis, Goodpasture dx,Chronic Glomerulonephritis, UTI, Renal calculi, Polycystic kidney dx, renal failure.

Front 9

6 biochemical assesments to determine renal dysfunction

Back 9

Proteinuria, Hematuria, Hydrogen Ion Conc, Specific Gravity,GFR, tubular function tests

Front 10

Proteinuria

Back 10

if greater than 150mg/day BAD! Simple dipstick test that is suggestive of glomerular problem.

Front 11

Hematuria

Back 11

Dipstick test or microscopic exam. Blood in urine is suggestive of UTI or renal dx.

Front 12

Hydrogen ion concentration

Back 12

Normal is 4.5-8 thruout day. pH inc post meal but Dec with sleep and fever (metabolic acidosis). Not really helpful for diagnosing.

Front 13

Specific Gravity

Back 13

measure oSm. 1.01-1.025 norm but if dehyd then it can be 1.04. Kidney loses ability to concentrate urine 1st with chronic renal dx.

Front 14

GFR

Back 14

115-125ml/min but dec with age. Measure with creatinine. BUN also good because when BUN inc GFR will dec.

Front 15

Tubular function test

Back 15

Four test: PAH excretion, conc/dilut test, Sodium conc test, and urine acidification tests. Challenge kidneys to determine capacity for secretion and reabs.

Front 16

6 types of morphological test for renal dyfunctoin

Back 16

microscopic findings, intravenous pyelogram, retrograde pyleogram, renal angiography, renal biopsy, CT/MRI/ultrasound.

Front 17

Microscopic examinations for renal dysfunction

Back 17

RBC (>1 or 2)
WBC (3 or 4)
Bacteria
Cast exam

Front 18

Cast Exam

Back 18

na

Front 19

Intravenous Pyelogram (IVP)

Back 19

visualize kidney cortex with x-ray. If cortex is thin=glomerulonephritis.
If cortex look moth-eaten then it is pyelonephritis and ischemia.

Front 20

Retrograde pyelogram

Back 20

catheter advanced up the ureter. Contrast media inj into renal pelvis. Contrast media given then xray taken.

Front 21

Renal Angiography

Back 21

Will determine arterial stenosis, prescence of neoplasms, arrangements of arteries and veins.

Front 22

Renal Biopsy

Back 22

renal tissue taken for micro exam. Can have problems with intrarenal bleeding.

Front 23

ARF

Back 23

sudden impairment of renal function, oliguria. Etiology not implied. Dec renal function characterized by nitrogenous waste and azotemia.

Front 24

Pre-Renal ARF

Back 24

usually abnormal blood flow or myocardial dysfunction

Front 25

Renal ARF

Back 25

parenchymal injury

Front 26

Post Renal ARF

Back 26

usually tubular obstruction that interferes with elimination. oliguria.

Front 27

80-95% of ARF are which types?

Back 27

Pre-renal and Renal

Front 28

Normal manifestation of ARF

Back 28

fall in urine out put (less than 400ml/day) and dec GFR.

Front 29

The 2 broad categories of causes for ARF

Back 29

ischemia and nephrotoxic injury.

Front 30

3 conditions that must prevail for kidney function to be normal

Back 30

1. kidney must be adequately prefused with blood.
2. kidney must function normally
3.urine formed must be able to leave body

Front 31

Pre-Renal Pathogenesis

Back 31

See Notebook! Lots of INFO!

Front 32

Normal BUN to creatinine ratio vs pre-renal ARF BUN:C

Back 32

Norm ratio of BUN to Creatinine 10:1

ARF 20:1

Front 33

Why avoid aspirin with pre-renal ARF

Back 33

aspirin will inhibit prostaglandin synthesis. PG are vasodilators so ischemia is induced.

Front 34

Best treatment for pre-renal ARF

Back 34

restore adequate volume with whole blood or isotonic fluids.

Front 35

four main potential causes of pre-renal ARF

Back 35

Hypovolemia, dec vascular filling, heart failure/cardiogenic shock, dec renal perfusion.

Front 36

Post-Renal ARF

Back 36

obstruction which result in oliguria or anuria. Sometimes it's partial obstruction.

Front 37

partial obstruction in post renal ARF

Back 37

leads to polyuria because partial obstruction causes loss of concentrating ability and sodium wasting.

Front 38

Levels where obstruction can occur

Back 38

bladder (rarely causes arf), the outlet, ureter, prostate.

Front 39

prostatic hyperplasia

Back 39

most common underlying problem in men enlarged prostate.

Front 40

How to treat obstruction and effects?

Back 40

remove obstruction. diuresis and polyuria will occur and fluid replacement is needed.

Front 41

Most Renal Parenchymal dx is caused by

Back 41

acute tubular necrosis

Front 42

5 mechanisms of renal parenchymal dx

Back 42

1.immunological renal dx
2. allergic renal dx
3.obstruction which leads to necrosis
4.ischemia can lead to ATN
5.Toxic substances

Front 43

ATN causes tubular damage by...

Back 43

1.anoxia occurs with tub damage
2.vasoconstriction of pre-glom arterioles with damage
3.damage can led to oliguria
All will dec GFR

Front 44

cisplatin causes renal damage by

Back 44

accum in proximal tubules and causes mitochondrial damage

Front 45

Gentamicin causes damage where in the kidney?

Back 45

Proximal tubule with it's tubular toxic effects. Has some diuretic effects in addition to it's antibiotic effects so it can dec vol and inc damage.

Front 46

Myoglobunuria (ATN cause)

Back 46

myglobin in urine associated with rhabdomyolysis or muscle injury.

Front 47

BUN:Creatinine ratio in pre-renal oliguria vs. ATN

Back 47

pre-renal: >20:1
ATN:>10:1

Front 48

Urine concentration in pt with pre-renal oliguria vs ATN

Back 48

Pre-renal urine is concentrated. Atn is not.

Front 49

Pre-Renal VS ATN
Urinary Sodium

Back 49

Pre: less than 20mEq/L
ATN:>40mEq/L

Front 50

Pre-renal vs ATN
urinary protein

Back 50

pre-renal: none
ATN: +1

Front 51

Pre-renal vs ATN
Urinary sediment

Back 51

Pre:normal
ATN:dirty

Front 52

a consequence of uremia

Back 52

neurological manifestations

Front 53

Some primary causes of ATN

Back 53

trauma with blood loss, major loss of fluids, pregnancy can change bp, hypovolemia, anoxia.

Front 54

Chronic Kidney Dx

Back 54

decline in kidney function due to permanent loss of nephrons

Front 55

Chronic kidney dx can result from

Back 55

HTN, diabetes, glomerulonephritis, and other kidney dx

Front 56

5 stages of kidney dx and their GFR values

Back 56

stage 1- >90
stage 2- 60-89
stage 3-30-59
stage 4-15-29
stage 5 less than 15

Front 57

stages 1 and 2 of CKD

Back 57

no symptoms usually. the symptoms could be the underlying renal dx itself.

Front 58

Stages 3 and 4 of CKD

Back 58

Dec GFR. all organ systems affected but notable changes are anemia, loss of apetite, abnormalities in ionic, water, and acid base.

Front 59

Stage 5 CKD

Back 59

toxin accumulate and uremic syndrome occurs.

Front 60

Kidney Failure definition

Back 60

GFR less than 15 and accompanied by signs and symptoms or uremia or condition that need a kidney replacement (or dialysis).

Front 61

End Stage renal dx

Back 61

Term NOT syn with KF. end stage is used when pt is treated with dialysis and transplantation.

Front 62

Functional Reserve of kidneys

Back 62

as many as 90% of nephrons maybe destoryed b4 impairment is seen.

Front 63

Mechanism of damage associated with CKD can be two types

Back 63

initiating which is specific to the etiology (immune, toxins, or inflamm) OR progresssive involving hyperfiltration and hypertrophy of viable nephrons.

Front 64

Albuminuria is helpful to measure what?

Back 64

monitoring nephron injury and the response to therapy in many forms of CKD.

Front 65

2 major types of CKD

Back 65

Disorders of glomerular function and tubulointerstitual disorders (pyelonephritis).

Front 66

pyelonephritis

Back 66

infection of kidney parenchyma and renal pelvis

Front 67

Chronic tubulointersitial disorders produce

Back 67

intersitial fibrosis, atrophy, mononuclear infiltrates.

Front 68

fluid and electrolyte imbalance in CKD can lead to

Back 68

inability to concentrate urine, polyuria,nocturia,metabolic acidosis and diminished sodium tubular reabsorption.

Front 69

Chronic Polynephritis

Back 69

Scarring and deformation occurs. Often occurs in people with recurrent UTI or acute polynephritis. Can lead to polyuria/nocturia.

Front 70

Chronic obstructive polynephritis

Back 70

associated with recurrent bouts of inflammation and scarring.

Front 71

Chronic polynephritis responsible for what % f ESRD?

Back 71

10-20%

Front 72

Kidney's tolerance to drugs can vary with

Back 72

age, hydration,renal function, BP and pH of urine.

Front 73

Drug-related nephropathies

Back 73

functional or structural damage after exposure to a drug

Front 74

Drug-Related nephropathies can cause damage by..

Back 74

dec renal blood flow, obstructing urine flow, damaging tublointestitial structure, prd hypersensitivity rxn.

Front 75

how can NSAIDS cause drug related nephropathy?

Back 75

reduce renal blood flow and cause pre-renal failure. Can cause intersitial nephritis with papillary necrosis.

Front 76

Drug-related hypersensitivity rxns present how?

Back 76

about 2 weeks post exposure and pt will experience fever, eosinophilia, hematuria, mild proteinuria. Can cause tubulointerstitial nephritis which will damage the tubule and interstitium.

Front 77

seven types of glomerular dx

Back 77

1. actue prolif glomerulonephritis
2. rapid progressive glomerulonephritis
3.nephrotic syndrome
4.membranous glomerulonephritis
5.minial change dx (lipoid nephrosis)
6.focal segmental glomerulosclerosis
7. chronic glomerulonephritis

Front 78

Cellular changes associated with glomerular dx

Back 78

most take place at basement membrane. Basement membrane thickening, sclerosis, fibrosis.

Front 79

potential causes of glomerular dx

Back 79

1. dx that cause inflammation of endothelial,mesangial, or epithelial cell of the glomeruli
2. inflammation damages capillary wall and permits rbc and proteins to get into urine.
and DEC GFR

Front 80

glomerular dx can be a manifestation of which three dx?

Back 80

lupus, diabetes, and HTN.

Front 81

Major characteristic of glomerulonephritis

Back 81

1. antibodies against glomerular basement membrane in a LINEAR pattern.
2. antibody-antigen complexes. Type 3 injury.
3. urinary changes
4. mixed nephrotic and nephritic syndromes. def diagnosis needs biopsy.

Front 82

Urinary changes in glomerulonephritis

Back 82

proteinuria, hematuria, pyuria, edema, dec gfr, azotemia, oliguria, htn.

Front 83

Def of Nephrotic sydnrome

Back 83

dx of the glomerular basement membrane and inc perm to plasma proteins

Front 84

Major characteristic of nephrotic syndrome

Back 84

Edema, dec in plasma osmotic presure which mean dec ECF which inc RAS. Inc in RAS mean inc in aldosterone so more fluid retention.

Front 85

More characteristic of nephrotic syndrome

Back 85

hypoalbumina, massive proteinuria (more than 3.5gm.day). Hyperlipidia cholesterol (more than 300mg/dl).

Front 86

three types of nephrotic syndromes

Back 86

1.minial change glomerulonephritis (lipoid nephrosis)
2. membraneous glomerulonephritis
3.Focal segmental glomerulosclerosis

Front 87

Characteristics of minimal change glomerulonephritis

Back 87

glomeruli look normal under light microscope, selective protein loss to lose electroneg charge. Common in children and responds well to steroids.

Front 88

Characteristics of membraneous glomerulonephritis

Back 88

Most common type in adults. Caused by thickening GBM due to immune complex deposition. Non-selective protein loss. 1 in 1000 respond to steriod treatment.

Front 89

Focal Segment Glomerulosclerosis

Back 89

portions of the glomeruli sclerotic. More common in african americans and hispanics. Can be associated with dec oxygen, HIV, drug use. HTN present. Can treat with roids.

Front 90

Nephritic Syndrome

Back 90

Acute glomerular inflammation

Front 91

Characteristic of Nephritic Syndrome

Back 91

hematuria, oliguria and some proteinuria. Caused by inflammation that occuldes glomerular capillary lumen and damage capillary walls. DEC GFR and retention of salt and water. Edema and HTN.

Front 92

HTN manifestations

Back 92

inc vascular volume, elevated peripheral resistance, dec renal vasodilators, inc RAS

Front 93

peripheral neuropathy

Back 93

symmetrical and includes both motor and sensory nerves. Atrophy and demyelination of nerve fibers due to toxic agents and electrolyte abnormalities.

Front 94

uremic encephalopathy

Back 94

CNS disturbance. inability to fix attention and loss of memory.

Front 95

possible cause of nausea and vomitting in pt with CKD?

Back 95

decomposition of urea by intestinal flora and resulting in high conc of ammonia.

Front 96

why infection more likely in pt with CKD?

Back 96

defective phagocytic function, impaired humoral and cell-mediate immunity, dec granulocytes. Skin and mucosal infection may also be defective.

Front 97

causes of impotence for men on dialysis

Back 97

endocrine derangements, loss of libido due to anemia and dec testoterone. In women it's due to same factors.

Front 98

Women on dialysis experience

Back 98

Amenorrhea

Front 99

cystic dx of kidney

Back 99

fluid or semiseolid filled sacs of a dilated nephron.

Front 100

3 types of cystic dx

Back 100

1.simple/acquired
2.medullary cystic dx
3.polycystic dx (autsomal recessive and autosomal dominant).

Front 101

Causes of cystic dx

Back 101

tubular obsruction that inc intratubular pressure. Changes in the basement membrane of renal tubules that predispose to cystic dilation.

Front 102

Three main dx that lead to dialysis

Back 102

glomerulonephritic, polynephritic, and polycystic dx.

Front 103

Recessive polycystic dx

Back 103

cysts are derived from collecting tubule. very rare and common in children.

Front 104

some systemic maifestations associated with polycystic kidney dx

Back 104

aneurysm, LV hypertrophy, hepatic cyst.

Front 105

Medullary cystic dx complex

Back 105

autsomal renal disorders with onset in childhood. Small kidneys with varying number of cyst. Initial insult is in distal tubule with progressive tubular atrophy involving both medulla/cortex. polyuria,polydipsia then salt wasting and growth retard.

Front 106

simple/acquired renal cyst

Back 106

common, in cortical region only, asymptomatic, tend to be in ppl over 50. If symptomatic will see HTN, pain, hematuria.

Front 107

General info about Renal Obstructive disorder

Back 107

1. can be insidous, partial or complete. Bi and unilateral.
2.partial occulsion of flow or complete.
3. reversible if resolved.
4. if unresolved can lead to chronic kidney dx

Front 108

Causes of UT obstruction

Back 108

1.developmental deficits
2.calculi
3.pregnancy
4.Benign prostatic hyperplasia
5.scar tissue
6. neurological disorders (spinal cord injury)

Front 109

Damaging effects of Urinay obstruction

Back 109

1.predisposes infection and stone formation. Calculi can contribute to infection.
2. develops back pressure that leads to kidney dilation and compresses renal vasculature. atrophy of kidney.

Front 110

Hydronephrosis

Back 110

urine filled dilation of renal pelvis associated with atrophy of kidney due to obstruction

Front 111

acute bilateral obstruction can mimic

Back 111

pre-renal failure

Front 112

Manifestation of partial bilateral obstruction

Back 112

inability to concentrate urine. Polyuria and nocturia as well.

Front 113

HTN is secondary to what disfunctions?

Back 113

reduced renal blood flow and stimulation of renin release.

Front 114

Most common cause of upper urinary tract obstruction is what?

Back 114

urinary calculi

Front 115

stone formation is dependent on what factors?

Back 115

1. pH and ionic strength
2.presence of Nidus for crystal formation
3.deficiency of inhibitors for stone formation. Citrate!

Front 116

What causes body to lack citrate?

Back 116

Metabolic acidosis, fasting and hyperkalemia.

Front 117

calcium stones

Back 117

most common, inc if bone dx, renal tubulat acidosis.

Front 118

Magnesium ammoniun phosphate stones

Back 118

form in alkaline urine and in prescnce of bacteria ( bac splits urea into ammonia and CO2)

Front 119

Uric Acid stones

Back 119

develop in gout and form in urine if ph is 5-6

Front 120

Cystine stones

Back 120

seen in cystinuria (genetic defect) in which renal transport of cystine is dysfunctional. RARE.

Front 121

Treatment for stones

Back 121

diet, passing, calcium salt supp, thiazide diuretics, cellulose phosphates. Removal can also be done. Antibiotic for infections and treatment of pain with meds.

Front 122

Protective mechanisms of the kidney against UTI infections

Back 122

1.washout phenom
2.Mucin layer is protective.
3.IgA immune response. Local and secretory.
4.Normal flora
5.prostate secretion in men

Front 123

What hormone is important in Mucin and normal flora prd?

Back 123

Estrogen

Front 124

Most common cause of UTI and most common entry path

Back 124

E.Coli and Urethra

Front 125

4 types of UTI

Back 125

asymptomatic
symptomatic
lower UTI (cystitis)
Upper UTI (pyelonephritis)

Front 126

Causes of UTI assosiated with stasis of urine flow (anatomical)

Back 126

stones, prostatic hyperplasis, pregnancy, malformations of ureterovesical junction. Inc P results in reflux.

Front 127

Causes of UTI assosiated with stasis of urine flow (functional)

Back 127

neurogenic bladder, infrequent voiding, detrusor instability, constipation.

Front 128

Urethrovesical Reflux

Back 128

when urine from urethra moves into bladder. interrupted voiding, coughing, squatting.

Front 129

Vesicoureteral Reflux

Back 129

occurs ar level of bladder to kidney. Short intravesical ureter.

Front 130

hormones produced by kidneys

Back 130

erythtopoietin, renin, calcitrol

Front 131

juxtaglomerular apparatus

Back 131

area where the late thick ascending limb of the distal tubulr passes between the afferent and efferent arterioles at the vascular pole of the renal corpuscle.

Front 132

Cells with function in the JGA

Back 132

Granule cells-seceret renin
Extraglomerular mesangial cells-continous with those in b.capsule
Macula Densa cells- senses sodium in lumen of nephron at end on tubule.controls gfr and renin.

Front 133

tubular secretion

Back 133

moving substances into lumen from capillaries

Front 134

tubular reabsorption

Back 134

moving substances into capil from lumen.

Front 135

normal GFR

Back 135

125ml/min

Front 136

Renal blood flow

Back 136

1.1L/min

Front 137

two main factors that affect RBF

Back 137

Mean pressure of renal artery vs renal vein
Resistance

Front 138

GFR is set by 3 factors

Back 138

hydraulic permeablity of capillaries, SA of capill, and net filtration pressure.

Front 139

Concept of filtered load

Back 139

GFR * plasma concentration. The filtered load is what is presented to the nephron to handle.

Front 140

autoregulation

Back 140

broad term for a collection of mechanisms thru which renal blood flow and GFR are kept constant across a wide range systemis arterial pressure.

Front 141

why is autoregulation necessary?

Back 141

excretion of salt and water is strongly regulated by GFR. and GFR is strongly regulated by arterial pressure.

Front 142

Mechanisms of autoregulation

Back 142

myogenic response and tubuloglomerular feedback.

Front 143

Myogenic response

Back 143

as MAP goes up, smooth muscle in the walls of the arteriloes are stretched and this induces constriction which induces inc vascular resistance.

Front 144

Tubuloglonerular feedback

Back 144

intrarenal process through which the distal tubules affect GFR. MAcula densa cells responsd to sodium levels in d.tubule.

Front 145

Mechanism of tubuloglomerular feedback

Back 145

high na in the d.tubule release transmitter agents from JGA. these agents loower GFR by constricting afferent arteriole. Also contract glomerular mesangial cells to dec capill SA.

Front 146

Renal clearance equation

Back 146

clearance= urine conc * (volume per unit time/plasma conc of s)

Front 147

In order to provide an accurate measure of GFR a compound must meet the following criteria (5)

Back 147

1. freely filtered
2.not reabsorbed
3.not secreted
4.not synth in tubulues
5.not metab by tubules

Front 148

creatintine meets all the criteria for GFR measurement except

Back 148

it's secreted by tubules in small amt

Front 149

two mechanisms of reabsorption

Back 149

transcellular and paracellular

Front 150

Transcellular reabsorption

Back 150

1.sodium pumped into interstitial space.
2. sodium enters epithelial cells from lumen of tubule
3.there is an electr and osm gradient
4. sodium,anions, and water from interstitium move into peritubular capill

Front 151

major substances reabsorbed thru paracellular reabs

Back 151

urea, potassium, chloride, calcium, magneium.

Front 152

tubular maximum limited system

Back 152

transport mechanism which can reach an upper limit because transporters are saturated. At saturation inc plasma conc does not mean inc excretion.

Front 153

Gradient limited system

Back 153

transport mechanism where limit is reached because of leaky junctions. substances leak back into lumen of tubule.

Front 154

substances that are heavily secreted

Back 154

H, K, anions and foreign chemicals.

Front 155

Tubular secretion requires

Back 155

active transport, usually coupled with sodium

Front 156

Familial Renal Glucosuria

Back 156

abnomality in the Na/glucose co transporter that mediates reabs of glucose in prox tubule.

Front 157

Proximal tubule main role

Back 157

reabsorb most the filtered water and non-waste solutes.

Front 158

total daily intake of water and salt

Back 158

water: 2850ml
salt:8.5g

Front 159

both salt and water

Back 159

are freely filtered and undergo considerable reabsorp but no secretion.

Front 160

four mechanism by which reabsorption of sodium drives reabs of other substances

Back 160

1. Osmolarity gradient
2. reabsorption of organic nutrients by co-transport
3.secretion of hydrogen ion by countertransport
4. reabs of chloride by indirect cotransport.

Front 161

How is Osm not changes in the prox tubule throughout these processes?

Back 161

Prox tubule highly perm to water, iso-osmotic volume reabs,

Front 162

Vasopressin (ADH) stimulates insertion of....

Back 162

aquaporins. When aquaporins are present water reabs is high and urine conc is increased.

Front 163

Urina concetration when there is maximal reabs...

Back 163

can contain less than 1% water. So urine is very hyperosmotic to plasma.

Front 164

Thin ascending vs thick ascending limg in loop

Back 164

thin- uses na/cl co-transporters to move salt
thick-uses diffusion
BOTH IMPERM to water!

Front 165

Descending limb

Back 165

no salt reabs but highly perm to water

Front 166

Distal convuluted tubule

Back 166

uses symport. transport salt out of lumen (like ascending limg) but is imperm to water.