Patho Ii, Exam 2 - Cumulative

Front 1

The kidney is ___% of total body weight and
receives ___% of CO
works with systems in intergrated manner to maintain____

Back 1

0.5%, 20%
homeostasis

Front 2

Total # of Nephrons
the 2 functional components are

Back 2

2.5 million
vascular (blood) and tubular( eventually urine)

Front 3

The 3 basic renal processes

Back 3

1 Glomerular filtration
2 Tubular reabsorption
3 Tubular secretion

Front 4

GFR: ~____l/day
Regulate ____ composition and filter out unwanted substances.
_____is being regulated, NOT _____.

Back 4

180L/day
ECF
ECF , urine

Front 5

Molecules have their own ______ capacities. Anything over this value, the molecules will be...?

Back 5

maximum transport
excreted in the urnine
(ex: glucose spillage)

Front 6

_____ act on different molecules/ions for reabsorption.

Back 6

transporter proteins

Front 7

______ have hight Tm values to preserve nutrients.

Back 7

Amino Acids

Front 8

_____ is absorbed by active transport mechanisms

Back 8

Na

Front 9

_____ is permeable to Na-->ions flow down gradient across membranes.

Back 9

Proximal Tubule

Front 10

Microvilli have a _____ for better absorption.

Back 10

microvilli

Front 11

When Na is transported, ___ is also transported do to an ______. ____ also follows.

Back 11

Cl
electrical gradient
H2O

Front 12

After Na absorption, the fluid left in the tubule is _____.

Back 12

concentrated

Front 13

This section makes final adjustments to urine osmolality, pH and ionic composition

___________controls the reabsorption of water
__________ controls the secretion of potassium

Back 13

Distal Tubule & Collecting Duct
Antidiuretic hormone (ADH)
aldosterone

Front 14

Glucose absorption dependent upon ______ gradient.

Most reabsorbed in _________.

Back 14

Na+
proximal tubule

Front 15

Apical membrane needs __/__ cotransporter. But at the basolateral membrane glucose crosses via ______ which do not need Na

Back 15

Na/Glucose
glucose transporters

Front 16

Product of protein catabolism.
Absorbed in GI tract,
transporters dependent upon Na+ gradient.

Back 16

Amino Acid

Front 17

K+ Reabsorption occurs at _________.
Secreted in __________

Back 17

proximal tubule
distal tubule

Front 18

What are normal K levels?

Back 18

4-5.5
hyper=VF, death
hypo=arrhythmias, paralysis and death

Front 19

K reabsorption is largely _____, follows Na and fluid.
(body keeping what it needs).

Back 19

passive

Front 20

K secretion relies upon _______ of K across basolateral membranes. Passively exits into tubular fluid.
(body getting rid of what it doesn't need)

Back 20

active transport

Front 21

Useful in concentrating urine. Toxic at high levels

Back 21

Urea

Front 22

low protein diet=less ____ and impaired ability to concentrate urine.

Back 22

urea

Front 23

Kidneys ____, ____ and _____ urea. The excretion is increased with an increase in _____ flow. Urea also creates an osmotic gradient.

Back 23

filter, reabsorb and secrete
urinary

Front 24

_____ allows rapid, graded control of urine conc.
and released in response to plasma osmolality and ECF volume (osmoreceptors and baroreceptors).

Back 24

ADH
(if osmo is low, more ADH secreted)

Front 25

ADH increases the permeability of ______ to H2O.

Back 25

Collecting ducts
-helps to produce small amounts of concentrated urine and increases recycling effects

Front 26

Total body water is ___%. It is made up of _____ and ____. _____ can be further broken down into interstitial and intravascular.

Back 26

60
Intracellular (40%) and extracellular (20%).
ECF

Front 27

_____ are substances that dissociate in solution to form charged particles (ions); opposites attract.

Back 27

Electrolytes

Front 28

Cations are ____. Anions are ____.

Back 28

positive
negative

Front 29

Diffusion is?

Back 29

movement of particles down a concentration gradient. (High to low)

Front 30

Osmosis is?

Back 30

movement of H2O across a semi-permeable membrane.
-Particles pull H2O by NUMBER, not size.

Front 31

What is a normal serum osmo?

Back 31

275-295 mOsm/L

Front 32

_______
Lower osmo than intracellular fluid
Ex: Half normal saline
_________
Same osmo as intracellular fluid
Ex: 0.9% saline (normal saline, NS) or lactated Ringer’s solution
________
Higher osmo than intracellular fluid
Ex: 3.0% saline

Back 32

Hypotonic (swollen cell)
Isotonic (normal cell)
Hypertonic (shrink cell)

Front 33

The most important characteristic of body fluid is_____. It protects circulatory volume.

Back 33

homeostasis

Front 34

What are the two mechanisms to protect vascular volume?

Back 34

1. Hemodynamic Alterations
-vasoconstriction and increased HR
2. Na and H2O alterations
-takes hours to be effective

Front 35

The solution to pollution is?

Back 35

dilution

Front 36

We need ____ to dissolve and eliminate metabolic wastes.

Back 36

H2O

Front 37

Water is gained from?

Back 37

-oral intake
-absorbed from GI tract

Front 38

Water is lost from?

Back 38

-kidneys
-GI tract
-Skin, lungs=insensible losses
-Increased BMR
-Increased RR

Front 39

_____ regulates intake. It responds to ECF change in osmo and volume. This is a conscious sensation and emergency response.

Back 39

thirst

Front 40

Polydipsia is?

Back 40

chronic thirst/chronically dry
(diarrhea,vomitting, DM, DI)

Front 41

____ regulates output. It is in response to ECF chnage in osmo and volume. Acute conditions produce a greater change than chronic conditions.

Back 41

ADH

Front 42

_____ regulates movement of fluids at the cell membrane. It controls ___ and ____ osomolality. Also regulates _____ balance.

Back 42

Na
ECF and ICF
acid base

Front 43

Na enters through the _____ tract. It is eliminated via the _____, _____ and ____.

Back 43

GI tract
kidneys, GI tract and skin

Front 44

We require _____ mg/day of Na.

Back 44

500

Front 45

What are hemodynamic and physical factors that affect tubular Na reabsoroption?

Back 45

-medullary blood flow
-renal perfusion pressure
-peritubular capillary starling forces

Front 46

what are hormonal factors that affect tubular Na reabsorption?

Back 46

-RAAS
-atrial natriuretic peptide
-renal prostaglandin synthesis
-renal kinin system

Front 47

Renal ______ activity also affects tubular Na reabsorption.

Back 47

sympathetic nerve

Front 48

What is the principle factor controlling Angiotensin II levels?

Back 48

renin

Front 49

If you have a ____ circulating volume you have increased renin release.

Back 49

decreased
-decreased BP
-decreased NaCl
-decreased renal perfusion pressure

Front 50

Angiotensin II causes _____. It also stimulates thirst and ____ relase by acting upon the _____.

Back 50

-vasoconstriction
-ADH, hypothalamus

Front 51

The macula densa becomes more sensitive to promote?

Back 51

Na reabsorption

Front 52

Aldosterone stimulates ___ reabsorption and ___ excretion by the renal tubule.

Back 52

Na, K

Front 53

____ is important in conserving Na and H2) while preventing massive changes in ____ levels.

Back 53

Aldosterone
K
(indirect negative feedback)

Front 54

ANP promotes ____.

Back 54

natriuresis (loss of sodium)

Front 55

The atrial myocytes synthesize, store and release ANP in response to _____.

Back 55

stretch (baroreceptors)

Front 56

ANP causes renal _____ --> increased blood flow and and increased ___. This causes more Na to reach macula densa and more Na to be excreted.

Back 56

vasodilation
GFR
(may inhibit renin and generally opposes effects of angiotensin II)

Front 57

Hyponatremia is defined as Na less than ____. It can also be ____ from increased H2O.

Back 57

135
dilutional

Front 58

Manifestations of hyponatermia are?

Back 58

-BRAIN AND CNS most affected-->headache, lethargy, sz, coma
-cramps, weakness

Front 59

hypernatremia is defined as Na greater than?

Back 59

145 meq/L

Front 60

Hypernatremia can occur from increased serum ____ or decreased ____.

Back 60

Na
H2O

Front 61

Manifestations are due to water loss and cellular _____. The manifestations are?

Back 61

-thirst
-decreased UO
-decrease reflexes
-AGITATION, HEADACHE, RESTLESSNESS, SZ, COMA

Front 62

K is mainly _____. K intakes come from ____ sources and is lost through the _____.

Back 62

intracellular
dietary
kidneys

Front 63

The function of K is to? It is regulated by?

Back 63

-regulate electrical membrane potentials controlling excitability of the skeletal, cardiac and smooth muscle tissues.
-Aldosterone

Front 64

Hypokalemia is K less than ____. It can occur from decreased ____, increased losses or redistribution from ____ to ____.

Back 64

3.5 meq/l
intake
ECF to ICF

Front 65

Manifestations of hypokalemia are?

Back 65

-N/V/D, weakness, fatigue, cramps, confusion, depression, neruomuscular excitability
-CARDIAC RHYTHM CHANGES
(max replacement: 20meq over 1 hr in large bore)

Front 66

Hyperkalemia is K greater than? This occurs from increase ____, decreased _____ or redistribution.

Back 66

5 meq
intake, elimination

Front 67

The manifestations of hyperkalemia are?

Back 67

-CHANGES IN EKG
- can cause periodic paralysis

Front 68

_____ balance is important in the renal and respiratory systems. Biochemical processes must occur within an optimal pH so we must prevent _____ or _____.

Back 68

Acid-Base
acidosis or alkalosis

Front 69

Lungs are responsible for excreting ____. While kidneys excrete ______ agents

Back 69

CO2
non volatile (HCO3)

Front 70

How do you gain H ions?

Back 70

-CO2 in blood
-non volatile acids from metabolism
-loss of HCO3 (GI or Urine)
*loss of HCO3 is like gaining H

Front 71

How do you lose H ions?

Back 71

-use H in metabolism
-Loss of H in vomit or urine
-Hyperventilation
*loss of H is like gaining HCO3

Front 72

HCO3 is the main physiological _____.

Back 72

buffer

Front 73

HCO3 is filtered and then practically all ______ under normal conditions.

Back 73

reabsorbed
When gains=losses you maintain homeostatsis

Front 74

The secreted H combines with filtered HCO3 in tubule to form _____ and ____.

Back 74

CO2 and H2O

Front 75

Normal Urine pH?

Back 75

6.0

Front 76

Blood pH?

Back 76

7.4

Front 77

Blood HCO3?

Back 77

24 mM

Front 78

Blood PCO2?

Back 78

40 mmHg

Front 79

Plasma osmolality?

Back 79

285 mOsm/kg water

Front 80

Urine osmolality?

Back 80

600 mOsm/kg water

Front 81

Acid base disorders can be _____ or _____ in nature.
_____ can be chronic or acute but _____ is always chronic.

Back 81

respiratory or metabolic
respiratory
metabolic (marked changed in HCO3)

Front 82

________ are homeostatic mechanisms that kick in to correct pH causes by a dysfunctional primary or initiating event. The adjust pH towards ____ but do not correct the underlying problem.

Back 82

compensatory mechanisms
7.4

Front 83

The respiratory system compensates for pH by increasing or decreasing ______. The kidneys compensate by conserving ______ or _____ ions.

Back 83

ventilation
HCO3 or H ions

Front 84

Compensatory mechanisms require mechanisms different than those that caused the primary disorder, for example?

Back 84

lungs don't compensate for respiratory acidosis from respiratory failure, the kidneys do.

Front 85

What are the labs to assess GFR?

Back 85

-blood urea nitrogen
-serum creatinine
-endogenous creatinine clearance

Front 86

What are the labs to assess renal tubular function and integrity?

Back 86

-urine concentrating ability
-protenuria
-urinary sodium excretion

Front 87

Normal BUN value?

Back 87

10-20 mg/dL
*the higher, the worse the renal fxn

Front 88

BUN Metabolism: major nitrogenous end product of protein and amino acid catabolism. Produced by the _____ and distributed throughout the ICF and ECF. In the kidneys almost all ____ is filtered out of blood by glomerular fxn. Some urea is reabsorbed with water but most excreted in urine.

Back 88

liver
urea

Front 89

Decreased BUN

Back 89

-fluid excess
-SIADH
-Liver failure
-malnutrition
-anabolic steroid use
-pregnancy (dilutional)

Front 90

Increased BUN

Back 90

-dehydration
-high protein diet
-GI bleed
-impaired renal fxn
-CHF
-Shock
-MI
-excess protein catobolism

Front 91

What are normal creatinine levels in men and women?

Back 91

men: 0.8-1.3
women: 0.6-1.0

Front 92

Creatinine is a nonketone waste product of creatinine phosphate metabolism by skeletal ______tissue. Proportional to muscle mass

Back 92

muscle

Front 93

Decreased Creatinine

Back 93

-elderly
-persons with small stature
-inadequate dietary protein
-muscle atrophy

Front 94

Increased Creatinine (loss of more than 50% nephrons)

Back 94

-impaired renal fxn
-chronic nephritis
-urinary tract obstruction
-muscle diseases
-CHF
-Shock

Front 95

What is a normal creatinine clearance test?

Back 95

110-115 ml/min

Front 96

The total amount of creatinine excreted in urine in a 24 hour period is called?

Back 96

creatinine clearance

Front 97

Creatinine is excreted entirely by the _____ and is directly _____ to the GFR.

Back 97

kidneys
proportional

Front 98

During renal failure if there is a decreased GFR, secretion of creatinine will _____. But there will be an eventual reduction in excretion

Back 98

increase

Front 99

What is a normal urine specific gravity?

Back 99

1.003-1.030

Front 100

What are the 3 factors that can influence urine concentrating gradient?

Back 100

1. decreased Na absorption: chronic polyuria, altered Na reabsorption
2. Lack of ADH: hypokalemia, hypercalcemia
3. Increased Medullary blood flow: hypokalemia, hypercalcemia, thyroid hormone.

Front 101

Proteinuria is described as?

Back 101

protein in the urine

Front 102

Transient proteinuria resolves with treatment of _____ condition.

Back 102

underlying
-fever, CHF, sz, exercise

Front 103

Orthostatic proteinuria is not associated with deteriorating ____ fxn. It is defined as increased protein excretion in the ____ position and normal protein excretion in the _____ position.

Back 103

renal
upright
supine

Front 104

Persistent proteinuria indicates significant renal disease.
Glomerular: alterations in _______ filtration
Tubular: impainrment of _______ reabsorption.

Back 104

-basement membrane
-tubular

Front 105

What is the normal Na urinary excretion?

Back 105

<=40 meq/L

Front 106

Increased Na excretion can be from?

Back 106

-damage to renal tubules
-drug induced diuresis

Front 107

Decreased Na excretion can be from?

Back 107

-hypovolemia

Front 108

Renal failure is defined as?

Back 108

failure of the kidneys to remove metabolic end products from the blood, regulate fluid, electrolytes and pH balances of the ECF. Can be acute or chronic

Front 109

Acute renal failure?

Back 109

abrupt in onset usually reversible with early treatment

Front 110

Chronic renal failure?

Back 110

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

Front 111

What are the three types of kidney failure?

Back 111

1. Pre-renal
2. Intra-renal (intrinsic)
3. Post-renal

Front 112

Pre-renal failure is from _____ to the kidneys.

Back 112

decreased blood flow

Front 113

Intra-renal failure is from disorders that disrupt the _____ of the kidney

Back 113

structures

Front 114

Post-renal failure is from disorders that impair ______ from the kidneys.

Back 114

urine outflow

Front 115

Prerenal failure causes a decrease in RBF which leads to decreased ____ and ____. This leads to decreased O2 delivery to the cells and cell _____. The decreased GFR allows for accumulation of toxins in the blood.

Back 115

-GFR and UO
-death

Front 116

Accumulation of nitrogenous waste products in blood is known as?

Back 116

azotemia

Front 117

Prerenal azotemia leads to and increased ____ and ____.

Back 117

BUN and Creatinine
*BUN greater than 15

Front 118

What can prerenal azotemia be caused by?

Back 118

-inadequate blood supply to the kidneys
-decreased CO
-hemorrhage
-volume depletion
-shock
-CHF
-anesthetic drug induced (decreases perfusion pressure)

Front 119

If prerenal azotemia is sustained it can lead to?

Back 119

acute tubular necrosis

Front 120

Intrarenal azotemia is from damage to kidney structures. Injury to the tubules is most commonly _____, _____ drrugs, or _____.

Back 120

-ischemia
-toxic drugs
-obstruction

Front 121

The three types of intrarenal disorders are?

Back 121

1. glomerular disorders (5%)
2. Interstitial nephritis (10%)
-inflammatory respons
3. Acute Tubular Necrosos (85%)
-ischemia, nephrotoxic drugs,dyes, myogloburia

Front 122

In intrrenal azotemia there is usually an initial decrease in renal blood flow leading to ____ of the renal tubular cells.

Back 122

ischemia

Front 123

What are the manifestation of intrarenal?

Back 123

-profound decrease in GFR leading to...
increase BUN and creatinine
retention of Na and H2O
acidosis
hyperkalemia

Front 124

Intrarenal BUN is?

Back 124

normal or less than 15
*irreversible renal necrosis can occur if ischemia is severe or prolonged

Front 125

Acute tubular necrosis (ATN) is defined as destruction of tubular _____ cells which leads to _____ tubular function.

Back 125

-epithelial cells
-decreased

Front 126

ATN is the most common cause of ______ renal failure.

Back 126

-intrinsic renal failure
from: ischemia, nephrotoxic drugs, tubular obsruction, toxins from infectious agents
-usually irreversible

Front 127

What are the three phases of ATN?

Back 127

1. Onset/Initiating (hours/days from insult)
2. Maintenace Phase
3. Recovery Phase

Front 128

What happens during the maintenance phase of ATN.

Back 128

-decreased GFR
-retention of metabolites (urea, K, sulfate, Cr)
-decreased UO
-generalized and pulm edema
-metabolic acidosis
-Oliguric vs. nonoliguric (<0.5ml/kg/hr)

Front 129

What happens during the recovery phase of ATN?

Back 129

-repair of renal tissues, gradual improvement in UO, BUN and Cr.

Front 130

Postrenal azotemia is from ______ of urine outflow from kidneys. It can be in the ureters (calculi, strictures), Bladder (tumor, neurogenic bladder) or urethra (BPH or strictures).

Back 130

obstruction

Front 131

Increased resistnace to urine flow can caus bac up into the kidneys, leading to ______.

Back 131

hydronephrosis

Front 132

BUN:Cr is?

Back 132

greater than 15

Front 133

what are the two most damaging effects of obstruction?

Back 133

1. stasis of urine, bacteria ascend urethra which leads to infection and stone formation
2.development of back pressure which leads to decreased renal blood flow and destroys kidney tissue.

Front 134

______ is distention of the kidney with ____ caused by backward pressure on the kidney when the flow of urine is obstructed.

Back 134

hydronephrosis
urine

Front 135

_____ is obstruction in distal ureter which leads to increased pressure above it and _____ of the ureter.

Back 135

hydoureter
ureter

Front 136

Manifestions of Obstruction are _____ & signs of ______

Back 136

Pain & signs of UTI
-Pain is usually why pt. seeks medical care. It results from distension of bladder, collecting system, renal capsule.

Front 137

Renal Colic Pain is more common with acute/chronic obstruction?

Back 137

Acute

Front 138

Dull Flank Pain is more common with acute/chronic obstruction of renal pelvis/upper ureter?

Back 138

Chronic

Front 139

Nephrolithiasis is formed of _______ structures-material the kidney normally excretes in urine.

Back 139

Crystalline structures

Front 140

Nephrolithiasis is uni/bi-lateral?

Back 140

unilateral

Front 141

In Nephrolithiasis, ______ is saturated with stone components- Calcium salts, Mg-ammonium phosphate, cystine, uric acid

Back 141

Urine

Front 142

In Nephrolithiasis, organic materials are produced by ______ cells and the lack of ______ inhibit crystallization

Back 142

epithelial cells & proteins

Front 143

Stones are associated with ______ secondary to hyperparathyroidism, vit D intoxication, diffuse bone disease (immobility)

Back 143

Hypercalcemia

Front 144

Stones are composed of calcium ____ & calcium ____.

Back 144

oxalate & calcium phosphate

Front 145

Stones are also related to renal tubular ____

Back 145

acidsis

Front 146

Treatment of stones depends on ____ & ____

Back 146

type and cause

Front 147

Stones ____ mm in size usually pass spontaneously

Back 147

<5mm

Front 148

Three tx to help small stones to pass spontaneously

Back 148

increase water consumption
physical activity can move a stone
NSAIDS or opioids for pain control

Front 149

When should a stone be removed surgically?

Back 149

Infection, blockage, or a risk of kidney damage

Front 150

If a stone is caused by infection is should first be treated with?

Back 150

antibiotics

Front 151

Stones ____ mm require some intervention, especially if stuck, causing obstruction or infection is present

Back 151

>6mm

Front 152

Most common method for large stone removal?

Back 152

Extracorporeal Shock Wave Lithotripsy (ESWL)
-Most common method,does not involve a surgical operation. Ultrasound waves are used to break the stones into crystals small enough to be passed in the urine. The shock waves do not hurt, although some people feel some discomfort at the time of the procedure and shortly afterwards.

Front 153

If lodged in the ureter, a _____ can be passed up through the urethra and bladder, known as Ureterscopic Stone removal

Back 153

Cytoscope
-The stone is "caught" and removed, or shattered into tiny pieces with a shock wave. This procedure is usually done under a general anesthetic.

Front 154

If ESWL doesn't work or a stone is particularly large, it may be surgically removed under general anesthetic with a ____ procedure.

Back 154

Percutaneous Nephrolithotomy (PCNL)
-The surgeon makes a small cut in the back and uses a nephroscope to pull the stone out or break it up with shock waves.

Front 155

Acute/Chronic renal failure is progressive, irreversible destruction of nephrons?

Back 155

Chronic

Front 156

Chronic renal failure requires ___ & ____

Back 156

dialysis and kidney transplants

Front 157

Causes of Chronic renal failure (3)?

Back 157

Diabetes, hypertension, glomerulonephritis
-s/s's are not evident until dz is advanced

Front 158

One primary presentation of diabetes:
-excretion of glucose with resulting excessive ____ excretion -> early influence on kidney function

Back 158

water

Front 159

Pathology of diabetic nephropathy early events (2):
-thinning/thickening of the glomerular basement membrane?
-thinning/thickening of efferent and afferent arterioles?

Back 159

Thickening & Thickening

Front 160

Pathology of diabetic nephropathy is often superimposed by ____ or ____ damage which can lead to progression of thinning/thickening of arteries and arterioles; scarring and fibrosis

Back 160

hypertensive or infective
-progression of thickening of arteries and arterioles
-scarring and fibrosis

Front 161

Stages of Chronic Renal failure:
Mild renal impairment:
GFR ____; Symptoms of uraemia ___; Serum biochemical degrangement ___

Back 161

GFR >90
Symptoms of uraemia: none
Serum biochemical degrangement: none
comment: not clearly progressive

Front 162

Stages of Chronic Renal failure:
Mild:
GFR ____; Symptoms of uraemia ___; Serum biochemical degrangement ___

Back 162

GFR 60-80
Symptoms of uraemia: none
Serum biochemical degrangement: subtle
comment: early bone disease

Front 163

Stages of Chronic Renal failure:
Moderate:
GFR ____; Symptoms of uraemia ___; Serum biochemical degrangement ___

Back 163

GFR 30-59
Symptoms of uraemia: mild
Serum biochemical degrangement: mild
comment: anemia starts

Front 164

Stages of Chronic Renal failure:
Severe:
GFR ____; Symptoms of uraemia ___; Serum biochemical degrangement ___

Back 164

GFR 15-29
Symptoms of uraemia: moderate
Serum biochemical degrangement: moderate
comment: Sodium & water retention evident

Front 165

Stages of Chronic Renal failure:
End-Stage:
GFR ____; Symptoms of uraemia ___; Serum biochemical degrangement ___

Back 165

GFR <15
Symptoms of uraemia: severe
Serum biochemical degrangement: Severe
comment: Dialysis or transplantation necessary

Front 166

Signs/Symptoms of Renal Failure:
-fluid & electrolyte imbalance
-_____ in blood levels of metabolic acids & other small, diffusible particles (e.g., urea)?

Back 166

Increase

Front 167

Signs of uremic encephalopathy _________

Back 167

Lethargy, decreased alertness, loss of recent memory, delirium, coma, seizures, asterixis, muscle twitching and tremulousness

Front 168

Signs of neuropathy ______

Back 168

Restless leg syndrome, paresthesias, muscle weakness and paralysis

Front 169

Signs/Symptoms of Renal Failure:
-Anemia ____
-Hyperparathyroidism ____
-High concentration of metabolic end products in body fluids ___

Back 169

-Pale, sallow complexion
-Pruritus
-Uremic frost and odor of urine on skin & breath

Front 170

Consequences of Renal Failure: Cardiovascular
-Activation of renin-angiotensin mechanism,
increased vascular volume and failure to
produce vasopressor substances leads to ____

Back 170

Hypertension

Front 171

Consequences of Renal Failure: Cardiovascular
-Fluid retention and hypoalbuminemia leads to ___

Back 171

Edema

Front 172

Consequences of Renal Failure: Cardiovascular
-Excess extracellular fluid volume, left ventricular hypertrophy and anemia leads to ___

Back 172

CHF: pulmonary edema

Front 173

Consequences of Renal Failure: Body Fluids
-Decreased ability to synthesize ammonia
and conserve biocarbonate leads to ___

Back 173

Metabolic acidosis

Front 174

Consequences of Renal Failure: Body Fluids
-Inability to excrete K+ leads to ___

Back 174

Hyperkalemia

Front 175

Consequences of Renal Failure: Body Fluids
-Inability to regulate Na+ excretion leads to ___

Back 175

-Sodium wasting or Na+ retention

Front 176

Consequences of Renal Failure: Body Fluids
-Impaired ability to excrete phosphate leads to ___

Back 176

Hyperphosphatemia, Hypocalcemia

Front 177

Consequences of Renal Failure: Body Fluids
-Hyperphosphatemia & inability to activate vitamin D leads to ___

Back 177

Hyperparathyroidism, Osteodystrophy

Front 178

Consequences of Renal Failure: Hematologic
-Impaired synthesis of erythropoietin & effects of uremia leads to ___

Back 178

Anemia

Front 179

Consequences of Renal Failure: Hematologic
-Impaired platelet function leads to ___

Back 179

bleeding tendencies

Front 180

Hematologic consequences arise because the kidney fails to perfom the usual excretory, regulatory, metabolic and ____ functions

Back 180

biosynthetic

Front 181

Chronic renal failure treatment:
Treat underlying causes and contributing factors
(3)

Back 181

-Control blood glucose (strict/tight controlA1C<7)
-Control high blood pressure (ACEI, BB, CCB)
-Diet (protien restriction-0.6g/kg/d)

Front 182

Chronic renal failure treatment:
Slow/speed progression of disease?

Back 182

Slow

Front 183

Chronic renal failure treatment:
Treat complications of disease (4)

Back 183

Fluid retention (CPD vs HD)
-Anemia (Hgb>12)
-Bone disease
-Acidosis

Front 184

Chronic renal failure treatment:
Replace lost kidney function via ___ & ___

Back 184

Dialysis & transplant

Front 185

Stages of CRF are associated with a progressive decrease of ___?

Back 185

GFR

Front 186

Chronic renal failure is a ____ chronic disease

Back 186

progressive
-Different primary diseases can cause CRF Diabetic nephropathy
-Symptoms can vary, dependant upon primary disease and stage of CRF
-Consequences are complex, based on function of the kidney
-May involve multiple organ systems

Front 187

Two factors to consider with Hypertension ___ & ___

Back 187

extra cellular fluid volume (ECF) & degree of vasoconstriction

Front 188

it is important to maintain ___ blood pressure with hypertension

Back 188

normal BP

Front 189

___ Hypertension is a specific underlying cause cannot be defined & it has No identified pathology in any organ system

Back 189

Essential

Front 190

___ Hypertension is High blood pressure as the result of another condition.

Back 190

Secondary

Front 191

Secondary HTN
the Kidney: Renal parenchymal disease & Renal artery stenosis
two possible mechanisms: ___ & ___

Back 191

-activation of the renin-angiotensin system?
-antihypertensive organ?

Front 192

FYI: Management of Hypertension: Proper examination of persistence and causes
-urine and plasma examination
-examination of lifestyle factors
->detecting stage and type of hypertension

Back 192

Management of HTN: physiological targets

Front 193

Hypertension TX:
-drugs that
-reduce ECF volume ___ (3)
_reduce heart force
-reduce vascular resistance (2)

Back 193

drugs that
-reduce ECF Volume (diuretics, water-, sodium excretion)
-reduce heart force (b-Blocker)
-reduce vascular resistance (ACE inhibitors, general vasodilating drugs)

Front 194

Renal diseases can produce ___

Back 194

hypertension

Front 195

Damages to the kidney by hypertension can cause ___

Back 195

renal diseases

Front 196

Uremic Syndrome
-A variety of signs and symptoms that reflect severity of renal disease
-Include but not limited to ____

Back 196

-N/V, anorexia, pruritis, anemia, fatigue
-Correlates to BUN

Front 197

Renal Osteodystrophy
-Component of hyperparathyroidism and decraese in Vit. D synthesis which leads to ___ ?
-Bone resorption & demineralization over time

Back 197

hypocalcemia

Front 198

Anemia
d/t decreased ____
-Bone marrow replaced with fibrous tissue (PTH)
-Usually tx w/epoetin to maintain HCT ___-___%
-Avoidance of transfusions, d/t ___

Back 198

erythropoietin
~36-40%
-antigen sensitization

Front 199

Bleeding
-test ___as an indicator
-Cryoprecipitate, DDAVP to increase VIII & decrease BT
Act within <___ hour

Back 199

bleeding time
- <1 hour

Front 200

Neurologic
-Mild thought process impairment to obtunded responses
-___ and ___ neuropathy, paresthesias/hyperesthesias, LE weakness

Back 200

Motor & Sensory

Front 201

Cardiac
HTN, CHF, CAD, CVD, ___, volume status, uremic pericarditis

Back 201

dysrhythmias

Front 202

Anesthetics: treat ARF & CRF ___

Back 202

similarly

Front 203

Never give ____ in renal pt

Back 203

Hespan

Front 204

Renal pt should have ___ before elective surgery

Back 204

HD

Front 205

Anesthetic considerations:
Cryoprecipitate or ___

Back 205

desmopressin

Front 206

Goals of Anesthesia in Renal pt.: (3)
Preservation ___
Maintain ___
Minimize ___

Back 206

-Preservation of renal function
-Maintain adequate intravascular fluid volume
-Minimize drug-induced cardiovascular depression

Front 207

Preoperative management:
-Concomitant drug therapy
-Blood volume status
-___ management
-Drug induced CV depression
·Dialysis
·Serum potassium <___ Meq/L on DOS
·Cardiac evaluation: EKG, stress, Echo

Back 207

Glucose
<5.5

Front 208

Preop Labwork to include: (4)

Back 208

CBC
Chem 7 or 13
Blood glucose (recent fingerstick)
Coagulation studies

Front 209

Preop management:
Continue antihypertensive drug therapy except ___

Back 209

ACEi

Front 210

Intraop Mngmt:
Use medications that are not cleared by the kidneys
examples ___

Back 210

Propofol, etomidate, succinylcholine (K), cisatracurium, atracurium, isoflurane, desflurane

Front 211

Patients with diabetes or uremia may exhibit decrease/increase gastric emptying

Back 211

decrease

Front 212

Induction agents ___
Action Partially Terminated by Renal Excretion

Back 212

Barbituates

Front 213

Muscle relaxants ___
Action Partially Terminated by Renal Excretion

Back 213

Pancuronium, vecuronium, rocuronium

Front 214

Muscle relaxants ___
Action Terminated by Renal Excretion

Back 214

Gallamine, metocurine

Front 215

Cholinesterase inhibitors ___
Action partially Terminated by Renal Excretion

Back 215

Neostigmine, edrophonium

Front 216

Cardiovascular drugs ___
Action terminated by renal excretion

Back 216

digoxin, inotropes

Front 217

Cardiovascular drugs ___
Action partially terminated by renal excretion

Back 217

Atropine, glycopyrrolate, milrinone, hydralazine

Front 218

Antimicrobials ___
Action terminated by renal excretion

Back 218

Aminoglycosides, vancomycin, cephalosporins, penicillin

Front 219

Antimicrobials ___
Action partially terminated by renal excretion

Back 219

sulfonamides

Front 220

Renal pt. responds as if they are ___

Back 220

hypovolemic

Front 221

Medications may have a shortened/exaggerated effect on CNS

Back 221

exaggerated

Front 222

Due to decrease/increase in protein binding, duration of action of drugs is prolonged

Back 222

decreased

Front 223

___ is avoided d/t seizures

Back 223

meperidine

Front 224

___ avoided d/t FL nephrotoxicity & compound A

Back 224

Sevo

Front 225

IVFs __%NS
-no NPO loss replacement

Back 225

0.9%NS

Front 226

Replace intra-op EBL with ___

Back 226

blood

Front 227

Prone to ___ & ___ injuries

Back 227

infection & nerve injuries

Front 228

Using N2O increases/decreases need for muscle relaxants & narcotic need

Back 228

decreases

Front 229

Muscle relaxants: depolarizing or non-depol?

Back 229

non-depol

Front 230

___, ___, & ___ are non renal dependent

Back 230

Atr, Cis, mIv

Front 231

___ is the metabolite of ATr., Cis,. which causes CNS excitability

Back 231

Laudanosine

Front 232

Use ___ which are short acting to avoid accumulation of metabolites

Back 232

opioids

Front 233

Fluid management: Avoid ___ & ___ containing fluids;
Avoid ___ & ___ diuretics
Boluses: ___-___ml 0.9%NS
CRF/HD pt: replace IO losses with ___ or ___

Back 233

Avoid LR, K+ containing fluids
Avoid osmotic & tubular diuretics
Boluses: 250-500cc 0.9%NS
CFR/HD patients: replace IO losses with NS or Albumin

Front 234

___ blocks for graft/fistula placement

Back 234

brachial plexus

Front 235

with ___ anesthesia, r/o LA toxicity, coag status, metabolic acidosis and seizure threshold

Back 235

central neuroaxial anesthesia

Front 236

-Monitor for skeletal muscle weakness after ___ of muscle relaxants
-Monitor for respiratory depression after ___ use
-Monitor EKG for ___ changes
-Keep patient on O2 especially if ___

Back 236

Reversal
opioids
Hyperkalemic
anemic

Front 237

Transplant Surgery
close monitoring of BP
Maintence of ___/CVP
Anti rejection drugs/steroids/diuretics

Back 237

euvolemia

Front 238

Acute Rejection requires

Back 238

removal/DIC

Front 239

4 things that happen w/ Release of arterial anastomotic clamp

Back 239

Releases K+ containing effluent
Cardiac implications  arrest
Addition of intravascular space
Release of vasodilators in donor kidney

Front 240

FYI: Transplant surgery considerations
Comorbidities-HTN, DM, CVD
Side effects of drugs/nephrotoxicity
Renal function/tests
Volume status
Maintain renal blood flow

Back 240

fyi

Front 241

BPH is enlargement of the ___, usually non-malignant

Back 241

prostate

Front 242

Treatment of BPH is ___

Back 242

TURP

Front 243

Introp concerns w/ TURP

Back 243

blood loss masked by irrigating fluids

Front 244

TURP syndrome- intra/extra-vascular volume shifts/solutes?

Back 244

intravascular

Front 245

Absorption of glycine (nonconductive fluid) = ___ change when under regional anesth.

Back 245

neurologic status

Front 246

Signs and Symptoms of Transurethral Resection of the Prostate Syndrome
Cardiovascular: Hypertension, reflex bradycardia, pulmonary edema, cardiovascular collapse Hypotension ECG changes (wide QRS, elevated St segments, ventricular arrhythmias)
Cause?

Back 246

Rapid fluid absorption(reflex bradycardia may be secondary to hypertension or increased ICP) Third spacing secondary to hyponatremia and hypo-osmolality; cardiovascular collapse Hyponatremia

Front 247

Signs and Symptoms of Transurethral Resection of the Prostate Syndrome
Respiratory: Tachypnea, oxygen desaturation, Cheyne-Stokes breathing
Cause?

Back 247

Pulmonary edema

Front 248

Signs and Symptoms of Transurethral Resection of the Prostate Syndrome
Neurologic: Nausea, restlessness, visual disturbances, confusion, somnolence, seizures, coma, death
Cause?

Back 248

Hyponatremia and hypo-osmolality causing cerebral edema and increased ICP, hyperglycinemia (inhibitory neurotransmitter, potentiates NMDA receptor activity), hyperammonemia

Front 249

Signs and Symptoms of Transurethral Resection of the Prostate Syndrome
Hematologic: Disseminated intravascular hemolysis
Cause?

Back 249

Hyponatremia and hypo-osmolality

Front 250

Signs and Symptoms of Transurethral Resection of the Prostate Syndrome
Renal: Renal failure
Cause?

Back 250

Hypotension, hyperoxaluria (metabolite of glycine)

Front 251

Signs and Symptoms of Transurethral Resection of the Prostate Syndrome
Metabolic: Acidosis
other: visual disturbances
Causes?

Back 251

Deamination of glycine to glyoxylic acid NH3
increase in Glycine, Usually resolves in 24h

Front 252

The ___ is a key component of fluid, electrolyte, neurohormonal balancing mechanisms

Back 252

renal system

Front 253

5 steps in prevention of ARF ___

Back 253

maintenance of blood flow
avoidance of nephrotoxic drugs
Tx is supportive
Close regulation of HTN
Anesthetic interventions that preserve renal function