Renal Assessment Flashcards
(201 cards)
1
Q
What is the role of antidiuretic hormone (ADH) in fluid and volume homeostasis?
A
ADH increases water and Na+ retention
2
Q
What percentage of total body water (TBW) is water? What factors affect this composition?
A
~60%. TBW varies with age, gender and body fat % (higher muscle will lead to higher water)
3
Q
Where is the fluid outside of cells located?
A
Extracellular fluid (ECF) (includes ISF and Plasma)
4
Q
Which fluid compartement is more immediately altered by kidneys? ICF or ECF?
A
ECF
5
Q
What regulates the majority of osmolar homeostasis? How is osmolar homeostasis maintained? (What does body do to improve fluid volume)
A
Osmlolar homeostasis mainly mediated by osmolality-sensors in anterior hypothalamus. These sensors stimulate thirst and cause pituitary release of ADH.
The cardiac atria release ANP which acts on kidneys to increase sodium and H20 excretion.
6
Q
How is volume homeostasis regulated?
A
Volume homeostasis is maintained by juxtaglomerular apparatus.
7
Q
What does a decrease in volume at the juxtaglomerular apparatus (JGA) trigger?
A
Renin-Angiotensinogen-Aldosterone system (RAAS) for Na+/H2O reabsorption
8
Q
What is the normal range for sodium?
A
135-145mEq/L
9
Q
What levels of sodium require correction prior to elective surgery?
A
sodium levels ≤125 or ≥155
10
Q
What are the potential causes of hyponatremia in the Hypovolemic category?
A
From ppt notes section: Na+/H20 loss (diuretics, gi loss, burns, trauma)
Full list:
Renal losses: Mineralcorticoid deficiency, salt-losing nephritis, renal tubular acidosis, metabolic alkalosis, ketonuria, osmotic diuresis.
Extrarenal losses: vomiting, diarrhea, 3rd space lossed, burns, pancreatitis, muscle trauma
11
Q
What are the potential causes of hyponatremia in the Euvolemic category?
A
Salt restriction, endocrine related -Hypothyroid, SIADH, gluccocorticoid deficiency, high sympathetic drive.
12
Q
What are the potential causes of hyponatremia in the Hypervolemic category?
A
ARF/CKD, heart failure, nephrotic syndrome, cirrhosis
13
Q
What percentage of hospitalized patients are hyponatremic?
A
15%
14
Q
What is a contributing factor to hyponatremia in hospitalized patients?
A
Over fluid-resuscitation and increased endogenous vasopressin
15
Q
Treatment of hyponatremia involves treating the underlying conditions. What are some common methods of correcting low sodium
A
electrolyte drinks, normal saline, diuretics (for dilutional hyponatremia). If ineffective hypertonic saline can be used.
16
Q
What are the signs and symptoms of Na level 120-130 mEq/L
A
17
Q
What are the signs and symptoms of Hyponatremia 130-135 mEq/L
A
18
Q
What are the signs and symptoms of Na level <120 mEq/L
A
19
Q
What are the two initial signs of hyponatremia
A
hyponatremia starts with headache and confusion
20
Q
What is the dose for 3% NaCl?
A
80 mL/hr over 15 hours.
21
Q
How often should Na+ level be checked while treating hyponatremia?
A
q 4 hr
22
Q
What is the recommended rate for Na+ correction in hyponatremia?
A
Na+ should not exceed 1.5 mEq/L/hr
23
Q
Why should Na+ correction be done slowly in hyponatremia treatment?
A
Rapid correction (>6 mEqL in 24 hr) can cause Osmotic Demyelination Syndrome (often leading to permanent neurological damage)
24
Q
Hyponatremic seizures are a medical emergency that can lead to what?
A
neurological damage
25
What is the initial treatment for hyponatremic seizures?
3-5ml/kg of 3% over 20 min until seizures resolve.
26
What is DI often associated with?
Loss of dilute urine
27
What are common causes of hypernatremia?
Excessive evaporation, Poor oral intake, Overcorrection of hyponatremia, DI, GI losses, Excessive sodium bicarb (when treating acidosis)
28
What are the diagnostic algorithms for different types of electrolyte imbalances?
Hypo: Renal/GI loss
Euvo: DI/insensible loss (skin, respiratory)
Hyper: ↑Na+ intake (IV)/aldosteronism/Cushings
29
What are the causes of hypernatremia?
IV intake, hyperaldosteronism, Cushings
30
What are the symptoms of Hypernatremia?
Orthostasis, Restlessness, Lethargy, Tremor/Muscle twitching/spasticity, Seizures, Death
31
What is the initial step in treating Hypernatremia?
Identify root cause, Assess volume status (VS, UO, Turgor, CVP)
32
What treatment is recommended for Hypovolemic Hypernatremia?
Normal saline
33
What treatment is recommended for Euvolemic Hypernatremia?
Water replacement (PO or D5W)
34
What treatment is recommended for Hypervolemic Hypernatremia?
Diuretics
35
What is the target Na+ reduction rate to avoid cerebral edema, seizures, and neurologic damage in Hypernatremia?
≤0.5 mmol/L/hr, and ≤ 10 mmol/L per day
36
Normal Potassium Level?
3.5-5 mmol/L
37
Percentage of Potassium in ECF?
< 1.5%
38
What does Serum K+ level reflect?
Transmembrane K+ regulation
39
Effect of Aldosterone on K+?
Causes distal nephron to secrete K+ and reabsorb Na+
40
What happens to K+ excretion in renal failure?
Renal excretion of K+ declines and excretion of K+ shifts towards GI system.
41
What are the 3 major categories of causes for hypokalemia?
Renal loss, GI loss, Transcellular shift
42
What are common causes of hypokalemia related to renal loss?
Diuretics, Hyperaldosteronism
43
What are common causes of hypokalemia related to GI loss?
N/V/D, malabsorption
44
What are some common causes of hypokalemia related to intracellular shift?
Alkalosis, β-Ag’s, Insulin
45
What medical condition can lead to hypokalemia due to osmotic diuresis?
DKA
46
Which medication in blood pressure management can cause hypokalemia?
HCTZ
47
What dietary item in excess can lead to hypokalemia?
Excessive licorice
48
What are the symptoms of hypokalemia?
Generally cardiac (dysrhythmias, U wave) and neuromuscular (muscle weakness/cramps and ileus)
49
How can hypokalemia be treated?
Treatment of underlying cause.
Potassium PO > IV (CVC) may take days to correct.
50
What is the IV dose range for IV potassium? How much will IV potassium increase serum K+ levels?
Generally 10-20meq/L/hr IV.
EAch 10 mEq IV K+ will increase serum K+ by 0.1mmol/L
51
What should be avoided in the treatment of hypokalemia?
Avoic excessive insulin, β-agonists (decrease speed of Na+/K+ pump), bicarb, hyperventilation, diuretics
52
What are some symptoms of hyperkalemia?
Chronic may be minimally symptomatic (Malaise, GI upset)
Skeletal muscle paralysis, cardiac dysrhythmias, decrease fine motor function
53
What are some EKG changes associated with hyperkalemia?
Peaked T wave, P wave disappearance, prolonged QRS complex, sine waves, asystole
54
What can cause hyperkalemia?
Renal failure, hypoaldosteronism, drugs inhibiting RAAS/K+ excretion, Succinylcholine, Acidosis, cell death, massive blood transfusion.
55
How does succinylcholine affect serum K+ levels?
Increases by 0.5-1 mEq/L
56
What is the initial consequence of dialysis?
Hypovolemia
57
What is the initial treatment for hyperkalemia? Why is this the initial treatment?
Calcium administration. Calcium will stabilize cell membrane quickly.
58
How does hyperventilation affect potassium levels?
Hyperventilation will increase pH (more alkalotic). Increase of pH by 0.1 will decrease K+ by 0.4-1.5 mmol/L.
59
What is the dose of insulin and D50 in hyperkalemia treatment? How long will it take for insulin to work in hyperkalemia treatment?
10 units IV insulin: 25 g D50. Onset of 10-20 min
60
What should be avoided in hyperkalemia management?
Succs, hypoventilation, LR & K+ containing IV fluids
61
In addition to Calcium, hyperventilation and insulin what other drugs are utilized to decrease potassium?
Bicarb, loop diuretics, Kayexalate (hours to days)
62
How much of the body's Calcium is in ECF? Where is the majority of Calcium stored? What percentage of plasma Ca++ is protein bound?
Only 1% of Calcium is in ECF; the other 99% is stored in bone.
Of the 1% of calcium in ECF 60% of it is bound to proteins (mainly Albumin)
63
How does pH affect the binding of Ca++ to albumin?
↑pH/Alkalosis→↑Ca++ binding
64
Which form of plasma Ca++ is physiologically active?
Ionized calcium is physologically active whereas protein bound calcium is not active.
65
What is the normal range for ionized Ca++?
1.2-1.38 mmol/L
66
Which hormones regulate Calcium
parathyroid, Vitamin D (calcitriol), Caclitonin.
67
What hormone stimulates the release of of Ca++ from the bones into plasma?
Parathyroid hormone
68
Which hormone augments intestinal Ca++ absorption?
Vitamin D
69
What hormone promotes calcium storage into the bone?
Calcitonin
70
What is required for PTH production?
Magnesium
71
How does pH influence the binding of Calcium to albumin?
increased pH/alkalosis leads to increase calcium binding to albumin (therefore decreasing ionized calcium levels)
72
When should iCa++ be checked in relation to PRBC transfusions?
After 4+ units
73
A major cause of Hypocalcemia is a decrease in what hormone?
PTH (Parathyroid hormone)
74
What role does Magnesium play in Hypocalcemia?
Deficiency can cause Hypocalcemia
75
How does Renal failure contribute to Hypocalcemia?
Kidneys not responding to PTH
76
What is a consequence of massive blood transfusion on calcium levels?
Citrate preservative binds Ca++, causing Hypocalcemia
77
Most common causes of hypercalcemia
Hyperparathyroidism or cancer
78
Hyperparathyroidism serum Calcium level range
<11
79
Cancer serum Calcium level range for those with hypercalcemia
>13
80
Less common causes of hypercalcemia
Vit D intoxication, Milk-alkali syndrome (excess GI Calcium absorption), Granulomatous diseases (sarcoidosis)
81
What caution should be taken when extubating after parathyroidectomy?
Have laryngospasm plan
82
What are signs and symptoms of hypercalcemia?
Confusion, lethargy, hypotonia/decreased deep tendon reflexes, abdominal pain, n/v, short QT interval.
83
What are signs and symptoms of hypocalcemia?
Paresthesias, irritability, hypotension, seizures, myocardial depression, prolonged QT interval.
84
What can chronic high calcium levels lead to?
Hypercalciuria & nephrolithiasis
85
What is a life-threatening complication post-parathyroidectomy related to hypocalcemia?
Laryngospasm. Due to calcium absoprtion dependent on PTH.
86
What are the causes of hypo-magnesium?
Low dietary intake or absorption, Renal wasting
87
What are the symptoms of hypo-magnesium?
Muscle weakness or excitation, seizures, Ventricular dysrhythmia (polymorphic v Tach, Torsades)
88
How is hypo-magnesium treated for torsades or seizures?
2g Mag Sulfate
89
What are the symptoms of hypermagnesemia at 4-5 mEq/L?
Lethargy, N/V, Flushing
90
What are the symptoms of hypermagnesemia at >6 mEq/L?
HoTN, ↓DTR
91
What are the symptoms of hypermagnesemia at >10 mEq/L?
Paralysis, apnea, heart blocks, cardiac arrest
92
How is hypermagnesemia treated?
Diuresis, IV Calcium (cell membrane stabilization), Dialysis
93
Where are the kidneys located?
Retroperitoneal between T12-L4
94
Which kidney is slightly caudal to accommodate the liver?
Right
95
What is the primary structural and functional unit in the kidney? How many are present in each kidney?
Nephron. There are approximately ~1 million per kidney.
96
What are the components of a nephron?
Glomerulus,
Tubular system: Bowman capsule, PCT, Loop of Henle, DCT, Collecting duct
97
What percentage of cardiac output do the kidneys receive? What does this equate to in L/min
20% of CO, 1-1.25 L/min
98
Which part of the kidney receives the majority of renal blood flow? What % of RBF does it receive?
Cortex receives majority of RBF (85-90%)
99
Which part of the kidney is particularly vulnerable to necrosis in response to hypotension?
Loop of Henle
100
What system is responsible for increasing Na+/H2O reabsorption?
RAAS (Renin Angiotensin Aldosterone system)
101
What hormone, secreted from the cardiac atria, decreases Na+/H2O reabsorption?
Atrial Natriuretic Peptide (ANP)
102
What is crucial for pH balance in the body?
Reabsorption & excretion of HCO3- & H+
103
What role does EPO play regarding blood?
Involved in RBCs production. Renal patients often on EPO supplements.
104
What maintains serum calcium levels?
Calcitriol
105
What are prostaglandins' roles in the kidneys?
Inflammatory modulators, vasodilatory effects, maintain renal blood flow
106
What additional role do kidneys play in metabolism?
Gluconeogenesis and filtration & reabsorption of glucose
107
How do kidneys help in regulating blood pressure?
RAAS, ANP
108
Name a function of the kidneys related to excretion.
Excrete toxins/metabolites
109
How do kidneys contribute to maintaining acid/base balance?
By managing the balance of HCO3- and H+
110
Which hormones are produced by the kidneys?
Renin, Erythropoietin, Calcitriol, Prostaglandins
111
What is the role of the kidneys in blood glucose homeostasis?
Gluconeogenesis, filtration & reabsorption of glucose
112
What is the best measure of renal function over time? What is this lab heavily influenced by? How does aging affect this lab?
Glomerular filtration rate (125-140 mL/min) is best measure of renal function over time. GFR is heavily dependent on hydration status. GFR decreases by 10 mL/min per decade after 20's.
113
What does Creatinine Clearance measure? What is the normal range?
Most reliable measure of GFR. Conducted using 24 hour urine test. Normal level (110-140 mL/min)
114
What is normal serum creatinine level? What is serum creatinine relationship to GFR?
Serum Creatinine (0.6-1.3 mg/dL).
It is inversely related to GFR.
115
What can a double serum creatinine in an acute case indicate?
Drop in GFR by 50%
116
What is the normal range for Blood Urea Nitrogen (BUN)?
10-20 mg/dL
117
What could a low BUN level indicate?
Malnourished or volume diluted
118
What could a high BUN level indicate?
High protein diet, dehydrated, GI bleed, trauma, muscle wasting
119
What is the normal BUN:Creatinine ratio?
10:1
120
Why is the BUN:Creatinine ratio a good measure of hydration status?
BUN reabsorbed, creatinine not reabsorbed
121
Normal proteinuria level? What could proteinuria (>750 mg/day) suggest?
Normal level is (<150 mg/dL). >750 mg/day is indicative of Glomerular injury or UTI
122
What is the normal range for specific gravity? What is it used to assess?
1.001-1.035. Measures nephron's ability to concentrate urine.
123
What should you consider when assessing volume status?
Hydration status, history, physical exam
124
What is oliguria?
<500mL in 24h
125
What is the normal range for urine output (UOP)?
0.5-1ml/kg/hr
126
What does a compressed IVC indicate? How is this assessed?
compressed IVC is indicative of dehydration. It can be assessed via Ultrasound
127
What does PCWP stand for and what does it stimulate?
Pulmonary Capillary Wedge Pressure; renal vasoconstriction
128
What assumption is made when measuring stroke volume variation?
Patient is ventilated and in sinus rhythm
129
What does >50% IVC collapse indicate?
Fluid deficit
130
What can be considered to determine fluid responsiveness in addition to IVC collapsibility?
Passive leg raise
131
What is a common hallmark of Acute Kidney Injury? Is Acute Kidney injury reversible?
Azotemia: buildup of urea and creatinine
Yes, it is Reversible with timely interventions
132
AKI with Multiple System Organ Failure (MSOF) requiring dialysis results in a mortatility rate of?
> 50%
133
What are some risk factors of AKI?
Primary risk: Pre-existing renal disease
Others: Advanced age (GFR decreases with age), CHF, PVD, Diabetes, Sepsis (via hypotension), Jaundice, Major operative procedures, IV Contrast
134
What is the diagnostic criteria for AKI?
SCr increase by 0.3 mg/dL within 48h, SCr increase by 50% within 7 days, Creatinine clearance decrease by 50%, and abrupt oliguria (although not always seen in AKI)
135
Physical symptoms of AKI
Can be asymptomatic, malaise, hypotension, hypo or hypervolemia
136
What is the cause of pre-renal azotemia?
↓ renal perfusion
137
What is the cause of renal azotemia?
nephron injury
138
What is the cause of post renal azotemia?
outflow obstruction
139
Which type of azotemia is the easiest to treat? Which is the most common form of AKI?
Postrenal Azotemia easiest to treat.
Pre-renal is the most common form of AKI.
140
Name the causes of prerenal azotemia.
141
Name the causes of renal azotemia.
142
Name the causes of postrenal azotemia.
143
What is the typical BUN:Cr ratio in Pre-Renal AKI?
>20:1
144
Is Pre-renal azotemia reversible? What can it lead to if it is not reversed in a timely manner?
Yes, pre-renal AKI is usually a volume issue.
If not reversed it can lead to Acute tubular necrosis (progressives from a pre-renal issue to a renal issue)
145
What is the primary goal in treating Pre-renal azotemia? How is this achieved?
Restore RBF is primary goal and can be achieved via: fluids, mannitol, diuretics, maintain MAP, pressers.
146
What is the typical BUN:Cr ratio in renal azotemia?
< 15:1
147
In renal AKI, why does BUN:Cr decrease compared to pre-renal AKI?
Decreased urea reabsorption in proximal tubule
148
What are the characteristics of renal azotemia?
Intrinsic renal disease, potentially reversible, decreased GFR (late sign), decreased urea reabsorption in proximal tubule (decreased BUN), decreased creatinine filtration (elevated blood creatinine)
149
What is hydronephrosis?
Obstruction causing renal pelvis dilation
150
What is post-renal azotemia?
Result of outflow obstruction
151
How is reversibility related to the duration of obstruction in hydronephrosis?
Inversely related. (longer duration/less reversible) and vice versa
152
What is the treatment for hydronephrosis?
Remove obstruction if possible
153
What does persistent obstruction in hydronephrosis lead to?
Damage to tubular epithelium
154
What are some neurological complications of AKI?
Uremic Encephalopathy (improved with HD), mobility disorders, neuropathies, myopathies, seizures, stroke
155
What are the cardiovascular complications of AKI?
Hypertension (not excreting fluid), LVH, CHF, pulmonary edema, Uremic cardiomyopathy, Arrhythmias
156
What is the order of cardiovascular complications in AKI?
HTN → LVH → CHF → ischemic heart disease →anemic heart failure →Arrhythmias → pericarditis (with or without effusion) →cardiac tamponade, Uremic cardiomyopathy
157
What are some hematological complications of AKI?
Anemia (decreased EPO/RBC/RBC survival), Platelet dysfunction, vWF disruption (d/t uremia)
158
What can be done prophylactically to address vWF disruption in AKI?
Prophylactic DDAVP (increased vWF/Factor VIII)
159
What are some metabolic complications of AKI?
Hyperkalemia, Water/sodium imbalances, Hypoalbuminemia, Metabolic acidosis, malnutrition, hyperparathyroidism (parathyroid in overdrive to stimulate kidney reabsorption of Calcium)
160
What is preferred pressor for maintaining renal blood flow in acute kidney injury?
Vasopressin
161
What is the preferred fluid for renal issues? What is the preferred colloid?
NS preferred for renal (no K+)
Colloids: albumin is preferred over hetastarch
162
How should mean arterial pressure be maintained in AKI anesthesia?
20% of baseline
163
What role does sodium bicarb play in AKI prophylaxis?
decreases formation of free-radicals and prevents ATN from causing renal failure.
164
Why may a patient with AKI need post-op dialysis?
Can't clear drugs on their own
165
What are some anesthesia implications for a patient needing dialysis?
Low threshold for invasive hemodynamic monitoring, prefer preoperative dialysis, recent labs especially K+, want POC equipment available, tailored drug dosing, avoid drugs with active metabolites, drugs that decrease RBF, and renal toxins.
166
What are the leading causes of chronic kidney disease (CKD)?
Diabetes, Hypertension
167
What are common presentations of chronic kidney disease (CKD) patients?
Surgery for dialysis access, Non-healing wounds, Diabetic toe/foot debridements/amputations, often frequent flyers
168
What is the formula for estimating GFR?
GFR = 186 x (SCr)-1.154x (age)-0.203x (0.742 if female) x (1.210 if African American)
169
What are the 5 stages of CKD based on GFR levels?
170
How are CKD stages typically discovered?
Often found during routine testing (focus on trends)
171
What are some cardiovascular effects of CKD?
Systemic hypertension
172
How does CKD lead to retention of sodium and water?
Activation of renin-angiotensin-aldosterone system
173
What is the 1st line treatment for CKD in terms of medications? What additional medications may be needed for CKD?
Thiazide Diuretics are 1st line.
Other meds: ACE-I/ARB
174
Why ACE's and ARB's often used in CKD?
Reduces systemic BP and glomerular pressure
Reduces proteinuria by reducing glomerular hyperfiltration
Reduces glomerulosclerosis
175
Why should ACE-I/ARBs be withheld on the day of surgery? If ACE-I/ARBs on board, what other medications may be required during surgery?
To reduce the risk of profound HoTN.
Vasopressin, NE, EPI may be needed if medication effects still present during surgery.
176
Which populations are high risk for silent MI?
CKD, Women and Diabetics
177
What are common lipid abnormalities in CKD patients?
Triglycerides often > 500, LDL often > 100
178
What neuropathies may CKD patients experience?
Peripheral & autonomic neuropathy. Sensation may be blunted.
179
What hematologic effects are associated with chronic kidney disease?
Anemia, Platelet dysfunction
180
How is anemia in chronic kidney disease managed?
Exogenous erythropoietin with a target Hbg of 10
181
What should be considered when transfusing blood in chronic kidney disease patients?
Risks vs benefits, Excess Hgb leads to sluggish circulation
182
What are indications to consider dialysis?
Volume overload, Severe hyperkalemia, Metabolic acidosis, Symptomatic uremia, Failure to clear medications
183
Why might peritoneal dialysis (PD) be more suitable for some patients?
Slower, less dramatic volume shifts, suitable for patients intolerant of fluid swings/volume shifts such as poor cardiac function
184
What is the most common side effect of hemodialysis (HD)?
Hypotension
185
What is the leading cause of death in dialysis patients?
Infection (due to impaired immune system/healing)
186
What are some anesthesia concerns for patients with ESRD?
Stability of ESRD, glucose management, well controlled BP, body weight pre-post dialysis within 24 hrs post op, aspiration precautions, pressers, uremic bleeding.
187
Why should body weight pre/post dialysis be assessed within 24 hours of surgery?
To monitor fluid shifts
188
What is the onset time and duration of desmopressin? What is a limitation of desmopressin?
Peak 2-4h; lasts 6-8h
Can develop tachyphylaxis therefore should only be used when needed.
189
What is important to consider about many anesthetic agents in patients with CKD?
Many anesthetic agents are lipid soluble, reabsorbed by renal tubular cells, lean towards agents not dependent on renal elimination, and avoid active metabolites (morphine and demerol)
190
What are examples of lipid insoluble drugs? What is renal dosing usually based on?
Thiazide diuretics, Loop diuretics, Digoxin, Many antibiotics.
Renal dosing usually based on the GFR.
191
What is important about lipid insoluble drug elimination? Especially with renal patients?
Lipid Insoluble meds are eliminated unchanged in urine. Longer duration of action in renal impaired patients.
192
What is the class of the drug Edrophonium?
Cholinesterase inhibitors
193
What percentage of Morphine is cleared through urine?
40%
194
What is the inactive metabolite of Morphine? What is the active metabolite of Morphine?
Inactive: morphine-3 glucuronide
Active: morphine-6 glucuronide
195
What is the main adverse effects of Demerol?
Neurotoxicity: nervousness, tremors, muscle twitches, seizures
196
Why does multiple doses of meperidine result in the accumulation of normeperidine?
Long elimination half-life of normeperidine (15-30 h) compared to (2-4 hr) for meperidine.
197
What level should potassium be under for elective surgery?
K+ < 5.5 mEq/L
198
What is recommended for dialysis patients before elective surgery?
Dialyzed within 24 h before
199
How do anesthesia and surgery affect renal blood flow (RBF) and glomerular filtration rate (GFR)?
Decrease RBF & GFR
200
What effect does blood loss have on baroreceptors and sympathetic nervous system (SNS) outflow?
Activates SNS outflow
201
How do catecholamines decrease renal blood flow (RBF)?
Catecholamines activate alpha 1 Receptors, this constricts afferent arterioles which decreases renal blood flow.
