Exam 1 Flashcards
1
Q
What are the functions of the kidney?
A
Excretory (urine)
Regulates BP
Hormones- erythropoietin, calcitriol, renin
Metabolism
2
Q
Typical GFR
A
125mL/min
Needs to be relatively constant
3
Q
Net filtration pressure
A
Has to be positive for the kidney to filter
NFP= GBHP-CHP-BCOP
4
Q
How does the kidney increase perfusion pressure?
A
RAAS system
5
Q
What systems decrease NFP
A
Myogenic stretch
Tubuloglomerular feedback
ANP
6
Q
Myogenic stretch
A
Allows blood flow to remain the same even with risking BP.
When arterial BP rises, the afferent arteriole is stretched, which increases blood flow.
Vascular smooth muscle responds by contracting and increasing resistance and decreasing GFR. This increases vascular tone and returns the flow to normal.
7
Q
Tubuloglomerular Feedback
A
Activated with disturbance in homeostasis (Increased BP)
Cells on the JGA detect increased delivery of Na, Cl, and water. This causes the JGA to decrease secretion of nitric oxide (a natural vasodilator). This causes the afferent arteriole to constrict and decrease blood flow to the glomerulus.
This in turn decreases GFR and BP
8
Q
ANP
A
Released with increased NaCl, ECF volume, and BP
Decreases the sympathetic NS causing a decrease in BP
9
Q
ATII Stimulus, MOA, and effect
A
Stimulus- decreased renal perfusion
Mechanism of action- Enhances Na and H2O reabsorption in PCT
Effect- Increases blood volume
10
Q
Aldosterone stimulus, MOA, and effect
A
Stimulus- Increased ATII and K
MOA- Enhances Na (exchanges K) and H2O reabsorption in the late distal and collecting duct
Effect- Increases blood volume, lowers K
11
Q
ADH stimulus, MOA, and effect
A
Stimulus- increased osmolarity of ECF or decreased blood volume
MOA- Inserts aquaporin channels in the DCT and collecting duct.
Effect- Increases BV
12
Q
ANP stimulus, MOA, and effect
A
Stimulus- Atrial stretch due to increased blood volume
MOA- Suppresses Na and H2O reabsorption, decreases ATII and aldosterone
Effect- Increases Na (and H2O) excretion to decrease BV
13
Q
PTH stimulus, MOA, and effect
A
Stimulus- low serum Ca
MOA- enhances Ca reabsorption in the DCT
Effect- Increases serum Ca
14
Q
Kidney and calcium
A
PTH controls calcium
PTH stimulates reabsorption of calcium from urine and activation of vitamin D in the kidney
15
Q
Kidney and erythropoietin
A
When there is a decreased oxygenation to the kidneys the kidneys secrete EPO into the blood, which stimulates erythropoiesis and increase the RBCs in the blood stream
16
Q
When do you use adjusted BW?
A
In obesity BMI >25
Adj BW= IBW + 0.4(ABW-IBW)
17
Q
Why is CrCl not an accurate representation of GFR?
A
CrCl OVERestimates GFR due to the fact that creatinine is secreted by the proximal tubule as well as filtered by the glomerulus. Insulin would be the ideal substance.
18
Q
MDRD vs CG
A
Use MDRD for detection, evaluation, and monitoring of CKD. More accurate when GFR <60mL/min, equation in labs
Use CG for drug dosing decisions
19
Q
Why is SCr lower in elderly patients?
A
Because they have less muscle mass
20
Q
For AKI or critically ill patients, what do you use to measure?
A
No formula is accurate
21
Q
Osmolality
A
The concentration of solutes in a fluid
22
Q
Osmolar gap
A
A difference in plasma osmolality >10
Typically worried about alcohols (ethanol)
23
Q
Normal plasma osmolality
A
280-295mosmol/kg
24
Q
Osmotic receptors vs pressure receptors
A
Osmotic receptors- Respond to osmolality
Pressure receptors- Respond to plasma volume
Thirst receptors and ADH and aldosterone
25
What is the role of ADH?
ADH is secreted in response to increased osmolality or decreased ECF volume
ADH binds to vasopressin 2 receptors resulting in the insertion of aquaporins into the collecting duct.
Net effect:
Reabsorption of FREE water (free of Na)
Increase plasma volume
Decrease plasma osmolality
26
What is the role of aldosterone?
Activated as a result of hypovolemia causing decreased perfusion to the kidneys
Aldosterone stimulates the reabsorption of sodium from the distal tubules and collecting ducts (water follows sodium)
Net effect:
Re-absorption of water and Na
Increase in plasma volume
27
Edema
Clinically detectable increase in interstitial fluid volume
Movement of fluids from the intravascular to interstitial space is influenced by BP and oncotic pressure. The alterations in these pressures leads to edema (third spacing)
Tx with Na restriction and/or diuretics
28
Changes in fluid physiology with aging
```
Decreased total body water
Decreased GFR
Decreased urination
Decreased thirst mechanism
Decreased aldosterone
Increased ADH levels but a decreased response to ADH
```
29
BUN:SCr ratio
Normally 20:1
Any higher and worry about patients being dry
Increased BUN and SCr= Dryer
30
Hct in relation to fluid status
Increased Hct concentration may mean decreased fluid
31
FENa
UNa(SCr)/ SNa(Ucr) x100
Tells us if the patient is dry
Less than 1% indicates hypovolemia
32
Osmolality vs tonicity
Osmolality is the number of osmoles of solute per liter of solution. This includes both ineffective and effective osmoles
Tonicity is the total concentration of solutes which exert an osmotic force across a membrane (effective osmoles)
Dextrose is an INEFFECTIVE osmole
33
Hypotonic IVF
D5W
Low Na
Cells swell, can burst if given too much
34
Hypertonic IVF
3% saline
| Cells shrink and can be damaged. Pulls water out of cells and into intravascular space
35
Max osmolality
Peripheral veins- 900mOsm/L
| Central- any
36
Where is D5W primarily found?
In the intracellular space
37
Where is LR and NS primarily found?
Interstitial space
38
Where is 3% NaCl primarily found?
Plasma space
| Pulls fluid from interstitial
39
What is the free water in 1L NS?
0
40
What is the free water in 1L D5W?
1000mL
41
Causes of volume deficit
```
Decreased intake
Abnormal losses
GI- vomiting, diarrhea, fistula
Renal- diuretics, hyperglycemia, adrenal insufficiency
3rd spacing
```
42
Presentation of volume deficit
Decreased BP, UOP, skin turgor, mental status, strength, temp (maybe)
Increased HR, BUN:Cr (prerenal azotemia), urine specific gravity or osmolality
43
Volume deficit treatment
Goal is to rapidly restore intravascular volume
| NS or LR
44
Volume overload causes
Chronic diseases- CHF, liver disease, cancer, starvation
Mobilization of interstitial fluid
Psychogenic polydipsia
45
Volume overload presentation
```
Edema
JVT
Rales
CHF
Increased BP
```
46
Volume overload treatment
Fluid restriction, diuretics, dialysis
47
Hyponatremia/ Hypernatremia
Imbalance of sodium relative to the amount of water
48
Hyponatremia
Serum sodium <135mEq/L
| Assess measured serum osmolality
49
Isotonic hyponatremia
pseudohyponatremia
50
Hypertonic hyponatremia
Suggests the presence of excess, non-sodium osmoles in the ECF
Most commonly caused by hyperglycemia
Estimated decrease in Na: 1.6x(glucose-100)/100
51
Hypotonic hyponatremia
Need to assess patients extracellular fluid and determine if it is decreased, increased, or normal
52
Hypovolemic hyponatremia
Decreased water, very decreased Na
Need to check UNa
If >20, caused by renal losses (diuretics, adrenal insufficiency, cerebral salt wasting)
If <20, caused by extrarenal losses (third spacing)
Often caused by chronic hyperglycemia
53
Euvolemic hyponatremia
Normal sodium, increased water
Causes- SIADH, primary polydipsia, hypothyroidism
Tx- fluid restriction, 3% NS with furosemide
54
Primary polydipsia
Compulsive water consumption
| Could be caused by phenpthiazines or beer potomania
55
SIADH
Euvolemic hyponatremia
Urine osmolality >100mosm/L and UNa >20mEq/L
Caused by SSRIs, carbamazepine, TCAs, antipsychotics, NSAIDs, opioids, theophylline, ectasy
Fluid restriction is primary treatment
56
Hypervolemic hyponatremia
```
Increased sodium, very increased water
Most common
Occurs with chronic diseases (CHF, cirrhosis, renal dysfunction)
Volume overload/ascites present
Tx- water restriction
Diuretics
ADH antagonists
```
57
Treatment goals of hyponatremia
Asymptomatic or chronic patients- Increase plasma Na by no more than 0.5-1 mEq/L per hour and by <8mEq/L over 24 h
Severe (Na <115)
Increase Na by 1mEq/L per hour but no more than 8mEq/24 hours
58
What happens when you correct hyponatremia too rapidly?
Central pontine myelinolysis
| Osmotic demyelination
59
Hypernatremia
>145
Results from a deficit of water relative to ECF sodium volume
Most commonly observed in patients without access to water
60
Hypovolemic hypernatremia
Decreased Na, very decreased water
Most common
Occurs with hypotonic fluid loss
Tx with volume expansion and isotonic fluids
Then need a low Na fluid to replace free water deficit (D5W)
61
Free water deficit
Typically replace 1/2 of water deficit in the first 24 hours via feeding tube or IV D5W
62
Euvolemic hypernatremia
Normal sodium, decreased water
Causes- diabetes insipidus
Tx- hypotonic fluid, vasopressin, HCTZ
63
Diabetes insipidus
Central DI- impaired ADH secretion
Nephrogenic DI- renal resistance to the actions of AVP
Can be caused by lithium, hypercalcemia, and hypokalemia
64
What is the effect of ADH (vasopressin)?
Decreased urinary volume, increased urine Osm
65
Hypervolemic hypernatremia
Very increased Na, increased water
Causes- Na administration, hyperaldosteronism
Tx- hypotonic fluid, diuretics
66
Treatment goals of hypernatremia
Rate of correction depends on neurological dysfunction, rapidity of onset, and magnitude of Na rise
General- Decrease plasma Na conc. by no more than 0.5-1mEq/L and no more than 8mEq/day
67
What happens if you correct hypernatremia too rapidly?
Cerebral edema/seizures
68
Acidemia
pH less than 7.35
69
Alkalemia
pH greater than 7.45
70
Lungs (respiratory) acid/base
Pulls O2 to alveoli (inhalation) and takes pCO2 away from alveoli (exhalation)
ACID- pCO2
71
Kidneys (metabolic) acid/base
Maintain water, sodium, and acid-base balance
Maintain ionic balance through retention or excretion of cations and anions
Primary: base (HCO3)
Secondary: Acid (chloride)
72
If there is an increase in pCO2 what type of acidosis is it?
Respiratory acidosis
73
If there is a decrease in HCO3 what type of alkalosis is is?
Metabolic alkalosis
74
Respiratory vs metabolic compensation
Respiratory compensation occurs quickly and metabolic compensation is delayed
75
Causes of respiratory acidosis
Decreased respiratory drive (opioids, sedation)
Apnea: Cardiac arrest
Airway disorders: bronchospasm, edema, ARDS, etc.
Chronic causes- COPD
76
Compensation of respiratory acidosis
Increased pCO2 and HCO3
77
Respiratory alkalosis causes
```
Increased expiration (tachypnea)
Causes- anxiety, pain, CHF, sepsis, pneumonia, stroke, theophylline, salicylates
```
78
Respiratory alkalosis primary compensation
Decreased pCO2
| Decreased HCO3
79
Anion Gap metabolic acidosis causes
```
Anion gap >12mEq/L
Presence of accumulation of nonvolatile acids
Methanol toxicity
Uremia
DKA
Paraldehyde toxicity
Infection (sepsis)
Lactic acidosis
Ethylene glycol toxicity
Salicylate toxicity
```
80
Anion gap metabolic acidosis compensation
Decreased HCO3
| Decreased pCO2
81
Nonanion gap metabolic acidosis causes
HCO3 loss leading to hyperchloremia (diarrhea, pancreatic fistula, renal tubular acidosis)
Hyperchloremia (iatrogenic)
82
Nonanion gap metabolic acidosis compensation
Decreased HCO3, increase Cl
| Decreased pCO2
83
Metabolic alkalosis causes
Loss of chloride (vomiting, diuretics)
| Excessive bicarbonate administration
84
Metabolic alkalosis compensation
Increased HCO3
Decreased Cl
Increased pCO2
85
Rules of thumb for acidosis/alkalosis
Systems do not over compensate
| There can only be one respiratory disorder at a time
86
Calcium
Normal 8.6-10.2mg/dL
| You have to correct calcium for albumin and the ionized fraction will change
87
Corrected total calcium=
Measured Ca + [0.8x (4-measured albumin)]
If albumin is normal, calcium is likely low
Do formula in all ICU patients
88
Hypercalcemia
Total calcium >10.2
Severe >13 requires treatment even when asymptomatic
Commonly caused by cancer and hyperparathyroidism
89
Medication causes of hypercalcemia
```
Thiazides
Lithium
Vit D
Vit A
calcium
Aluminum/magnesium antacids
Theophyllines
Tamoxifen
Ganciclovir
```
90
Hypercalcemia presentation
Fatigue, weakness, anorexia, depression, anxiety, cognitive dysfunction, abdominal pain, constipation, kidney stones
Shortened QT interval
Coving of the ST wave
91
Treatment of hypercalcemia
May not treat if patient is asymptomatic
Nonpharm- hemodialysis, surgery if hyperthryoidism
Pharmacologic:
1st line- IV NS + loop
1st line for hemodialysis- Calcitonin
1st line for cancer- bisphosphonate
Other treatments- cinacalcet, denosumab, corticosteroids
92
Hypocalcemia
<8.5
Tetany, parathesia, muscle cramps, laryngeal spasms, dry puffy and coarse skin, hypotension
Prolonged QT interval
Arrhythmias
Bradycardia
93
Causes of hypocalcemia
```
Vit D deficiency
Post op hyperparathyroidism
Mag deficiency
Blood transfusions
Medications- furosemide, cinacaclet, biphophonates, calcitonin, fluoride, ketoconazole, phenytoin, phenobarbitol
```
94
Treatment of hypocalcemia
```
Give calcium in symptomatic patients
100-300 elemental calcium IV
Max rate of 60mg of calcium/minute
1g CaCl= 27% elemental
1g calcium gluconate= 9% elemental
Oral- give 1-3 g calcium/day +/- Vit D
```
95
Phosphorous
Normal 2.7-4.5mg/dL
96
Hypophosphatemia
<2.5mg/dL
Rarely signs/symptoms unless severe
Can have irritability, weakness, numbness, paresthesia, confusion
Seizures or coma in very severe cases
97
Hypophosphatemia causes
Decreased GI absorption- corticosteroids, Vit D deficiency
Increased excretion- diuretics, glucocorticoids, sodium bicarb
Internal redistribution- Refeeding syndrome, insulin, catecholamines, calcitonin, TPN, alcoholism, chronic antacid use
98
Treatment of hypophosphatemia
Mild to moderate (asymptomatic)- use oral therapy 50-60mmol/day. Be cautious of K in KPhos unless pt has low K levels
Severe- IV phosphorous
<2mg/dL- 0.32mmol/kg
<1.5mg/dL- give 0.64mmol/kg
99
Potassium
Most abundant cation in the body
Normal- 3.5-5mEq/L
Insulin is the most important regulator of K! Hypokalemia inhibits insulin secretion
Metabolic acidosis associated with hypokalemia
100
Hypokalemia
<3.5mEq/L
Cramping, weakness, myalgia, malaise, impaired muscle contractions
ST segment depression
T wave inversions
101
Causes of hypokalemia
```
V/D
Hypomagnesemia
Ephedrine
Catecholamines
Beta 2 agonists
Caffeine
Loop and thiazide diuretics
```
102
Tx of Hypokalemia
Correct magnesium first!
Oral- potassium chloride, phosphate, bicarbonate
20mEq/day prevention
40-100mEq/day treatment
Divide into 3-4 doses due to stomach upset
IV- 10mEq/hr peripheral, 20mEq/hr central
Too rapid administration can lead to death!
103
Hyperkalemia
>5mEq/L
Usually asymptomatic
Can cause heart palpitations or skipped beats
Peaked T wave
104
Causes of hyperkalemia
Decreased intake (fruits, veggies)
Decreased excretion- K sparing diuretics, Trimethoprim
Aldosterone resistance- ACEis, ARBs, NSAIDs, heparin
Redistribution- Beta blockers (blocks catecholamine receptors), digoxin (inhibits pump)
105
Treatment of hyperkalemia
1.) Stabilize cardiac membrane with calcium
2.) Hide K extracellularly with dextrose + insulin
OR
Eliminate K with furosemide, Na Bicarb, or albuterol
3.) Can give SPS to bind K and excrete in gut
4.) New drugs- patiromer, sodium zirconium cyclosulfite are great in chronic cases but not in acute patients due to long onset
106
Magnesium
Normal 1.4-1.8mEq/L
OR
1.7-2.3mg/dL
107
Hypomagnesemia
<1.4mEq/L
Usually asymptomatic
Can cause tetany, heart palpitations, widened QRS interval, prolonged PR interval, peaked T wave
108
Causes of hypomagnesemia
Low serum potassium and calcium
Decreased GI absorption, increased excretion, alcoholism
Thiazide and loop diuretics, cyclosporine, tacrolimus
109
Treatment of hypomagnesemia
Oral-magnesium containing laxatives or antacids, mg containing tabs
400-800mg 3-4 doses/day
IV- 8-12mg Mg in 1st 24 hours. May take 3-5 days to replete body stores because 50% is excreted in urine
110
Hypermagnesemia
Rare
>2mEq/L
Loss of tendon refluxes, lethargy, confusion, arrhythmias, muscle weakness
111
Hypermagnesemia Causes
acute renal failure, CKD, excessive intake, lithium, hypothyroidism, addisons disease, acute DKA
112
Tx of hypermagnesemia
Reduce intake, enhance elimination, antagonize physiologic effects
100-200mg IV elemental calcium if cardiac events present
Hemodialysis
Diuretics
