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Therapeutics II > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What are the functions of the kidney?

A

Excretory (urine)
Regulates BP
Hormones- erythropoietin, calcitriol, renin
Metabolism

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2
Q

Typical GFR

A

125mL/min

Needs to be relatively constant

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3
Q

Net filtration pressure

A

Has to be positive for the kidney to filter

NFP= GBHP-CHP-BCOP

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4
Q

How does the kidney increase perfusion pressure?

A

RAAS system

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5
Q

What systems decrease NFP

A

Myogenic stretch
Tubuloglomerular feedback
ANP

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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.

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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

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8
Q

ANP

A

Released with increased NaCl, ECF volume, and BP

Decreases the sympathetic NS causing a decrease in BP

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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

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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

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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

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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

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13
Q

PTH stimulus, MOA, and effect

A

Stimulus- low serum Ca
MOA- enhances Ca reabsorption in the DCT
Effect- Increases serum Ca

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14
Q

Kidney and calcium

A

PTH controls calcium

PTH stimulates reabsorption of calcium from urine and activation of vitamin D in the kidney

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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

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16
Q

When do you use adjusted BW?

A

In obesity BMI >25

Adj BW= IBW + 0.4(ABW-IBW)

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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.

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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

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19
Q

Why is SCr lower in elderly patients?

A

Because they have less muscle mass

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20
Q

For AKI or critically ill patients, what do you use to measure?

A

No formula is accurate

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21
Q

Osmolality

A

The concentration of solutes in a fluid

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22
Q

Osmolar gap

A

A difference in plasma osmolality >10

Typically worried about alcohols (ethanol)

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23
Q

Normal plasma osmolality

A

280-295mosmol/kg

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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

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25
Q

What is the role of ADH?

A

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

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26
Q

What is the role of aldosterone?

A

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

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27
Q

Edema

A

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

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28
Q

Changes in fluid physiology with aging

A 
Decreased total body water
Decreased GFR
Decreased urination
Decreased thirst mechanism
Decreased aldosterone
Increased ADH levels but a decreased response to ADH
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29
Q

BUN:SCr ratio

A

Normally 20:1
Any higher and worry about patients being dry
Increased BUN and SCr= Dryer

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30
Q

Hct in relation to fluid status

A

Increased Hct concentration may mean decreased fluid

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31
Q

FENa

A

UNa(SCr)/ SNa(Ucr) x100
Tells us if the patient is dry
Less than 1% indicates hypovolemia

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32
Q

Osmolality vs tonicity

A

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

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33
Q

Hypotonic IVF

A

D5W
Low Na
Cells swell, can burst if given too much

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34
Q

Hypertonic IVF

A

3% saline

Cells shrink and can be damaged. Pulls water out of cells and into intravascular space

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35
Q

Max osmolality

A

Peripheral veins- 900mOsm/L

Central- any

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36
Q

Where is D5W primarily found?

A

In the intracellular space

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37
Q

Where is LR and NS primarily found?

A

Interstitial space

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38
Q

Where is 3% NaCl primarily found?

A

Plasma space

Pulls fluid from interstitial

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39
Q

What is the free water in 1L NS?

A

0

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40
Q

What is the free water in 1L D5W?

A

1000mL

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41
Q

Causes of volume deficit

A 
Decreased intake
Abnormal losses
GI- vomiting, diarrhea, fistula
Renal- diuretics, hyperglycemia, adrenal insufficiency
3rd spacing
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42
Q

Presentation of volume deficit

A

Decreased BP, UOP, skin turgor, mental status, strength, temp (maybe)
Increased HR, BUN:Cr (prerenal azotemia), urine specific gravity or osmolality

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43
Q

Volume deficit treatment

A

Goal is to rapidly restore intravascular volume

NS or LR

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44
Q

Volume overload causes

A

Chronic diseases- CHF, liver disease, cancer, starvation
Mobilization of interstitial fluid
Psychogenic polydipsia

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45
Q

Volume overload presentation

A 
Edema
JVT
Rales
CHF
Increased BP
46
Q

Volume overload treatment

A

Fluid restriction, diuretics, dialysis

47
Q

Hyponatremia/ Hypernatremia

A

Imbalance of sodium relative to the amount of water

48
Q

Hyponatremia

A

Serum sodium <135mEq/L

Assess measured serum osmolality

49
Q

Isotonic hyponatremia

A

pseudohyponatremia

50
Q

Hypertonic hyponatremia

A

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
Q

Hypotonic hyponatremia

A

Need to assess patients extracellular fluid and determine if it is decreased, increased, or normal

52
Q

Hypovolemic hyponatremia

A

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
Q

Euvolemic hyponatremia

A

Normal sodium, increased water
Causes- SIADH, primary polydipsia, hypothyroidism
Tx- fluid restriction, 3% NS with furosemide

54
Q

Primary polydipsia

A

Compulsive water consumption

Could be caused by phenpthiazines or beer potomania

55
Q

SIADH

A

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
Q

Hypervolemic hyponatremia

A 
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
Q

Treatment goals of hyponatremia

A

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
Q

What happens when you correct hyponatremia too rapidly?

A

Central pontine myelinolysis

Osmotic demyelination

59
Q

Hypernatremia

A

> 145
Results from a deficit of water relative to ECF sodium volume
Most commonly observed in patients without access to water

60
Q

Hypovolemic hypernatremia

A

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
Q

Free water deficit

A

Typically replace 1/2 of water deficit in the first 24 hours via feeding tube or IV D5W

62
Q

Euvolemic hypernatremia

A

Normal sodium, decreased water
Causes- diabetes insipidus
Tx- hypotonic fluid, vasopressin, HCTZ

63
Q

Diabetes insipidus

A

Central DI- impaired ADH secretion
Nephrogenic DI- renal resistance to the actions of AVP
Can be caused by lithium, hypercalcemia, and hypokalemia

64
Q

What is the effect of ADH (vasopressin)?

A

Decreased urinary volume, increased urine Osm

65
Q

Hypervolemic hypernatremia

A

Very increased Na, increased water
Causes- Na administration, hyperaldosteronism
Tx- hypotonic fluid, diuretics

66
Q

Treatment goals of hypernatremia

A

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
Q

What happens if you correct hypernatremia too rapidly?

A

Cerebral edema/seizures

68
Q

Acidemia

A

pH less than 7.35

69
Q

Alkalemia

A

pH greater than 7.45

70
Q

Lungs (respiratory) acid/base

A

Pulls O2 to alveoli (inhalation) and takes pCO2 away from alveoli (exhalation)
ACID- pCO2

71
Q

Kidneys (metabolic) acid/base

A

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
Q

If there is an increase in pCO2 what type of acidosis is it?

A

Respiratory acidosis

73
Q

If there is a decrease in HCO3 what type of alkalosis is is?

A

Metabolic alkalosis

74
Q

Respiratory vs metabolic compensation

A

Respiratory compensation occurs quickly and metabolic compensation is delayed

75
Q

Causes of respiratory acidosis

A

Decreased respiratory drive (opioids, sedation)
Apnea: Cardiac arrest
Airway disorders: bronchospasm, edema, ARDS, etc.
Chronic causes- COPD

76
Q

Compensation of respiratory acidosis

A

Increased pCO2 and HCO3

77
Q

Respiratory alkalosis causes

A 
Increased expiration (tachypnea)
Causes- anxiety, pain, CHF, sepsis, pneumonia, stroke, theophylline, salicylates
78
Q

Respiratory alkalosis primary compensation

A

Decreased pCO2

Decreased HCO3

79
Q

Anion Gap metabolic acidosis causes

A 
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
Q

Anion gap metabolic acidosis compensation

A

Decreased HCO3

Decreased pCO2

81
Q

Nonanion gap metabolic acidosis causes

A

HCO3 loss leading to hyperchloremia (diarrhea, pancreatic fistula, renal tubular acidosis)
Hyperchloremia (iatrogenic)

82
Q

Nonanion gap metabolic acidosis compensation

A

Decreased HCO3, increase Cl

Decreased pCO2

83
Q

Metabolic alkalosis causes

A

Loss of chloride (vomiting, diuretics)

Excessive bicarbonate administration

84
Q

Metabolic alkalosis compensation

A

Increased HCO3
Decreased Cl
Increased pCO2

85
Q

Rules of thumb for acidosis/alkalosis

A

Systems do not over compensate

There can only be one respiratory disorder at a time

86
Q

Calcium

A

Normal 8.6-10.2mg/dL

You have to correct calcium for albumin and the ionized fraction will change

87
Q

Corrected total calcium=

A

Measured Ca + [0.8x (4-measured albumin)]
If albumin is normal, calcium is likely low
Do formula in all ICU patients

88
Q

Hypercalcemia

A

Total calcium >10.2
Severe >13 requires treatment even when asymptomatic
Commonly caused by cancer and hyperparathyroidism

89
Q

Medication causes of hypercalcemia

A 
Thiazides
Lithium
Vit D
Vit A
calcium
Aluminum/magnesium antacids
Theophyllines
Tamoxifen
Ganciclovir
90
Q

Hypercalcemia presentation

A

Fatigue, weakness, anorexia, depression, anxiety, cognitive dysfunction, abdominal pain, constipation, kidney stones

Shortened QT interval
Coving of the ST wave

91
Q

Treatment of hypercalcemia

A

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
Q

Hypocalcemia

A

<8.5
Tetany, parathesia, muscle cramps, laryngeal spasms, dry puffy and coarse skin, hypotension

Prolonged QT interval
Arrhythmias
Bradycardia

93
Q

Causes of hypocalcemia

A 
Vit D deficiency
Post op hyperparathyroidism
Mag deficiency
Blood transfusions
Medications- furosemide, cinacaclet, biphophonates, calcitonin, fluoride, ketoconazole, phenytoin, phenobarbitol
94
Q

Treatment of hypocalcemia

A 
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
Q

Phosphorous

A

Normal 2.7-4.5mg/dL

96
Q

Hypophosphatemia

A

<2.5mg/dL
Rarely signs/symptoms unless severe
Can have irritability, weakness, numbness, paresthesia, confusion
Seizures or coma in very severe cases

97
Q

Hypophosphatemia causes

A

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
Q

Treatment of hypophosphatemia

A

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
Q

Potassium

A

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
Q

Hypokalemia

A

<3.5mEq/L
Cramping, weakness, myalgia, malaise, impaired muscle contractions
ST segment depression
T wave inversions

101
Q

Causes of hypokalemia

A 
V/D
Hypomagnesemia
Ephedrine
Catecholamines
Beta 2 agonists
Caffeine
Loop and thiazide diuretics
102
Q

Tx of Hypokalemia

A

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
Q

Hyperkalemia

A

> 5mEq/L
Usually asymptomatic
Can cause heart palpitations or skipped beats
Peaked T wave

104
Q

Causes of hyperkalemia

A

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
Q

Treatment of hyperkalemia

A

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
Q

Magnesium

A

Normal 1.4-1.8mEq/L
OR
1.7-2.3mg/dL

107
Q

Hypomagnesemia

A

<1.4mEq/L
Usually asymptomatic
Can cause tetany, heart palpitations, widened QRS interval, prolonged PR interval, peaked T wave

108
Q

Causes of hypomagnesemia

A

Low serum potassium and calcium
Decreased GI absorption, increased excretion, alcoholism
Thiazide and loop diuretics, cyclosporine, tacrolimus

109
Q

Treatment of hypomagnesemia

A

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
Q

Hypermagnesemia

A

Rare
>2mEq/L
Loss of tendon refluxes, lethargy, confusion, arrhythmias, muscle weakness

111
Q

Hypermagnesemia Causes

A

acute renal failure, CKD, excessive intake, lithium, hypothyroidism, addisons disease, acute DKA

112
Q

Tx of hypermagnesemia

A

Reduce intake, enhance elimination, antagonize physiologic effects
100-200mg IV elemental calcium if cardiac events present
Hemodialysis
Diuretics

Therapeutics II (5 decks)

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