The Cellular Environment Flashcards

1
Q

Define Total Body of Water (TBW)?

A

The sum of all fluids within all the compartments of the body constitutes TBW. TBW = 55 to 60% of total body weight.

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2
Q

Ratio of Intercellular Fluid (ICF) to Extracellular Fluid (ECF) in the body?

A

1) ICF = 40% of TBW ~ 28L

2) ECF = 20% (4% IV and 16% Interstitial) of TBW ~ 14L

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3
Q

What is the percentage of TBW in the following populations:

1) Newborn
2) Childhood
3) Adults
4) Older Adults

A

1) Newborn - 75 to 90%
2) Childhood - 60 to 65%
3) Adults - 60%
4) Older Adults - declines with age

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4
Q

Define Aquaporin

A

A family of water channel proteins that provide permeability to water.

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5
Q

What allows water to move between plasma and the interstitial fluid?

A

Osmotic and hydrostatic pressure gradients

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6
Q

Describe Starling’s Law of Capillaries and Net Filtration Pressures on the arterial side?

A

Starling’s Law describes net filtration of arterial capillary pressures as follows:
1) Capillary Hydrostatic pressure - 35mmHg
2) Interstitial Fluid Hydrostatic Pressure - 2mmHg
Net Hydrostatic Pressure (pushing in) = 33mmHg
1) Capillary Oncotic Pressure - 24mmHg
2) Interstitial Fluid Oncotic Pressure - 0mmHg
Net Oncotic Pressure (pushing out) = 24mmHg
Net Filtration Pressure = 33 - 24 = 9mmHg

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7
Q

Describe Starling’s Law of Capillaries and Net Filtration Pressures on the venous side?

A

Starling’s Law describes net filtration of venous capillary pressures as follows:
1) Capillary Hydrostatic pressure - 18mmHg
2) Interstitial Fluid Hydrostatic Pressure 1mmHg
Net Hydrostatic Pressure (pushing in) = 17mmHg
1) Capillary Oncotic Pressure -25mmHg
2) Interstitial Fluid Oncotic Pressure 0mmHg
Net Oncotic Pressure (pushing out) = 25mmHg
Net Filtration Pressure = 17 - 25 = -8mmHg

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8
Q

What is Starling’s Equation? What does each component mean?

A

Ԛ=K(Pc -Pi)-σ(πc -πi) (gives the net hydrostatic pressure - oncotic pressure out of the capillary

1) Q = Flow out of capillary
2) K = Filtration coefficient (k of H20 perm. of the cap.)
3) Pc = Capillary hydrostatic pressure
4) Pi = Interstitial hydrostatic pressure
5) σ = reflection coefficient (relates cap. protein perm)
6) πc = capillary oncotic pessure
7) πi = interstitial oncotic pressure

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9
Q

What is Edema? What causes it?

A

Edema is the accumulation of fluid in the interstitial spaces caused y and increase in filtration or a decrease in reabsorption.

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10
Q

5 specific cause of Edema as mentioned in the Pos?

A

1) Increased capillary hydrostatic pressure from HTN or venous obstruction or insufficiency.
2) Decreased blood colloid osmotic pressure from low albumin, liver disease or malnutrition.
3) Increased capillary permeability from inflammation or severe burns.
4) Lymph obstruction aka lymph edema
5) Kidney disease causing sodium retention and/or protein loss.

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11
Q

Why is periopererative fluid mgmt important?

A

1) maintains intravascular volume
2) Augments CO
3) Maintains tissue perfusion
4) Promotes O2 delivery
5) Corrects/maintains electrolyte balance
6) facilitates delivery of nutrients
7) clearance of metabolic wastes
8) Vital component of ERAS (enhanced recovery after surgery) protocol

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12
Q

What are crystalloids? 3 most common?

A

Aqueous electrolyte solutions that are close to tonicity of plasma.

1) Plasmalyte/normosol
2) Lactated Ringers
3) 0.9% NaCl

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13
Q

Crystalloids are preferable for the resuscitation of dehydration from conditions leading to hypertonicity. Name 4 examples of such conditions?

A

1) Prolonged fasting states
2) Active GI losses
3) Polyuria
4) Hypermetabolic conditions

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14
Q

Even though 0.9% NaCl is the most commonly used isotonic solution, it is the least physiologic. What pH condition results if too much NaCl is given?

A

Hyperchloremic metabolic acidosis can happen because too much Cl- in the NaCl kicks out HCO3- via the kidney.

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15
Q

The only isotonic fluid that contains Phosphate, Mag, Acetate, and gluconate?

A

Plasmalyte/Normosol

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16
Q

What are Colloids?

A

Suspensions with high-molecular weight molecules in electrolyte solutions used for their plasma volume-increasing factors.

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17
Q

How do Colloids increase plasma volume?

A

Colloids increase πc (capillary oncotic pressure) & interacts with glycocalyx to decrease transcapillary filtration

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18
Q

(T/F?) Albumin is the only naturally occurring colloid available for infusion (besides PRBCs)?

A

True

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19
Q

What are the 3 types of Synthetic Colloids?

A

1) Hydroxyethyl Starches (Hetastarch)
2) Dextrans
3) Gelatins

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20
Q

Characteristics of Hetastarches?

A

1) Have allergic potential
2) Associated with coagulopathies
3) Can accumulate in interstitial tissues/organs causing nephrotoxicity.

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21
Q

Characteristics of Dextrans?

A

1) Oldest artificial colloid

2) Can cause ARF and coagulopathies

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22
Q

Characteristics of Gelatins?

A

1) Derived from bovine components
2) High incidence of anaphylaxis
3) Can transmit spongiform encephalopathy

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23
Q

What is the preferred replacement for blood volume in patients with intact endothelial glycocalyx undergoing acute volume loss.

A

Colloids

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24
Q

What will happen if you use Albumin and other colloids in patients with endothelial injuries?

A

Use of colloids in PT’s with endothelial injuries may lead to pulmonary edema and other end organ complications (i.e. hyperglycemia and sepsis).

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25
Q

Advantages of Colloids?

A

1) Replacement ratio of 1:1
2) Increases plasma volume in 3-6 hrs
3) Smaller volume needed
4) Less peripheral edema
5) Albumin has anti-inflammatory properties
6) Dextran 40 reduces blood viscosity which improves microcirculatory flow in vascular surgery.

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26
Q

Disadvantages of Colloids?

A

1) Albumin binds to Ca2+ causing hypocalcemia
2) Risk of renal failure with synthetic colloids (FDA black box warning)
3) Coagulopathy
4) Anaphylaxis (highest risk with Dextran)

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27
Q

Advantages of Crystalloids?

A

1) replacement ratio = 3:1
2) Expands ECF
3) Restores 3rd space loss

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28
Q

Disadvantages of Crystalloids?

A

1) Limited ability to expand plasma
2) Increased risk for peripheral edema
3) Possible hychloremic metabolic acidocis
4) Dillutional effect on albumin reducing capillary oncotic pressure
5) Dillutional effect on coagulation factors

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29
Q

How do you calculate Plasma Osmolarity? What is the normal range?

A

Plasma Osmolarity = 2[Na+] + Glucose/18 + BUN/2.8

Normal range = 280 to 290 mOsm/L

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30
Q

Whats the most important determinant of Plasma Osmolarity? What can cause an increase?

A

Sodium is the most important determinant.

Hyperglycemia or uremia can cause an increase

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31
Q

What are the main extracellular cation and anion?

A

1) Major ECF Cation = Na+

2) Major ECF Anion = Cl

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32
Q

What are the main intracellular cation and anion?

A

1) Main ICF Cation = K+

2) Main ICF Anion = HPO4^3-

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33
Q

Which ion is responsible for half of the osmotic pressure gradient between the interior of cells and the surrounding environment (attracts water).

A

Sodium

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34
Q

Major roles of Sodium in the ECF?

A

1) Neuron and muscle excitability
2) Acid-base balance
3) Cellular reactions
4) Transport substances

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35
Q

How is sodium regulated in the ECF?

A

By the RAAS and natriuretic peptides

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36
Q

What are the roles of the Chloride in the ECF?

A

1) contributes to the osmotic gradient between ICF and ECF.
2) Provides electroneutrality by balancing cations (follows sodium)
3) Propre hydration
4) Acid-base balance

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37
Q

Characteristics of Aldosterone?

A

1) It’s a steroid hormone of the Adrenal cortex
2) Stimulated by Angitensinn II
3) Reabsorption of Na2+/secretion of K+ by distal tubule

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38
Q

Characteristics of Natriuretic Peptides?

A

1) Comes from the heart when stretched
2) Decreases tubular reabsorption of sodium and promotes urinary excretion of sodium
3) 2 types: arterial natriuretic and brain natriuretic peptides

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39
Q

If you have too much volume, which natriuretic peptide is more prevalent?

A

ANP

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40
Q

What is Antidiuretic Hormone (ADH)? How does it work?

A

1) ADH aka argentine-vaopressin is secreted when plasma osmolality increases or blood volume decreases and BP drops. ADH stimulates thirst and water drinking, stimulates the posterior pituitary to release ADH and increases reabsorption in distal tubules.

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41
Q

Basic causes of Hypernatremia?

A

1) Excessive dietary intake
2) Over-secretion of aldosterone
3) Water loss

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42
Q

Manifestations of Hypernatremia?

A

1) Convulsions
2) Pulmonary edema
3) Hypotention
4) Tachycardia

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43
Q

Basic causes of Hyperchloremia?

A

1) Hypernatremia

2) Bicarbonate deficit

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44
Q

Basic causes of Hyponatremia?

A

1) Excess water accumulation in the body

2) Loss of sodium via vomiting or diarrhea, diuretics, polyuria (i.e. diabetes), acidosis (i.e. low aldosterone)

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45
Q

Manifestations of Hyponatremia?

A

1) Lethargy
2) Headache
3) Confusion
4) Apprehension
5) Seizures
6) coma

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46
Q

Treatment for Hyponatremia?

A

1) Treat underlying disorder

2) Restrict water intake

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47
Q

Treatment for Hypernatremia?

A

Isotonic salt-free fluids

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48
Q

Effects of hyponatremia on cells?

A

Causes swollen RBCs which have decreased oxygen-carrying efficiency and can be too large.
Causes swollen neurons which leads to damage or death

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49
Q

Basic causes of Hypochloremia?

A

1) Hyponatremia
2) Vomiting
3) Metabolic alkalosis
4) Cystic fibrosis

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50
Q

(T/F?) In general, K+ and Na+ move in opposite directions via sodium/potassium pumps?

A

True

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51
Q

Roles of Potassium as an ICF ion?

A

1) Maintains concentration via Na+/K+ pump
2) Establishes the resting membrane potential
3) Transmission and conduction of nerve impulses, normal cardiac rhythm
4) Responsible for Skeletal and smooth muscle contractions

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52
Q

Basic causes of hypokalemia?

A

1) Reduced K+ intake
2) Alkalosis causing increased K+ entry into cell
3) Increased potassium loss (polyuria, etc.)

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53
Q

Explain the relationship between pH and levels of potassium in the blood?

A

When PT is acidotic (too much H+ in ECF) H+ moves into the cell and switches places with the other proton:K+, which goes to the ECF and causes hyperkalemia. (it works vice-versa when PT is alkaloid).

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54
Q

(T/F?) Strenuous exercise facilitates the movement of K+ from the ICF to the ECF?

A

True

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55
Q

Explain the relationship between Potassium and glucose/insulin levels?

A

K+ follows glucose, so when the PT is hyperglycemic, potassium shifts from the ICF to the ECF to join glucose. When insulin is given and lowers the Blood glucose, the Potassium will go back into the ICF.

56
Q

Manifestations of Low potassium?

A

1) Decreased neuromuscular excitability
2) Skeletal muscle weakness
3) Smooth muscle atony
4) Cardiac dysrhythmias

57
Q

Basic causes of hyperkalemia?

A

Increased intake or decreased renal secretion

2) Acidosis
3) hyperglycemia (low insulin levels)
4) Cell trauma (releases K+ from ICF to ECF)

58
Q

Manifestations of Hyperkalemia?

A

1) Tingling of lips
2) Intestinal cramping and diarrhea
3) Abnormal T-waves on the ECG

59
Q

Treatment for Hyperkalemia?

A

1) Calcium glutinate (increases threshold potential)
2) Glucose
3) Na+ bicarb (counteracts acidosis, promotes K= movement from ECF to ICF)
4) Cation exchange resins
5) Dialysis

60
Q

Effects of altered potassium levels on ECG?

A

1) Hypokalemia - ST depression, shallow t-wave, u-wave shallow if present.
2) Hyperkalemia - Prolonged PR interval, widened QRS, ST depression, tall/peaked t-wave

61
Q

Where is Calcium mostly located in the body?

A

99% of Calcium is in the bones and 1% is in the plasma

62
Q

Roles of Calcium

A

1) Structure of bones and teeth
2) Muscle contractions
3) Blood clotting
4) Hormone and neurotransmitter secretion
5) Cell receptor function (secondary messenger)

63
Q

3 things that regulate calcium?

A

1) Parathyroid hormone
2) Vitamin-d
3) Calcitonin

64
Q

(T/F?) Calcium and Phosphate concentrations are rigidly controlled?

A

True - if the concentration of one increases, the concentration of the other increases as well.

65
Q

(T/F?) Most Phosphate in the body is located in the bones?

A

True - 85% of Phosphate is in the bones

66
Q

Roles of Phosphate?

A

1) Used in high-energy bonds (i.e. ATP and creatine phosphate)
2) Acts as an anion buffer
3) Muscle contraction energy

67
Q

Which 2 hormones are responsible for increasing levels of calcium the blood?

A

1) PTH - secreted in response to low calcium, increases calcium levels via kidney reabsorption. blocks reabsorption of phosphate and stimulates bone reabsorption by osteoclasts.
2) Vitamin-D - PTH upiregulates enzymes responsible for converting vitmamin D to its active form. Vitamin-d increases calcium absorption from the GI tract via calbindins.

68
Q

Which hormone is responsible for decreasing calcium levels in the blood?

A

Calcitonin - Parafolicular cells of the thyroid:

1) Inhibits calcium absorption by the intestines.
2) Inhibits osteoclast activity in the bones
3) Stimulates osteoblastic activity in the bones
4) Inhibits renal tubular reabsorption

69
Q

Basic causes of Hypocalcemia?

A

1) Inadequate intake or absorption
2) Decrease in PTH & vit-d
3) Blood transfusions (blood products contain citrate which binds calcium)

70
Q

Manifestations of Hypocalcemia?

A

1) Increased neuromuscular excitability (partial depolarization)
2) Muscle spasms and convulsions
3) Chvostek’s sign (nerve hypersensitivity when facial nerve is tapped)
4) Trousseau’s signs (spasms of hand muscles when brachial artery is occluded)

71
Q

Treatment for Hypocalcemia?

A

Calcium replacement or decreased phosphate intake

72
Q

Basic causes of Hypercalcemia?

A

1) Hyperparathyroidism/bone metastasis
2) Excess vitamin-d
3) Acidosis

73
Q

Manifestations of Hypercalcemia?

A

1) Muscle weakness (decreased neuromuscular excitability)
2) Kidney stones and constipation
3) Abnormal heart rhythms (Osborn wave)

74
Q

Treatment for Hypercalcemia?

A

1) Oral diphosphate and IV saline
2) Biphophnates
3) Calcitonin
4) Corticosteroids

75
Q

Basic causes of Hypophosphatemia?

A

1) Renal excretion
2) Intestinal malabsorption (GI damage, vit-d deficiency)
3) Alcohol abuse (impairs phosphate absorption)
4) Alkalosis (stimulates glycosides, makes phosphate move into the cell)
5) Certain antacids (binds phosphates)
6) Refeeding syndrome

76
Q

What is Re-feeding syndrome?

A

When the malnourished are given high carbohydrates, the cells uptake phosphate from blood for glucose metabolism and production of ATP) causing hypophosphatemia.

77
Q

Manifestations of Hypophosphetemia?

A

1) Muscle weakness
2) Osteomalacia (soft bones)
3) Increased affinity for oxygen in the blood
4) Bleeding disorders (platelet impairment)
5) leukocyte alterations (worsening infections)

78
Q

Treatment for Hypophosphatemia?

A

Treat underlying condition such as respiratory alkalosis or hyperparathyoidroidism

79
Q

Basic causes of Hyperphosphatemia?

A

1) Low calcium levels
2) Renal failure
3) Hypoparathyoidroidism
4) Heparin Therapy

80
Q

Manifestations of Hyperphosphatemia?

A

Same as hypocalcemia with possible calcification of soft tissue

81
Q

Treatment of Hyperphosphotemia?

A

1) Treat underlying condition
2) Aluminum hydroxide
3) Dialysis

82
Q

Characteristics of Magnesium?

A

1) Mostly and intracellular cation
2) Stored in the bones (60%) and muscle (20%)
3) Has a plasma concentration of 1.8 to 2.4 mg/dL

83
Q

Roles of Magnesium?

A

1) Is a co-factor in intracellular reactions
2) Protein synthesis
3) Nucleic acid stability
3) Neuromuscular excitability

84
Q

Causes of Hypo and Hyper - magnesia?

A

1) Hypomagnesemia - Malabsorption, diarrhea, diuretics, ABX, and PPI-use.
2) Hypermagnesemia - Renal failure

85
Q

Manifestations of Hypomagnesemia?

A

1) Neuromuscular excitability
2) Tetany and convulsions
3) Increased reflexes

86
Q

Manifestations of Hypermagnesemia?

A

1) Loss of DTR
2) Muscle weakness
3) N & V
4) Hypotension
5) respiratory depression
6) Bradycardia

87
Q

Treatment for Hypo and hyper-magnesemia?

A

1) Hypomagnesemia - magnesium sulfate

20 Hypermagnesemia - Avoid magnesium, dialysis

88
Q

How is pH calculate given the concentration of H+?

A

pH = -log[H+]

89
Q

How are acids formed?

A

Acids are formed as end products of proteins, carbohydrates and fat metabolism.

90
Q

To maintain the body’s normal pH between 7.35 - 7.45, the H+ ions must be neutralized by ______ and excreted by ________?

A

H+ ions are neutralized by buffers (bicarbonate) and excreted by the kidneys.

91
Q

How is Anion Gap calculated? what is the normal range?

A

AG = Serum cations - Serum anions

Normal AG = 8 - 12 meq/L

92
Q

Explain what it means when the PT is acidotic and has a high Anion Gap?

A

A high AG and acidosis means that the acidosis is being caused by an increase in organic acids. i.e. lactic acid, kept acids, formic acids, shock, etc.

93
Q

Explain what it means when the PT is acidotic but has a normal Anion Gap?

A

Acidosis with a normal Anion Gap means that the acidosis is being caused by a loss of HCO3-. There aren’t enough bicarbs in the body to buffer H+ ions and the body holds on to Cl- ions instead.

94
Q

What is a Buffer?

A

A Buffer is a chemical system that prevents a radical change in pH by dampening the change in hydrogen ion concentrations using a either a weak acid or a weak base.

95
Q

(T/F?) Buffers can be located in both the ECF and the ICF?

A

True

96
Q

What are the 3 Buffer Systems functioning in blood plasma?

A

1) Plasma Proteins
2) Phosphate
3) Bicarb/Acid system

97
Q

How are proteins able to act as a buffer?

A

Proteins are made up of amino acids, which contains positively charged amino groups and negatively charged carboxyl groups which are able to bind OH- and H+, thus acting as a buffer.

98
Q

What percentage of the buffering in the blood is accounted for by proteins?

A

2/3 and most of the buffering inside the cell.

99
Q

At the systemic capillaries, what is responsible for buffering liberated hydrogen ions from carbonic acid?

A

Reduced hemoglobins

100
Q

What are the 2 types of phosphate buffers in the blood?

A

1) Sodium Dihydrogen Phosphate (NaH2PO4-) - A weak acid.

2) Sodium Monohydrogen Phosphate (Na2HPO4^2-) - A weak base.

101
Q

What is the ratio of bicarbonate to carbonic acid present in the blood if the blood is pithing normal pH range?

A

20:1

102
Q

What regulates the amounts of carbonic acid and the levels of bicarbonate in the body?

A

1) Carbonic Acid levels are controlled by the expiration of CO2 via the lungs.
2) Bicarbonate levels are controlled by excretion of bicarbonate via the kidneys.

103
Q

Respiratory acidosis vs. Respiratory alkalosis

A

1) Respiratory Acidosis - Increase in pCO2 as a result of ventilation depression.
2) Respiratory Alkalosis - Depression of pCO2 as a result of hyperventilation.

104
Q

If inspired air contains no CO2, then how is the relationship of CO2 levels in the body expressed?

A

paCO2 is proportional to Vco2/Va
where Vco2 is CO2 production in the body
Va is alveolar ventilation

105
Q

Metabolic acidosis vs. Metabolic alkalosis

A

1) Metabolic Acidosis - Depression of HCO3- or an increase in noncabonic acids.
2) Elevation of HCO3-, usually as a result of an excessive loss of metabolic acids.

106
Q

What. are the 3 possible causes of Respiratory Acidosis?

A

1) Excess CO2 in the inspired gas
2) Increased production of CO2 in the body which is very rare but possible. i.e. malignant hyperthermia.
3) Decreased alveolar ventilation

107
Q

What are some of the causes of decreased alveolar ventilation leading to respiratory acidosis?

A

1) Respiration depression via drugs i.e. opiates
2) CNS trauma or tumor above c4
3) Obesity hypoventilation (Pickwickian Syndrome)
4) Poliomyelitis, tetanus
5) Nerve or muscle disorders i.e. GBS
6) Lung or chest wall defects i.e. COPD, aspiration
7) Airway disorders

108
Q

Acute Respiratory Acidosis vs Chronic Respiratory Acidosis?

A

1) ARA - Onset of acidosis. The body’s compensatory response is limited because it has to eliminate H+ and reabsorb HCO3- via the nephrons.
2) CRA - After a few days of acidosis when the renal system starts compensating and the pH returns to normal.

109
Q

Manifestations of Respiratory Acidosis (paCO2 > 44)?

A

1) Headache
2) Restlessness
3) Blurred vision
4) Apprehension
5) Lethargy
6) Muscle twitching
7) Tremors
8) Convulsions and coma

110
Q

Basic causes of Respiratory Alkalosis (paCO2 < 38)?

A

1) Hyperventilation
2) High altitudes, anxiety, or panic attacks
3) Hypermetabolic states like fevers and hyperthyroidism
4) Early salicylate intoxication
5) Improper use of mechanical ventilators

111
Q

Manifestations of Respiratory Alkalosis?

A

Dizziness, confusion, tingling of extremities, convulsions, and coma with signs of hypocalcemia

112
Q

Treatment of Respiratory Alkalosis?

A

1) Breathe into a paper bag
2) Treat hypoxemia and hyper metabolic states
3) Administer IV chloride fluids

113
Q

Ketoacidosis is a form of which type of pH imbalance?

A

Metabolic acidosis

114
Q

Manifestations of Metabolic Acidosis (HCO3- < 22)?

A

1) Headache
2) Lethargy
3) Hyperventilation (kussmaul respirations)

115
Q

Treatments for Metabolic Acidosis?

A

1) Bicarbonate (may not be necessary)
2) Lactate-containing solutions (lactate is converted to bicarbonate in the liver)
3) Treat underlying cause

116
Q

Metabolic Alkalosis Causes (HCO3- > 26)?

A

1) Increased Bicarbonate concentration, usually fro excessive loss of metabolic acids (i.e. Cl- depletion)
2) Vomiting, NG suctioning and diuretics
3) Excessive bicarbonate intake
4) Potassium depletion via hyperaldosteronism with hypokalemia

117
Q

Manifestations of Metabolic Alkalosis?

A

1) Weakness
2) Muscle cramps
3) Hyperactive reflexes with signs of hypocalcemia

118
Q

Treatments for Metabolic Acidosis

A

1) Sodium Chloride
2) Potassium
3) Chloride IV (replaces HCO3-)

119
Q

Clinical manifestations of hypotonicity: when water flows into the ICF and the cells swell?

A

1) Lethargy
2) Confusion
3) Seizures
4) Coma

120
Q

Which stimuli increases secretion of aldosterone from the Arenal cortex on top of the kidneys and what is the resulting physiological effect of doing so?

A

Angiotensin II and increased plasma potassium. Increases renal sodium and water reabsorption and increases renal excretion of potassium.

121
Q

Which stimuli increases secretion of parathyroid hormone and what is the resulting physiological effect of doing so?

A

Low plasma calcium - Increases resorption of bone, stimulates renal reabsorption of calcium and inhibits reabsorption of phosphate.

122
Q

Which stimuli increases secretion of Atrial Natriuretic Peptide and what is the resulting physiological effect of doing so?

A

Increased volume in the cardiac atria - increases renal sodium and water excretion.

123
Q

Which stimuli increases secretion of Calcitonin and what is the resulting physiological effect of doing so?

A

High plasma calcium - Inhibits osteoclasts in bone

124
Q

Which stimuli increases secretion of Antidiuretic hormone and what is the resulting physiological effect of doing so?

A

Increased plasma osmolality and substantially decreased arterial blood pressure - Increased renal water reabsorption and vasoconstriction

125
Q

What’s the difference between a volatile acid and a non-volatile acid?

A

1) Volatile acid (carbonic acid) is excreted by the lungs

2) Non-volatile acid (metabolic acid) is excreted by the kidneys.

126
Q

What’s the difference between Acidemia and Acidosis?

A

1) Acidemia - When pH is < 7.35

2) Acidosis - When you have to much acid or too little base regardless of pH.

127
Q

With regard to acid-base imbalance, what’s the difference between correction and compensation?

A

correction returns the concentrations back to normal, while compensation returns the normal ratio of bicarbonate carbonic-acid (20:1), but the concentrations are still abnormal.

128
Q

1/3 of the body’s fluid is located ________ while the other 2/3 is located ______?

A

ECF, ICF

129
Q

A standard 68kg man has how many liters of TBW?

A

40.8L

130
Q

What is Edema?

A

Excessive fluid within the interstitial space is called ________?

131
Q

Hyperphosphatemia can result in which other electrolyte imbalance?

A

Hypocalcemia

132
Q

(T/F?) Glucortocoids can cause edema and hypokalemia?

A

True

133
Q

In which direction does insulin move potassium?

A

From the ECF into the cell

134
Q

Which direction does epinephrine move potassium?

A

From the ECF into the cell

135
Q

In which direction does alkalosis move potassium?

A

From the ECF into the cell