Pathophysiology Exam #1

Total Body Water

- Intracellular and extracellular fluid
- 2/3 of TBW \= ICF
- 1/3 of TBW \= ECF

Intracellular Fluid

- 2/3 of TBW
- fluid inside the cells

Extracellular Fluid

- 1/3 of TBW
- fluid outside the cell
- Subdivided into 2 compartments;
1. Interstitial Fluid (between the cells) 80%
2. Plasma (bloodstream) 20%

T/F: Water shifts by diffusion/osmosis back and forth between the ICF and ECF based on concentration gradients between the 2 compartments?

True

T/F: If the ICF and ECF concentrations are in equilibrium then there will be no net shift of water between the 2 compartments?

True

T/F: Water only shifts between the ICF and ECF when there is a concentration gradient between the 2 compartments?

True

Intracellular/Extracellular makeup

- solutions comprised of water and solutes (dissolved substances) such as Na+, Cl-, K+, glucose, etc

Isotonic range

280-300

T/F: If there is a normal amount of water and a normal amount of solute, then the concentration of the solution is normal; Isotonic

True

Hypertonic

- relatively more solute/relatively less water
- \>300
- Solution is greater than the normal

Hypotonic

- relatively less solute/relatively more water
-

T/F: Water will always move from more dilute to more concentrated?

True

T/F: The abnormalities are not incredibly severe, 280-300 is normal, but even the slightest change either direction causes shifts?

True

If the ICF is isotonic and the ECF is hypotonic, how will the fluid shift?

The fluid will shift from the ECF to the ICF. The ECF is slightly more dilute/less concentrated than the ICF, therefore the fluid will shift to inside the cells causing them to expand.

If the ICF is isotonic and the ECF is hypertonic, how will the fluid shift?

The fluid will shift from the ICF to the ECF. The ICF is less concentrated/more dilute than the ECF, therefore the fluid will shift out of the cells and into the ECF, causing the cells to shrink.

T/F: The ECF concentration changes more easily than the ICF concentration?

True

Hydrostatic Pressure

- pressure trying to push water out
- In the plasma: water is trying to be pushed out by hydrostatic pressure
- Has a direct correlation to Blood Volume
- Increased BV, Increased HP
- Decreased BV, Decreased HP

Oncotic Pressure

- pressure trying to hold or keep water in
- In the plasma: water is trying to stay in by oncotic pressure
- Oncotic Pressure Plasma Protein: Albumin (made in the liver)
- Albumin establishes oncotic pressure

Edema

- accumulation of fluid in the interstitial space
- is a distribution problem

- can occur in almost every organ and can be focal (localized), regional, or diffuse (widespread)

4 Factors Contributing to Edema Formation

- Increased Plasma Hydrostatic Pressure
- resulting from increased BV
- ex: Pulmonary Edema, CHF (not enough cardiac output \= fluid retention)

- Decreased Plasma Oncotic Pressure
- resulting from reduced plasma albumin levels
- ex: liver failure

- Increased Capillary Permeability
- resulting from trauma and/or inflammation
- "increased leakiness"

- Lymphatic Obstruction
- resulting from internal blockage or external compression or lymphatic drainage
- reduced lymphatic circulation

Any of the above-contributing factors can occur alone or in combination

Normal Sodium Values/Affects

- 135-145 mEq/L
- Most abundant ECF electrolyte; sodium abnormalities affect ECF osmolarity and BV/BP
- Na+ homeostasis is regulated by the GI tract, kidneys, and endocrine system (aldosterone)

Hypernatremia

blood Na+ \>145 mEq/L

- most commonly occurs in hospitalized patients and the elderly; and is almost always caused by water deficit, reduced water intake, or increased water loss
- as a result of hypernatremia, ECF will be hypertonic, causing water to shift out of the cells (ICF to ECF) and causing shrinkage (cellular dehydration)
- If severe (blood Na+ \> 165), more significant effects are on the CNS
- Treat by correcting the water deficit

Hyponatremia

- blood Na+

Normal Postassium Values/ Affects

- Blood K+ 3.5-5.0 mEq/L

- K+ is the most abundant ICF electrolyte
- the vast majority of K+ is in the cells
- Abnormalities affect the NM excitability, most notably affecting the heart
- K+ homeostasis is regulated by the GI tract, kidneys, and endocrine system (aldosterone and insulin)
-Aldosterone: lower BP with release of K+; holds onto Na+, releases K+
- lowers K+ by shifting into cells

Hyperkalemia

- blood K+ \>5.0mEq/L

- most dangerous electrolyte abnormality due to the development of potentially lethal cardiac dysrhythmias
- Severe hyperkalemia (blood K+ \> 6.5) slows conduction velocity in the heart; can cause asystole or causes VFib (ventricular fibrillation)
- Common causes are drugs that increase K+ retention (K+ sparing drugs; ACE inhibitors and ARBs), renal impairment, adrenal insufficiency (both decrease K+ excretion), metabolic acidosis, cancer treatments, etc
- Resting potential goes up as a result of hyperkalemia
- Treat moderate to severe hyperkalemia with IV insulin (insulin shifts K+ back into cells), glucose (to compensate for the insulin), and Calcium gluconate to protect the heart

Hypokalemia

- Blood K+

Normal Calcium Values/ Affects

- Blood Ca+ 8.5-10.5 mg/dL

- Calcium is abundantly stored in the bones and teeth
- Calcium abnormalities affect NM excitability
- Calcium homeostasis is regulated by the GI tract, kidneys, skeletal system, and endocrine system (PTH [increases blood Ca+] & Vitamin D)

Hypercalcemia

- blood Ca+ \>10.5 mg/dL

- most commonly caused by hyperparathyroidism and cancer
- hypercalcemia causes a decrease in NM excitability (by moving threshold potential further away from resting membrane potential) possibly resulting in constipation and hypercalciuria (increased urine Ca+) with kidney stones
- If hypercalcemia is severe (blood Ca+ \>~13.0 mg/dL), skeletal muscle weakness, confusion, and coma can occur
- Treat underlying cause. Treatment can also include the administration of a loop diuretic (LASIX) to enhance urinary Ca+ excretion

Hypocalcemia

- Blood Ca+

Acid-Base Balance normal values/affects

pH: 7.35-7.45
Acidosis: arterial pH

3 Ways the Body Acts to Maintain Acid-Base Balance

1. Buffer systems work to resist pH changes
2. Kidneys: regulate acid/base excretion as needed
3. Lungs: regulate CO2 (volatile acid) excretion as needed

Buffer systems and kidneys collectively are responsible for the metabolic regulation of acid-base balance (Bicarbonate ion; HCO3- levels reflect the function of the metabolic component of acid-base regulation) HCO3- is a base/alkaline

Lungs are responsible for the respiratory regulation of acid-base balance. CO2 levels reflect the function of the respiratory component of acid-base regulation. CO2 is an acid/acidic

Acid-Base Disturbance

Acidosis: pH

Respiratory Acidosis/Alkalosis

Respiratory Acidosis: high CO2
Respiratory Alkalosis: low CO2

Metabolic Acidosis/Alkalosis

Metabolic Acidosis: low HCO3-
Metabolic Alkalosis: high HCO3-

Combination Acidosis/Alkalosis

Combination Acidosis: high CO2, low HCO3-
Combination Alkalosis: low CO2, high HCO3-

There's both a respiratory and metabolic cause for the acidosis/alkalosis

What test is used to determine the Acid-Base balance of a patient?

ABG (Arterial Blood Gas)

What is the ABG made up of?

pH, CO2, HCO3-

Normal Values for the ABG

pH: 7.35-7.45 (indicates acid-base balance)
CO2: 35-45 mmHg (respiratory component)
HCO3-: 22-28 mEq/L (metabolic component)

Respiratory Alkalosis

- occurs when CO2 is removed (exhaled) faster than it is produced; results in low CO2 (hypocapnia) and a corresponding increase in pH (\>7.45) because acid is being removed faster than it is replaced

- can be caused by anything that results in hyperventilation (increased ventilation rate), hypoxemia, panic attacks, severe anxiety, etc

Respiratory Acidosis

- occurs when CO2 is removed (exhaled) slower than it is being produced; results in high CO2 (hypercapnia) and a corresponding decrease in pH (

Metabolic Alkalosis

- occurs when HCO3- accumulates due to a loss of acid, reduced HCO3- excretion, or the addition of HCO3-, this results in a high HCO3- and a corresponding increase in pH (\>7.45) because base (HCO3-) is accumulating

- commonly caused by volume depletion (low blood volume) secondary to vomiting (loss of acid) or diuretic use (reduced HCO3- excretion)

Metabolic Acidosis

- occurs when HCO3- is reduced due to the accumulation of organic acid (lactic acid, keto acids, others) or increased HCO3- excretion (loss); resulting in low HCO3- and a corresponding decrease in pH (

Normal Anion Gap (AG)

- caused by loss of HCO3-; most common cause s prolonged diarrhea

-normal range\= 3-12 mEq/L

Elevated Anion Gap (AG)

- caused by the accumulation of organic acid
- most common causes are lactic acids (from hypoxia [low tissue oxygenation]), DKA (diabetic ketoacidosis; complication of Type 1 DM), or uremia associated with CKD (chronic kidney disease)

Formula for Elevated AG: AG\= Na+ - (Cl- + HCO3-)

Metabolic Acidosis formula to determine if respiratory compensation is appropriate

CO2\= (1.5 * HCO3-) +8 +/- 2

+/-2 gives us the range

Combinations

- in a combination acidosis/ alkalosis, there is BOTH a respiratory and metabolic cause for the acidosis or alkalosis

Compensation

- in acid-base regulation, compensation refers to physiologic changes that occur to try to maintain acid-base balance

- EX: metabolic acidosis; the pH is low because there is a primary metabolic cause. The respiratory component (reflected by CO2) may then compensate for the metabolic cause of the acidosis in an attempt to keep the pH as close to normal as possible

T/F: Compensation can occur for any acid-base disorder?

True