W2 PP2 Fluids& Electro Flashcards
2 main locations of fluids
Intercellular and extracellular
Extracellular spaces
Interstitial-fluid btn cell’s Intravascular Space- fluid within veins, arteries and capillaries Synovial Joints Lymph Space CSF Intraoccular space Intestinal space Pericardial space
Pleural effusion
When water accumulates in the pleural space could be serum, blood, chyle , or pus
Two main types of pleural effusions
The trasudative is secondary to starlings forces (change in hydrostatic pressure)
Causes by a disease process that causes a change in pressure like left ventricular failure or cirrhosis liver disease
Exudative pleural effusion is due to local factors that effect the secretion and absorption of water, usually a malignancy/cancer.
Pressure vs Hydrostatic pressure
Defined as the force exerted on an area
Hydrostatic pressure is the force exerted by a fluid due to the force of gravity
Hydrostatic pressure helps to determine the movement of fluid into or out of the cell along with other forces
Oncotic forces
Form of osmotic pressure exerted by the large osmolarity proteins found in serum. These proteins are too big to escape the vessel wall so water gets pulled into vessel. Albumin causes most of this pressure.
High oncotic pressure draws water into the vessel while a low oncotic pressure draws it out.
Starling’s forces
Discuss the movement of fluid secondary to their filtration through a semi-permeable membrane. Takes into account capillary, interstitial, oncotic and hydrostatic pressures. The movement depends on all of these factors
Not all capillaries are the same. The glomerular capillaries have no protein permeability so water is always coming in while the Hypatic Sinusoids of the liver are very permeabkento proteins. It’s where albumin is manufactured and it’s permeability allows it to enter blood
Water movement depends on
membrane permeability, hydrostatic pressure, oncotic pressures
It’s the different gradients btn these spaces that determines where water will move
Capillary and interstitial hydrostatic and oncotic pressures all interact to determine movement of water
Water coming out or out of vessels is determined by
Vessel permeability
The dimension of the lumen
The oncotic and hydrostatic pressures
What causes water to move from the ICF to the ECF
Aquaporins- integral membrane protein. Allows for rapid movement of water depending on cell’s needs
Sodium- in high concentration in ECF and draws ware out of the cell
Potassium- most prominent electrolyte inside he cell. Draws water back in
Proteins- in and outside the cell that are involved in water movement as well
Diabetes insipidous
Mutation in aquaporin is a disorder of the kidney and patients secrete large amount of dilute urine. Called diabetes insipidous. Usually secondary to a deficiency in anti diuretic hormone or bc or some toxicological events
How does posterior pituitary effect water flow?
Regulated by ADH
Osmoreceptors and baroreceotors detect changes in osmolarity and changes in BP. Constantly send signals to retain or excrete water. The body needs to retain water, ADH is secreted from the pituitary gland. ADH acts by inserting aquaporins in the distal tubules of the kidneys. Allow for the tea reabsorption of water and water is retained
ADH levels are low, water is excrete
SIADH
The Syndrome of Inappropriate ADH
Overexcretion of ADH
Excessive water retention leading to pulmonary edema, edema, and water overload
Is edema a disease in itself?
No it’s usually a manifestation of other disease processes
When does edema occur
1- proteins explain
- If there’s a < in plasma oncotic pressure (secondary to a < in plasma proteins-usually albumin)
- if proteins are not available in the vascular space water is gonna leak out like in liver failure. Liver doesn’t produce albumins so then there’s a decrease in intravascular oncotic pressure, when that happens, water can move out of the vessel and into the interstium manifesting as edema or ascities
When does edema occur
2- capillary HP
Increased capillary hydrostatic pressure
When there’s an > volume in the vessel. Secondary to > in water retention or > in water intake
Left Ventricular Hypertrophy
Increased Capillary Hydrostatic Pressure Example
When there’s failure of the left ventricle to affectingly pump blood which results in a backup of blood volume to the pulmonary vasculiture
This > the capillary hydrostatic pressures in the pulmonary vasculiture and fluid starts to leak out into the interstitium
This is pulmonary edema
High Altitude Pulmonary Edema
Increased Capillary Hydrostatic Pressure Example
Altitudes greater than 8200 ft. Incidence <1%
Hypoxia can ensue when people are at 8200ft or high for extended periods of time and hypoxia will induce pulmonary artery vasoconstriction
This > the pressure in that vessel and the capillary pressures which causes fluid to leak out giving you fluid in the interstitial space
When does edema occur
3- capillary permeability
Increased capillary permeability
Burns.
Increase vascular permeability and fluid leaks out
Second or third degree burns have lots of edema, it’s secondary to the capillary > in permeability
When does edema occur
4- lymph
Lymphatic obstruction
Causes backup of cellular recycling. Increase of pressure in vascular space and fluid will leak out
See this in people who have had lymph nodes removed bc if tumor or cancer. Mastectomy, one of their arms may have lymphodema
High Altitude &; Edema
Occurs at altitudes > 8200ft. Only occurs in 1% of people who probably have a different ACE enzyme. There are only low levels of o2in the atmosphere that that altitude, so hypoxia ensues. The pulmonary arteries construct/tighten up. >pulmonary capillary pressures, you’ll have a leaking of fluid through those capillaries into the interstitium giving you PE. Why it occurs in people with this Angiotensin-Converting Enzyme Polymorphism, no one knows
Sodium fun facts
Alkali metal
Large part of our diet, important for food preservation. Wars have been fought over salt. “Wich” towns were salt producing towns
Sodium affects water movement in the body (shocking)
Sodium is about 90% of ECF cations
Regulates osmotic forces and water balance
Serum Na:135-145 mEq/L
Controlled by Aldosterone
Excreting or retaining Sodium Pathway
If volume is < secondary to blood loss or dehydration or other volume loss states, you hold onto Na+ bc water will follow and total body volume will>. Barorecepters and osmoreceptors will notice this change but so will other cells
Name the 6 components involved in volume changes
Juxtaglomerular cells Angiotensinogen Angiotensin 1 (ACE) Angiotensin 2 ( intraglomerular mesangial cells) Aldosterone
Juxtaglomerular Cells and Sodium
Specialized smooth muscle cells found int the walls of the afferent renal arterioles. Have beta receptors that secrete renin enzyme in respond to a < in renal profusion. Renin will be released into the central circulation where it will cleave zymogen (inactive peptide) Angiotensinogen.
Zymogen
Inactive peptide
Angiotensinogen and salt
“A” is a liver derived peptide and it can circulate without any effect as an inactive molecule until it interacts with Renin. When this occurs, “A” is cleaved into Angiotensin 1, which is further metabolized by ACE (enzyme derived in the lung), into Angiotensin 2 then interacts with the smooth muscle of the renal arterioles causing them to constrict. “A”2 also stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone then interacts with kidney causing sodium retention, water follows.
What happens with aldosterone sodium and water retaining system is overactivated?
Hypertension (elevated BP)
ACE inhibitors PREVENT HP&>BP and block the system
ARBs “Angiotensin Receptor Blockers” also PREVENT the system
Direct renin inhibitors ALSO prevent
Chloride &; Potassium
Chloride sometimes follows sodium. Is important in membrane activity and inactivity.
Potassium is the major intracelular cation. Important in establishing the testing membrane potential of cells
An 83 yo F presents to her PC office bc of progressive weakness and malaise.
She hasn’t been feeling well due to a recent URI (Upper Respiratory Infection) and hasn’t been eating well either. She is on the diuretic chlorthalidone
Her measured K+ is 2.2 mEq/
Normals is 3.5-4.5
Hypokalemia
Hypokalemia
Low potassium level
Major intercellular cation, maintained by the Na+K+ ATPase pump, resting membrane potential of the cell
The electrical gradient of the cell at rest
A change has major effects
How does hypokalemia occur?
Can occur bc if < intake
Usually, from excess K+ loss bc of diuretic use, burns, or GI losses (vomiting diarrhea)
Weakness and fatigue due to muscles failure to repolarize
Can result in life threatening cardiac arrhythmias
A change in the resting membrane potential can result in a delayed repolarization of the ventricles making one susceptible to arrhythmias.
How does hypokalemia affect the heart?
Prolongation of P-R interval-> showing atrial repolarization
And T-wave flattening, the electrical manifestation of ventricular repolarization.
If hypokalemia ensues, this can make one prone to other arrhythmias like ventricular tachycardia or ventricular fibrillation
72 year old M s/p R hip replacement on ibuprofen for pain
Present to the ED with a complain of weakness, lethargy, and 2 days of abdominal cramping and diarrhea and dark urine
Cr (creatine): 2.2. K: 5.8
Normal Cr:0.5-1. K: 3.5-4.5
Hyperkalemia
Secondary to renal disfunction due to non-steroidal anti inflammatories (ibeprophen)
An > in K+ can be caused by:
Overt renal insufficiency
Medications that interfere with excretion (ibuprofen, some antibiotics)
Some diseases that cause hyperkalemia like Addison’s, or excess release of K+ from the cells from an injury, burn, or certain toxins
T or F
An increase in intraceullar levels of K+ can lead to an increase level of the extracellular levels of potassium
True!
This can lead to membrane excitability. This increase can result in a change of the Na/K+ channel/pump’s activity
The overall result is impaired function of muscles the GI tract. Life threatening arrhythmias are the most detremental manifestation.
What does hyperkalemia do to the heart
Very tall T waves, demonstrating a susceptible left ventricle to extra impulses that could induce ventricular fibrillation or ventricular tachycardia which are lethal arrhythmias.
42 yo marathon runner
Found lethargic, muscle twitching, hypotensive and confused on trolley
Measured Na: 128 mEQ/L
Normal range 135-145
Hyponatremia
Low sodium level
Causes of hyponatremia
Water loss
Sodium can flow water out of body!!
Also have water loss!, but with no electrolyte replacement
Over dilution an also have water overload like in CHF or liver failure, leading to hyponatremia
< in ability of cell to depolarize
Treat for hyponatremia
SLOW CAREFUL Na+ replacement Overaggressive sodium replacement (Central pontine monolynolysis) Complication of overaggressive sodium replacement, destroys myelin sheaths Coma, spasms, bad stuff
66 yo M w Hx of DM
Has been sick with pneumonia
Confused, lethargic, hypotensive, & tachycardic
Glucose: 760mg/dL
Na: 150 mEq/L
Hypernatremia
Not often caused by an increase in sodium but rather a deficit in fee water (volume or water loss like dehydration. Can occur if someone is drinking seawater (too much Na+) but usually lack of water. High glucose levels lead to excessive water loss. Glucose stuck outside of cells and water follows it outside
Tachycardic bc of increased excitability
Volume shifts too quickly=edema
Give insulin and carefully replace water
