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Pathophysiology > Patho: Fluids and Electrolytes > Flashcards

Patho: Fluids and Electrolytes Flashcards

1
Q

Intracellular compartment location and compostition

A
  • Fluids in cells.
  • 66% Body fluid and 40% body weight.
  • incr. K
  • moderate Mg
  • small Na, Cl, P, HCO3
  • No free calcium.
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2
Q

Extracellular compartment location and composition

A
  • Fluid outside the cells.
  • Includes interstitial spaces and blood vessels.
  • 5% body weight in plasma, and 14% body weight in interstitial fluid.
  • incr. Na, Cl
  • moderate HCO3
  • small K, Mg, Ca, P
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3
Q

Intersitial compartment location and roles.

A
  • Part of the ECF-Space surrounding the tissues
  • Transport for gases, nutrients, wastes, other.
  • Fluid resevoir for vascular system if fluid volume drops. (why may have sunken eyes when dehydrated)
  • Collagen fibers support the ISF creating a tissue gell that prevent free water from outside the ISF entering the Interstitial spaces causing edema.
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4
Q

Transcellular compartment locations and the effect of Third space accumulation.

A

Transcellular compartment:
-A small volume of fluid found in body cavities, including the cerebrospinal fluid, peritoneal, pleural and pericardial cavities
-Also includes joint spaces
-Accounts for 1% of ECF
-If this amount increases due to clinical causes, the fluid is inaccessible by the rest of the ECF and is ‘trapped’.
-It’s called third space accumulation
Ex: ascites in the peritoneal cavity.

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5
Q

Edema

A
  • Defined as palpable swelling produced by the expansion caused from increased interstitial fluid volume
  • Usually does not become notived until the volume has increased to 2.5 - 3L
  • Several mechanisms at play in edema, usually involving multiple organ systems (Ex: liver, Heart (right sided heart failure))
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6
Q

Etiology of Edema

A

1) Increased Capillary Filtration Pressure. (ICFP)
2) Decreased Capillary Colloidal Osmotic Pressure. (low plasma proteins) (DCCOP)
3) Obstruction to Lymph Flow. (OLF)
4) Increased Capillary Permeability. (trauma) (ICP)

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7
Q

Increased Capillary Filtration Pressure:

1) How does it lead to Edema?
2) 3 types of edema that can result from this.

A

1) -Decreased resistance to flow by precapillary sphincters
- Increased venous pressure or increased resistance in postcapillary sphincters
- Capillary distension caused by increased capillary volume

(Note: As the pressure within the capillary rises, the movement of vascular fluid into the interstitial spaces increases becuase there’s no where else to go. High pressure in vessels = edema in interstitial space.)

2) -Localized: inflammation, Histamine
- Generalized: Incr. vascular volume. Common with CHF= fluid retention and venous congestion.
- Dependant: Edema in areas that experience gravity (feet, hands)

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8
Q

Decreased Capillary Colloidal Osmotic Pressure:

1) How does it lead to Edema?
2) Tissue types affected

A

1) -A loss/decrease of plasma proteins.
- Plasma proteins are synthesized in the liver, therefore edema could indicate a problem with liver function (Ex: cirrhosis) or be an indicator of malnutrition.
- Kidney issues can cause increased loss of plasma proteins

(Note:This is just that osmosis doesn’t work b/c of low plasma proteins, so fluid stays in the interstitial compartment (face, legs, feet) and swells b/c there are no plasma proteins to trigger osmosis to bring the fluid back into the capillaries.)

2)-Affects all tissues in a generalized and non-dependent manner.-Swelling presents in the face, legs and feet

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9
Q

What are plasma proteins?

A

(Plasma proteins are needed to exert the osmotic force needed to pull fluid back into the capillary from the tissue spaces.)

Osmosis: low to high concentration.

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10
Q

Increased Capillary Permeability:

1)How does it lead to Edema?

A

1)-Occurs if the pores become enlarged or there is a break in the capillary wall or it’s injured.
(holes in capillaries)
-Plasma proteins leak into the ISF, drawing further fluid with them
-Conditions include trauma, burns, inflammation and immune responses to the capillaries

(Note: Plasma proteins will leak into ISF bringing fluid with them. This is caused by trauma or burns to the capillaries increasing their permeability (flow of substances))

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11
Q

Obstruction to Lymph Flow:

1)How does it lead to Edema?

A

1)Can be caused by a blockage to lymph nodes, or by removal of lymph nodes d/t surgery.
It’s termed “lymphedema”Prevent it because otherwise it will obstruct the lymphatic system, and you don’t want that.

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12
Q

S/s of Edema

A
  • Swelling: dependant or generalized.
  • Joint issues.
  • High risk tissues >Lungs (pulmonary edema decr. gas exchange >heart (overload) >brain (cerebral edema) >larynx
  • Downstream ischemia: edema can be so sever that it cuts of blood flow. CWSM.
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13
Q

Assessment of Edema

A
  • Daily weights
  • Visual assessment
  • Measurement of affected area and evaluation of pitting edema
  • CWSM
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14
Q

Treatment of Edema

A
  • Diuretics
  • Elevation of extremeties to help fluid drainage
  • Supportive stockings (TED): preventative Tx prior to the effects of gravity. and improves venous return.
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15
Q

What is Third Space accumulation?

A
  • Represents a loss of fluid into the transcellular compartments
  • Accumulation usually results from an error in lymphatic drainage
  • Can cause some functional impairment
  • Referred to as ascites in the peritoneal cavity and effusion elsewhere
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16
Q

Sodium and Water Balance

A

Movement of electrolytes occurs at the cell membrane

Water accounts for 90-93% of fluid and sodium salts account for 90-95% of the ECF electrolytes

Changes in sodium are usually accompanied by changes in water volume

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17
Q

What is Total Body Water?

A

Amount of water in the body.

  • Varies with gender.
  • largely dependant on the amount of fat and muscle a person has. (fat is hydrophobic)
  • Men: 60% when you and declines with age (50%)
  • Women: 50% when young and declines with age (40%)
  • Obesity decr. total body weight b/c of fat.
  • Infants: 75-80%. D/t their high metabolic rate, larger surace area in relation to body mass, and inability to concentrate urine.
  • infants are susceptible to dehydration, as well as obese people.
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18
Q

Water Gains and Losses of total body water over 24 hrs

A

Gain:

  • Individuals require 100mL of water for every 100 calories expended – why? For dissolving and eliminating wastes for metabolic purposes.
  • Fever requires an increase in fluid consumption as metabolic rate increases with fever**
  • Fluid intake occurs through oral intake and metabolism of nutrients

Loss:

  • Water is absorbed from the GI tract
  • Loss of body water occurs through the kidneys, GI tract, skin (sweat) and respiratory tract.
  • Kidneys function to regulate fluid volume and ECF solute concentration.
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19
Q

1) What is Obligatory Urine Output?
2) Average value of U/O
3) Conditions that incr./decr. fluid volume.

A

1) The minimun amount of urine that is lost from the body per day to rid the body of metabolic waste.
2) Min amount: 300-500ml/day relating to metabolic waste.
3) Vomiting and Diarrhea can cause incr. fluid loss (Dehydration)

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20
Q

Functions of Sodium

A

1) Regulate Extracellular fluid volume.
2) Plays a role in acid-base balance.
3) Electrical signalling by the nervous system.

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21
Q

What are the sodium Gains and Losses?

A

Gain:

  • Intake through the GI tract and exits through kidney excretion
  • Minimal intake needed is 500mg/day

Loss:

  • Renin-angiotensin-aldosterone system and the sympathetic nervous system aids in controlling sodium excretion
  • Sodium loss increases in instances of diarrhea and vomiting
  • Sodium also leaves via the skin through sweat glands that’s why sweat is salty and tears are too.
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22
Q

Mechanisms that regulate Total Body Water and Sodium Balance.

A

-Antidiuretic Hormone and Thirst:
Thirst regulates water intake and ADH regulates output

Both respond to changes in ECF osmolality and regulation of sodium concentration

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23
Q

What is thirst?

A

An emergency response to dehydration.
A conscious sensation to obtain fluids.
People usually drink before they are “thirsty”

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24
Q

What are two triggers of thirst?

A

1) Cellular dehydration (b/c of incr. ECF osmolality)

2) Decreased blood volume.

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25
Q

1) What are the body fluid sensors?

2) What are their functions?

A

1) Osmoreceptors, and Barorceptors.

2) Osmoreceptors: respond to osmolality.
- Sensory receptors located near the hypothalamus(controls thirst)
- Respond to changes in osmolality and stimulate the sensation of thirst.

Baroreceptors: help monitor BP (senses changes in blood volume)

  • Play a role in monitoring blood volume and can also stimulate thirst when low BP d/t dehydration.
  • Angiotensin II is released when blood pressure drops and triggers the sensation of thirst
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26
Q

What are the “Inappropriate Thirst Signals?”

A

Hypodpsia (Decreased ability to sense thirst)

  • occurs with head trauma to the hypothalamus.
  • also occurs wth incr. age.

Polydipsia- (Excessive thirst)
-Has 3 catagories: (true thirst, inappropirate thirst, compulsive water drinking)

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27
Q

What are the 3 categories of Polydipsia?

A

1) True thirst
- Develops when neeed, and disappears once fluid balace is restored.
- Can be caused by DM, Diarrhea, Vomiting.

2) Inappropriate thirst
- Thirst that persists after hydration is restored
- Common problem for ppl with Renal Failure or CHF.
- Could be a SE of meds.

3) Compulsive water drinking
- Usually with psychiatric disorders
- Lead to water intoxication b/c too much water that dilutes electrolytes and then there’s also the elimination of electrolytes when voiding.

Without Na, nerves and muscles cannot work properly and cannot conduct the signalling for the nervous system.
Tx: with water restriction and behavioural modification to decr. water intake.

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28
Q

1) What is the function of ADH in the body?
2) When is ADH released?
3) What is the control of ADH?4)What are some influences on ADH secretion?

A

1) Regulates reabsorption of water in the kidneys to not excrete too much (Anti diuretic)
2) Released by the hypothalamus and stored in posterior pituitary

The release is determined by the Osmoreceptors.

3) Prevent urinating too much.
4) Diabetes Insipidus, and SIADH

29
Q

What is Diabetes Insipidus?

A

-A Deficiency or dereased response to ADH.

  • People are not able to concentrate their urine and conserve water when it needs to be retained.
  • This make a person urinate a lot.
  • Can urnate 3-20L/day( will need to drink a lot to make up for the loss)
  • Accompanied by excessive thirst b/c urinating a lot and losing a lot of fluid.
  • Danger arises if not enough water is consumed to compensate for U/O
30
Q

Causes of Diabetes Insipidus

A

1) Neurogenic: A defect in ADH synthesis or release.
- Usually does not cause a complete lack of ability to produce concentrated urine.
- Temporary instances can result from head injury or neural surgery.

2) Nephrogenic: Kidneys don’t respond to ADH that’s circulatin. Results in not absorbing water.
- May be a genetic defect in kidney ADH receptors or as a SE of meds containing lithium.

3) Dipsogenic: A defect to thirst mechanism (hypothalamus).
- Results in an abnormal increae in thirst and fluid intake that suppresses ADH secretion and increase U/O

4)Gestational (Maternal): occurs during pregnancy and results when an enzyme made by the placenta destroys ADH in the mothr.

31
Q

Dx of Diabetes Insipidus

A

Urinalysis

  • urine will be less concentrated
  • salt and waste in low and water amount is high

Fluid deprivation test: If DI is caused by:

  • excessive intake of fluif-defect in ADH production (neurogenic)
  • defect in kidneys reponse to ADH (nephrogenic)
32
Q

Managment of Diabetes Insipidus

A

Depends on cause and severity

  • Possible self managment by appropriate intake of fluids.
  • Medications can be used to stimulate the hypothalamus, and thiazide diruetics act to decrease sodium excretion.
33
Q

1) What is SIADH

2) S/s of SIADH

A

1) Syndrome of Inappropriate ADH release.
- Results from a negative feedback system that regulates the release and inhibition of ADH causing it to be released too much.
- Results in extreme water retention and hyponatremia (b/c there’s too much water compared to sodium making it hyponatremia)

2)S/s: Peripheral edema, Pulmonary edema, Crackles,

34
Q

Chronic and Trasient SIADH

A

Transient:

  • Transient stimuli include surgery, pain, stress and temperature changes
  • Drugs can either stimulate ADH release from the hypothalamus or increase the effectiveness of ADH in the kidney tubules

Chronic:

  • Can result from lung tumours, chest lesions and CNS disorders
  • Tumours produce ADH
  • Chest conditions can change the response of stretch receptors, resulting in the release of ADH
35
Q

Dx of SIADH

A
  • U/O decrease despite normal fluid intake.

- Blood volume increases and results in decreased sodium osmolality, hematocrit and water intoxication.

36
Q

Tx of SIADH

A

Depends on sverity

  • Mild: Fluid restriction and diuretics
  • Severe: hypertonic solution is given IV and new drugs that are ADH antagonists are being developed.
37
Q

What are the Disorders of Water and Sodium Balance?

A

1) Isotonic Fluid Volume Deficit
2) Isotonic Fluid Volume Excess
3) Hyponatremia
4) Hypernatremia

38
Q

1) What is Isotonic Fluid Volume Deficit?

2) What is it’s Etiology?

A

1) A decrease in ECF including blood volume.
- Relationship b/w water and sodium,
- Hypovolemia occurs if the circulating lvl of blood volume is severely compromised.

2)Etiology: Loss of body fluid and decr. fluid intake.-caused by Vomiting, Diarrhea, polyuria, sweating a lot, exercise.-urinary losses can result from kidney disease or excessive use of diuretics-Is also a SE of Addisons disease.

39
Q

S/s of Isotonic Fluid Volume Deficit

A
  • Thirst
  • Attempted water conservation by the kidneys
  • loss of body weight
  • impaired temp regulation and reduced interstitial and vascular volume.
  • Weight LOSS : 2% mild. 5% moderate. 8% severe.
  • Sunken eyes
  • Decr. skin turgor
  • Decr. body temp
  • Decr. BP
  • Incr. HR but weak pulse.
40
Q

Dx of Isotonic Fluid Volume Deficit

A
  • Based on weight-Intake and output measurements
  • observations of altered physiological function
  • Cap refill and Vein refill to determine if there is a deficit in venous volume. (Slow)
41
Q

Tx of Isotonic Fluid Volume Deficit

A

Providing fluids and, treating underlying cause.

42
Q

What is Isotonic Fluid Volume Excess?

A

Causes an increase in ISF and vascular volume.

  • Almost always results from incr. Na, which causes conservation of water.
  • Caused by a decr. in Na excretion.

Decr. Na excreteion is caused by: heart failure (decr. blood flow to kidneys), Liver failure (loss of hormone/drug metabolism), Corticosteroids (target sodium reabsorption)

43
Q

S/s of Isotonic Fluid Volume Excess

A
  • an Increase is ISF and vascular fluids
  • Weight GAIN: 2% mild. 5% moderate. 8% severe.
  • Edema is often present.
  • Causes an increase in venous volume and HR.
  • Excess fluid in the lungs can cause resp.distress.
44
Q

Dx of Isotonic Fluid Volume Excess

A

Weight gain
Edema
Cardio/resp inolvement

45
Q

Tx of Isotonic Fluid Volume Excess

A

Diuretics

Limit Na intake.

46
Q

1) What is Hyponatremia?

2) What are the causes?

A

Low Sodium.
135-145mmol/L, anything below 135 is hyponatremia.

Possible Hyponatremic Causes:

  • Hypertonic shift of water from the ICF to ECF, diluting sodium in the ECF.
  • Water retention diluting Na.
  • Water is lost along with Na
  • Water is retained as normal lvls while sodium is reduced, like in SIADH.
  • Associated with edema
  • causing conditions such as heart failure, cirrhosis, nephrotic syndrome and advanced renal disease.
47
Q

S/s of Hyponatremia

A

Early:
Muscle cramps
Weakness/fatigue
Vomiting, diarrhea, nasuea, abdominal cramps

If brain swelling occurs (from water retention), it can lead to irreparable damage and water intoxication is usually Dx’d when neurological symptoms develop.

48
Q

How does hyponatremia alter homeostasis?

A
  • Low Na lvls impair nerve conduction.
  • Decreased osmotic pressure in the extracellular compartment may cause a shift into cells, resulting in hypovolemia and decreased BP.
  • The neurons and/or neuroglia may swell.
49
Q

Dx of hyponatremia

A

Lab results of Na serum.

s/s of the disorder

50
Q

Tx of hyponatremia

A

Tx underlying cause.

  • Water restrictions
  • Salt restriction (b/c Na lvls may quickly shift if given Na and become hypernatremia.)
  • Saline drip (to provide an adequate amount of salt)
  • Tx is slow and regulation to prevent neurological damage
51
Q

1) What is Hypernatremia?

2) What are the causes?

A

High Sodium.
Serum lvls greater than 145mmol/L
-Characterized by hypertonicity of the ECF resulting in cellular dehydrarion

Causes of Hypernatremia:

  • Increased sodium or decreased water.
  • Rapid ingestion of sodium without sufficient water intake.
  • A defect in thirst b/c then you won’t drink.
  • Excessive respiratory tract water loss
  • Watery diarrhea
  • Tube feedings without adequate water intake. (IV not enough, or not drinking enough)
52
Q

How does Hypernatremia alter Homeostasis?

A

1) Cellular dehydration, can alter the isotonic balance.
- cells will shrink
- neurons/muscle: alter transmembrane potential.
- Alters function.

2) Increased Plasma volume ( Incr. Na= Incr. water)
- Dilute other electrolytes-Incr. BP
- Change CO
- Kidney problems.

53
Q

S/s of Hypernatremia

A
  • Elevated body temp
  • Skin is flushed
  • U/O is decreased
  • Skin and mucus membranes are dry
  • Salivation decreases
  • Mouth is dry
  • Swallowing is difficult.
  • Neurological symptoms are significant causing: decreased reflexes, agitiation, headache and restlessness.
54
Q

Dx of Hypernatremia

A

Based on Hx
Physical exam indicatin dehydration
Na serum lab results

55
Q

Tx of Hypernatremia

A
  • Oral fluid replacement

- Water and salt balanced and regulated (slowly but not too slow)

56
Q

How does Potassium maintain homeostasis?

A
  • Potassium is major in the ICF with a concentration of 140-150mmol/L
  • About 65-75% of K is found in muscles.
  • Total Body Potassium therefore decreased with age b/c we lose muscle mass as we age b/c we’re not using it as much.
57
Q

What are some Gains and Losses of Potassium.

A

Gain:

  • Intake is derived from dietay sources where 50
  • 100mmoles are needed/day

Loss:
-Kidneys are the main source of potassium loss where 80-90% of loss occurs in the urine, the remainder is lost in stools and sweat.

58
Q

What are the Mechanisms of Potassium Regulation.

A

1) Renal regulation

2) Shifts between ICF and ECF

59
Q

Renal Regulation of Potassium

A

-Aldosterone: retains Na, and also regulates K balance in the kidney.
When present, Na is absorbed back into the blood and potassium is excreted.
-The kidney can excrete K when too high, exchanging it for Hydrogen, producing a decrease in pH and creating metabolic acidosis.
-When K lvls are low, K is reabsorbed and Hydrogen is secreted into the urine, resulting in metabolic alkalosis in order to bring the K lvls back up again.

60
Q

Extracellular -Intracellular Shift of Potassium

A

RBC’s, muscle, liver, and bone all act as a temporary reserve for potassium when there is too much in the blood.
This movement is controlled by the Na/K pump.

  • Insulin: incr. cellular uptake of K = Decr. in plasma potassium
  • Epinephrine: incr. muscle uptake of potassium= Decr. in plasma potassium.
  • Exercise: Released potassium into the ECF = incr. plasma potassium
61
Q

1) What is Hypokalemia?

2) What are the causes?

A

Low potassium K < 3.5mmol/L

Causes of Hypokalemia:

  • Inadequate intake: need 10-30mmoles/L to account for obligatory urine loss.
  • Excessive renal loss: Diuretics, metabolic alkalosis(from H and K exchangeing if K was too low), magnesium depletion, trauma, stress, vomiting and increased aldosterone.
  • Redistribution from ECF to ICF: Drugs can cause temporary hypokalemia, insulin also incr. uptake of K into cells.
62
Q

S/s of Hypokalemia

A
  • Altered membrane potential and excitability of cardiovascular, neuromuscular and GI function.
  • U/O is increased, urine specific gravity is decreased, polyuria and thirst are common.
  • GI: anorexia, nausea, vomiting, constipation, abdominal distention
  • Postural HTN, ECG changes, arrhythmias and bradycardia
  • Weakess, fatigue, muscle cramps (arise during exercise)
  • Pralysis of resp muscles with SEVERE hypokalemia
  • May cause atrophy if chronic.
63
Q

Dx of Hypokalemia

A

K lvls and s/s

64
Q

Tx of Hypokalemia

A
  • Increased potassium intake (foods)

- Potassium IV when oral route is not tolerated, but monitor closely to prevent death by cardiac arrest d/t too much K.

65
Q

1) What is Hyperkalemia?

2) What are the causes?

A

High potassium.
over 5mmoles/L
Rarely occurs in healthy ppl b/c the body is effective in preventing an excess of ECF potassium.

Causes of Hyperkalemia:

1) Decreased renal elimination of Potassium:-Renal failure (acute for hyperkalemia to be a problem)
- acidosis results in slowed potassium excretion.
- Decreased aldosterone excretion (to excrete K) or kidney response to aldosterone can also result in decreased renal elimination.
2) Excessive administration:
- If IV potassium is infused too quickly (renal function must be assessed prior to administration of potassium IV)
3) ICF to ECF movement:
- Movement can be caused by tissue injury such as burns and trauma b/c it causes cell death and release of potassium into ECF
4) Transiet Hyperkalemia
- Extreme exercise/seizures can incr. K b/c it releases K from the muscles.

66
Q

S/s of Hyperkalemia

A

paresthesia
Muscle weakness
dyspnea d/t resp muscle weakness
Most serious effect is on the heart b/c it can become very slow and cause conduction issues.
HR may slow, ventricular fibrillation and cardiac arrest can be terminal

67
Q

Dx of Hyperkalemia

A

K lvl

s/s

68
Q

Tx of Hyperkalemia

A
  • Focus on decr. intake or absorption and increasing renal excrtion and increasing cellular uptake ( Ex: Give insulin)
  • Intake of K is limited.
  • Ppl with renal failure may need dialysis or peritoneal dialysis or an IV infusion of Insulin (and glucose to prevent hypoglycemia) can be used to increase cellular uptake.

Pathophysiology (7 decks)

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