Patho Chapter 8 Disorders Of Fluid, Electrolyte, And Acid Base Balance Flashcards

1
Q

Fluid,Ions, Nonelectrolytes, and electrolytes

A
  • Body fluids
  • Ions
  • Nonelectrolytes
  • Electrolytes
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2
Q

Functions of Body Fluids

A
  • Transport gases, nutrients, and wastes
  • Helps generate the electrical activity needed to power body functions
  • Take part in the transformation of food into energy
  • Maintain overall functions of the body
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3
Q

Distributions of Body fluids

A
  • Intracellular Compartment
    . Consists of fluid contained within all of the billions of cells in the body
    . Larger of two compartments, with approximately two thirds of the body water in high adults
    . High concentration of K+

-Extracelluar Compartmeng (ECF)
.Contain the remaining one third of body water
.Contains all the fluids outside the cells, including that in the interstitial or tissue spaces and blood vessels
.High Concerntration of Na+

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4
Q

Composition of the ECF, Plasma, and Interstial Fluids

A

. Large amounts of sodium and chloride
. Moderate amounts of bicarbonate

. Small quantities of potassium,magnesium, calcium, and phosphate

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5
Q

Composition of the ICF

A

.Almost no calcium

.Small amounts of sodium, chloride, bicarbonate, and phosphate

. Moderate amounts of magnesium

. Large amounts of potassium

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6
Q

Diffusion and Osmosis

A

. Concerntration Gradient
- Difference in Concerntration over a distance
. Diffusion
-The movement of charged or uncharged particles along a concentration gradient from an area of higher concentration to one of lower concentration
.Osmosis
- The movement of water across a semipermeable membrane from the side of the membrane with the lesser number of particles and greater concentration of water to the side with the greater number of particles and lesser concentration of water.

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7
Q

Tonicity

A

. The tension or effect that the effective osmotic pressure of a solution with impermeable solutes exerts on cell size because of water movement across the cell membrane.

. Solutions can be classified according to whether or not they cause cells to shrink

  • Isotonic: neither shrink nor swell
  • Hypotonic: Swell
  • Hypertonic: Shrink
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8
Q

Mechanisms Protecting Extracellular Fluid Volume

A

. Alterations in Hemodynamics Variables
- Vasoconstriction and an increase in heart rate

. Alterations in Sodium and water balance

  • Isotonic Contraction or expansion of ECF volume
  • Hypotonic dilution or hypertonic Concerntration of extracellular sodium brought about by changes in extracellular water
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9
Q

Edema

A

.Accumulation of fluid in extracellular space

  • Pitting edema
  • Nonpitting edema
  • Brawny edema
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10
Q

Edema Formation

A

.The physiologic mechanisms that contribute to edema include factors that

  • Increase the capillary filtration pressure
  • Decrease the capillary colloidal osmotic pressure
  • Increase capillary permeability
  • Produce Obstruction to lymph flow

. Localized edema
.General edema
.Dependent edema

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11
Q

Method for Assessing Edema

A

. Daily weight

. Visual assessment

. Measurement of the affected part

. Application of finger pressure to assess for putting edema

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12
Q

Physiologic Mechanisms Assiting in Regulating Body Water

A

.Thirst
-Primarily a regulator of water intake

. ADH
-A regulator of water output

-Both mechanisms respond to change in extracellular osmolality and volume

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13
Q

Water and Na+ Balance

A

. Baroreceptors regulates effective volume
.Modulating sympathetic nervous system outflow and ADH secretion
. ANP
. RAAS
-Angiotensin II
-Aldosterone

.Gain
-Water
-Oral intake and metabolism of nutrients
-Na+
.Loss
-Kidneys
-Skin
-Lungs
-Gastrointestinal tract
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14
Q

Regulators of Sodium

A

.The kidney is the main regulator of sodium

  • Monitors arterial pressure; retain sodium when arterial pressure is decreased; and eliminates it when arterial pressure is increased
  • The rate is coordinated by sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS).
  • Atrial natriuretic peptide (ANP) may also regulate sodium excretion by kidney
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15
Q

Assessment of Body Fluid Loss

A

. History of conditions that predispose to sodium and water loses, weight loss, and observations of altered physiologic function indicative of decreased fluid volume

  • Heart rate
  • Blood pressure
  • Venous volume / filling
  • Capillary refill rate
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16
Q

Phychogenic Polydipsia

A

. Compulsive water drinking
.Psychiatric disorders
.Schizophrenia
.Drinking large amounts of water and excrete large amounts of urine
. Cigarette smoking
-ADH
-Interferr with water excretion by the kidneys
. Antipsychotic medications increase ADH levels.

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17
Q

ADH and Aquaporin-2 Channels

A
. ADH
-V1 receptors
. Vasoconstriction 
-
-V2 Receptors
. Control water reabsorption
. Aquaporins
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18
Q

Disorders of ADH Expression

A

. Diabetes insipidus
-Deficiency of or a decreased response to ADH
-Patients unable to concentrate urine during periods of water restrictions and excrete large volumes of urine
-Neurologenic diabetes insipidus
-Central diabetes insipidus
.SIADH
-Failure of the negative feedback system that regulates the release and inhibition of ADH

19
Q

Types of Diabetes Insipidus

A

.Central or Neurologenic Diabetes Insipidus
-Occurs because of a defect in the synthesis or release of ADH

.Nephrogenic Diabtes Insiy
-Occurs because the kidney do not respond to ADH

20
Q

Causes of Fluid volume Excees

A

.Inadequate sodium and water elimination
.Excessive sodium intake in relation to output
. Excessive fluid intake in relation to output

21
Q

Isotonic Fluid Volume Excess

A

. Isotonic expansion of the ECF compartment with increases in both interstitial and vascular volumes
. An increase in total body sodium that is accompanied by a proportionate increase in body water
. Causes of decreased sodium and water elimination
- Renal function
- Heart failure
-Liver failure
-Corticosteroid excess

22
Q

Potassium Distribution and regulation

A

.Intracellular Concerntration of 140 to 150 mEq/L
. The extracellular concentration of 3.5 to 5.0 mEq/L
. Body stores of potassium are related to the body size and muscle mass
. Is normally derived from dietary sources
. Plasma potassium is regulated through two mechanisms:
- Renal mechanisms that conserve or eliminate potassium
-A trans cellular shift between the ICF and ECF compartments

23
Q

Abnormal potassium

A

. Hypokalemia refers to a decrease in plasma potassium levels below 3.5 mEq/L
1. Inadequate intake
2. Excessive gastrointestinal, renal, and skin losses
3. Redistribution between the ICF and ECF compartments
.Hyperkalemaia refers to an increase in plasma levels of potassium in excess of 5.0mEq/L
4. Decreased renal elimination
5.Excessively rapid administration
6. Movement of potassium from the ICF to ECF compartments

24
Q

Diagnosis and Treatment of Potassium Disorders

A

. Diagnosis is based on complete history, physical examination to detect muscle weakened and signs of volume depletion, plasma potassium levels, and ECG findings.

. Treatment

  • Calcium antagonizes the potassium-induced decrease in membrane excitability
  • Sodium bicarbonate will cause K+ to move ICF
  • Insulin will decrease ECF K+ concentration.
  • Curtailing intake or absorption, increasing renal excretion, and increasing cellular uptake
25
Q

Vitamin D, Calcium and Parathyroid Hormones

A

. Calcium , phosphate and magnesium are the major divalent cations in the body
. Vitamin D acts to sustain normal plasma levels of calcium and phosphate by increasing their absorption from the intestine.
. Calcitonin acts on the kidney and bone to remove calcium from the extracellular circulation

26
Q

Mechanisms Regulating Calcium, Phosphate and Magnesium Balance

A

. Calcium, phosphate, and magnesium are the major divalent cations in the body
. They are
- ingested in the diet
-Absorbed from the intestine
- Filtered in the glomerulus of the kidney
- Reabsorbed in the renal tubules
-Eliminated in the urine

27
Q

Physiological Calcium

A

. ECF calcium exists in three forms
-(1) protein bound
. 40% of ECF calcium is bound to albumin
- (2) complexed
. 10% is chelates with citrate, phosphate, and sulfate
-(3) Ionized
- 50% of ECF calcium is present in the ionized form

28
Q

Calcium Gain and Loss

A

. Gains
- Dietary dairy foods
- PTH and Vitamin D stimulate calcium reabsorption In this segment of the nephron
. Loses
- When dietary intake is less than intestinal secretion

29
Q

Causes and symptoms of hypocalcemia

A

.Causes

  • Impaired ability to mobilize calcium from bone stores
  • Abnormal loses of calcium from the kidney
  • Increased protein binding or chelation such that greater proportions of calcium are in the non ionized form
  • Soft tissue sequestration

Symptoms

  • Increased neuromuscular excitability
  • Cardiovascular effect
  • Nerve cells less sensitive to stimuli
30
Q

Causes and symptoms of hypercalcemia

A
.Increased intestinal absorb
- excessive vitamin D and calcium 
-Milk -alkali syndrome
. Increased bone reabsorption
-Parathyroid hormone
- Malignant neoplasms 
-Prolonged immobilization 
. Decreased elimination 
-Thiazides, lithium therapy

Symptoms

  • Changes in neural excitability
  • Alterations in smooth and cardiac muscle function
  • Exposure of the kidneys to high concentration of calcium
31
Q

Role of phosphate in the body # 1

A

. Plays a major role in bone formation
. Essential to certain metabolic processes
- The formation of ATP and the enzymes needed for metabolism of glucose, fat and protein

. A necessary component of several vital parts of the cell
. Incorporated into the nuclei acids of DNA and RNA and the phospholipids of the cell membrane

32
Q

Role of phosphate in the body # 2

A

. Serve as an acid - base buffer in the extracellular fluid in the renal excretion of hydrogen ions
. Necessary for delivery of oxygen by red blood cells
. Needed for normal function of other blood cells
- white blood cells and platelets

33
Q

Causes of hypophosphatemia and hyperphosphatemia

A

. Hypophosphatemia

  • Depletion of phosphate because of insufficient intestinal absorption
  • Transcompartmental shifts
  • Increased renal loses

Hyperphosphatemia

  • from failure of the kidneys to excrete excess phosphate
  • Rapid redistribution of Intracellular phosphate to the ECF compartment
  • Excess intake of phosphate
34
Q

Magnesium Balance

A
. Essential to all reactions that require ATP
. .Regulation at the kidney level
. Ingested in the diet
. Absorbed from the intestine
. Excreted by the kidneys
35
Q

Manifestations of Hypomagnesemia

A

. Laboratory values
- Serum magnesium level less than 1.8mg/do
. Neuromuscular manifestations
- Personlaity change, athetoid or choreiform movements, nyastagmus tetany, positive Babinski, Chvostek, Trousseau signs
. Cardiovascular manifestations
-Tachycardia, hypertension, cardiac dysrhythmias

36
Q

Causes of hypermagnesemia

A

. Excessive Intake
- Intravenous administration of magnesium for treatment of preeclampsia
-Excessive use of oral magnesium-containing medications
. Decreased Excretion
-Kidney disease
-Acute renal failure

37
Q

Mechanisms of Acid -base Balance

A

. Acid -base Chemistry
. Metabolic acid and bicarbonate production
-carbon dioxide and bicarbonate production
. Carbon dioxide transport
- production of fixed or nonvolatile acids and bases
. Calculation of Ph

38
Q

Regulation of ph

A
. Calcium buffer system
-Intracellular 
-extracellular 
. Respiratory control mechanisms 
. Renal control mechanisms
39
Q

Laboratory tests

A

. Carbon dioxide and bicarbonate levels
. Base excess or deficit
. Anion gap

40
Q

Disorders of Acid- base Balance

A

. Metabolic versus respiratory acid-base disorders
. Compensatory mechanisms
. Single versus mixed acid-base disorders

41
Q

Metabolic acidosis

A

. Etiology
. Clinical manifestations
. Treatment

42
Q

Metabolic Alkalosis

A

. Etiology
. Clinical manifestations
. Treatment

43
Q

Respiratory acidosis

A

.Etiology
.clinical manifestations
.Treatment

44
Q

Respiratory Alkalosis

A

.etiology
. Clinical manifestations
. Treatment