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Pathophysiology > Fluid Electrolyte > Flashcards

Fluid Electrolyte Flashcards

1
Q

Intracellular Compartment ICF

A

Contains 2/3 of body water in healthy adults
Larger of the 2 compartments
Major Cation K+

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2
Q

Extracellular Compartment ECF

A

Contains 1/3 of body water
Contains all fluid outside the cells
Major cation : Na+

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3
Q

Capillary Hydrostatic Pressure

A

pushes water out of the capillary into the interstitial space

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4
Q

interstitial hydrostatic pressure

A

pushes water into the capillary

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5
Q

Capillary colloidal osmotic pressure

A

pulls water back into the capillary

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6
Q

Antidiuretic Hormone (ADH)

A

made in hypothalamus

affects kidneys to hold H2O

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7
Q

Aldosterone

A

affects kidneys and what is being excreted in urine

Retains sodium and H20 and excretes potassium

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8
Q

Renin Angiotensin System

A

a critical regulator of blood volume and systemic vascular resistance.

composed of three major compounds: renin, angiotensin II, and aldosterone

It can retains sodium and water
or
excrete potassium

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9
Q

Parathyroid Hormone

A

Monitors calcium levels and responds appropriately

  1. promotes release of calcium in bone
  2. helps further to activate vitamin d
  3. stimulates calcium and magnesium conservation by the kidneys while increasing phosphate exrection
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10
Q

Vitamin D

A

converted by kidneys into functional

essential to absorb calcium from GI tract

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11
Q

Calcitonin

A

inhibits calcium levels by preventing bone breakdown

tells the body not to give up calcium

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12
Q

Threshold Potential

A

critical level to which a membrane must be depolarlized to initiate an action potential

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13
Q

capillary permability

A

edema

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14
Q

Hypovolemia

A

exists when a net loss of sodium and water (eg, via skin, gut, or kidney) leads to ECF volume depletion.
IE : to little volume on board

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15
Q

Causes of Hypovolemia

A

inadequate fluid intake, excessive, GI Renal losses, excessive skin losses, third space losses

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16
Q

hypervolemia

A

to much fluid in your body

excessive sodium or fluid intake in relation to output

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17
Q

Causes of Hypervolemia

A

renal issues , heart failure, liver failure

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18
Q

Acid - Base is mainly concerned with 2 ions

A

hydrogen (H+)

Bicarbonate (HCO3-)

19
Q

Acids release

A

Acids release H+ when dissolved in water

20
Q

Bases bind

A

Bases bind free H+ in water

21
Q

Increased capillary hydrostatic pressure

A

Increased vascular volume

Increased venous obstruction

22
Q

Increased vascular volume =

A 
Increased vascular volume =  how much pressure are in your vascular system 
heart dx
kidney dx
pregnancy 
venous obstruction
23
Q

Increased venous obstruction =

A

Increased venous obstruction = talking about exit, back up of traffic, they are fluid overloaded
liver dx
acute pulmonary edema
venous thrombosis (clot)

24
Q

Decreased capillary Osmotic (oncotic) Pressure edema

A

Decreased capillary Osmotic (oncotic) Pressure
increased loss of plasma proteins
typically have liver disease

25
Q

types of edema

A

Increased capillary hydrostatic pressure edema

Decreased capillary Osmotic (oncotic) Pressure edema

Increased capillary permeability

Obstructed lymphatic Drainage

26
Q

Hyponatremia

A

low na
causes a delay in the depolarization of membranes via Na-K pump
causes : maybe due to diuretics ,vomiting ,D
manifestations : lethargy, headache wt gain, edema

27
Q

hypernatremia

A 
na high
causes water deprivation or water loss
sodium increases
oversecretion of aldosterone
patients become twitchy 
manifestations : thirst, fever, dry mucous membranes, pulmonary edema
28
Q

hypokalemia

A

low K
causes : inadequate intake, excessive losses from GI and Renal, and ECF - ICF shift
prolongs the rate of repolarization ; have S-T depression
patient becomes sluggish
lowers resting membrane potential
manifestations : weakness, cardiac dysrhythmias, glucose intolerance

29
Q

hyperkalemia

A

high K
causes : decreased renal excretion , cellular injury, excessive rapid admin , shifts of K from ICF to ECF
T- waves peak
patients become twitchy
raises resting membrane potential
manifestations : neuromuscular excitability increases (cardiac arrest)

30
Q

Calcium

A

important for bone health, muscle contraction, cardiac and skeletal muscle
you must have calcium to clot / activates clotting factors
affects threshold potential

31
Q

Hypercalcemia

A

nerves are less about to fire
the start line for threshold is farther ; these people end up being more sluggish
causes : cancer , hyperthyroidism
manifestations : muscle weakness / flacciditiy, behavior changes, slows down smooth muscle , kidney stones

32
Q

Hypocalcemia

A

nerves fire more easily
the start line for threshold potential is closer; these people tend to be twitchy
causes : unable to mobilize Ca from bone, decreased intake or absorption, increased chelation
manifestations : skeletal muscle issue (hyperactive), cardiovascular issues (sluggish), weakened bones, fail to respond to drugs

33
Q

Magnesium

A

cofactor in multiple metabolic reactions

affects cardiac and smooth muscle function

34
Q

hypomagnesemia

A

causes : alcoholism, insufficent intake, excessive losses,

effects : twitchy

35
Q

hypermagnesemia

A

causes : renal failure or Mg containing medications

effects : skeletal muscle depression, muscle weakness, respiratory depression, bradycardia

36
Q

compensatory mechanisms for pH balance

A

Chemical buffer systems immediate

Respiratory Response (second line of defense)

Renal Control

37
Q

Chemical buffer systems

A 
** immediate**
Bicarbonate buffer system
proteins 
transcellular H+/K+ exchange systems
bones serve as an additional source
38
Q

Respiratory Response (second line of defense)

A

lungs regulate levels of CO2

39
Q

Renal Control

A 
final control
has 3 major roles
erection of H+
Production of HCO3-
Retention of HCO3

long term adjustment
reabsorb acids and bases or excrete them in urine
produce bicarb

40
Q

respiratory acidosis

A

the body believes your not getting enough CO2
Manifestations : tachycardia and hypertension transitioning to bradycardia and hypotension, dyspnea, tachypnea, pale or cyanotic skin, anxiety, irritability, dysrhythmias
causes : anything that can depress or limit RR ( because your holding onto CO2), sepsis, burns
compensation occurs through elimination of acid or through reabsorption of base through kidneys

41
Q

respiratory alkalosis

A

causes : hypoxemia stimulated by hyperventilation, salicylate toxicity ( aspirin overdose), increased RR,
Manifestations
increased protein binding of extracellular calcium ,tachypnea, tachycardia possible dysrhythmias
compensations

kidneys eliminate alkaline or base and pH returns to normal

42
Q

metabolic acidosis

A

causes: excess production of hydrogen ion(DKA sepsis, burns) , inadequate elimination of hydrogen ion, inadequate production of HCO3 (renal failure, liver failure,dehydration) , or loss of bicarbonate (renal failure, pancreatitis , D)

Compensation mechanisms :
increase RR, decrease binding of calcium to proteins, depresses neuronal excitability,
blood becomes more acidic , respiratory centers stimulated

43
Q

metabolic alkalosis

A

causes : to much HCO3, oral ingestion of bases, acid loss

manifestations : asymptomatic , tachycardia, hypoventilation, dysrhythmias, seizures

compensation : short term : RR decreases, kidneys eliminate bicarb

Pathophysiology (4 decks)

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