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Lytes acid and base Flashcards

1
Q

All lytes are measured in

A

mEq/L

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2
Q

Sodium level

A

135-145

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3
Q

K+ level

A

3.5-5.0

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4
Q

Ca2+ level

A

4.5-5.5

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5
Q

Phosphate level

A

2.5-4.5

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6
Q

Mg level

A

1.5-2.5

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7
Q

Sodium function

A 
90% of ECF cations
Regulates osmotic forces and H20 balance
For muscle and nerves with K and Ca
Helps with pH through sodium bicarb and sodium phosphate
Particaptes in cell reactions
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8
Q

Hypernatremia

A

> 145
From extra sodium or too little water
It causes intracellular dehydration and movement of water to ECF which may cause hypervolemia

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9
Q

Hypernatremia etiology

A 
1. Excessive water loss from
Diabetes insipidus
Fever
Resp infections (tachypnea)
Diarrhea (osmotic)
2. Too little water
3. Too much sodium
too much Nabicarb
Saltwater near drowning
Over secretion of aldosterone
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10
Q

ADH

A

Vasopressin
Increases solute free water reabsorption
Constricts arteries
Released from hypertonicity

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11
Q

Clinical manifestations

A
  1. Thirst and signs of high ADH (polydipsia, oliguria, anuria)
  2. Intracellular dehydration
  3. H20 out of cells (headache, agitation, restlesness, decreased reflexes, seizures)
  4. Decreased vascular volume - tachy, weak and thready pulse, low BP
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12
Q

Hyponatremia

A

<135
Vomiting, diarrhea (inflammatory) GI suctioning, burns, sweating, lack of salt intake
Some diuretics
Hormone imbalances (low aldosterone high ADH)
Too much water
Kidney failure
Hypeglycemia as it draws water into ECF, lowering serum Na

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13
Q

Clinical manifestations of hyponatermia

A

Cramps, weakness, headache, depression, apprehension, impending doom, personality changes, lethargy, stupor, coma (from nerves not being able to depolarize)
GI - anorexia, nausea, vomting, cramps, diarrhea
Increased ICF causing pitting edema and hypotension

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14
Q

Potassium function

A

Maintaining RMP

Predominant ICF cation

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15
Q

Regulation of K+

A

Kidneys via diffusion, distal tubular cells determines whether it will be secreted into urine or reabsorbed into distal tubules

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16
Q

K+ and diuretics

A

increase flow rate of K+ through distal tubules increasing K+ secretion
There are K+ sparing diuretics which can counter this

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17
Q

K+ and pH

A

H+ accumulate in ICF and kick K+ out of cell

decreased ICF decreases secretion of K+ by distal tubular cells creating a state of hyper K

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18
Q

Hyper K causes

A

> 5.5 mEq/L
From increased K+
or a shift out of cells from
Trauma, burns, crush injuries, acidosis, insulin deficiency, hypoxia
Also decreased renal excretion from renal failure, aldosterone deficit, K+ sparing diuretics, ACE inhibtors, Angiotensin II receptor blockers

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19
Q

Hyper K clinical manifestation

A 
GI
-nausea, vomiting, cramps, diarrhea
Muscles
-paraesthesia
-muscle weakness
Cardiovascular
-arrythmias, cardiac arrest
Oligura
Acidosis
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20
Q

Hypo K

A

<3.5 from

  • Inadeqaute intake
  • Renal loss (non K+ sparing, cushings, aldosteronism, steroids)
  • Vomiting, diarrhea, GI suction, draining GI fistula
  • Transcompartmental shift from ventolin, alkalosis, insulin
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21
Q

Hypo K presentation

A

Impaired ability to concentrate urine (polyuria nocturia)
Anorexia, nausea, vomiting, constipation, abdo distension, paralytic ileus
Muscle flabbiness, weakness, fatigue, paresthesia, paralysis, cramps
ECG changes, postural hypotension
Confusion, depression
Alkalosis

22
Q

Where is calcium

A

99% in bone
.4 ionized
.6 non ionzed (bounded to albumin)

23
Q

Calcium is needed for

A 
Structure (bone teeth)
Clotting
Hormone secretion, cell function
Plasma membrane stability
Transmission of nerve impulses
Contraction of muscles
24
Q

Calcitonin

A

Opposes PTH, and REDUCES blood calcium

25
Calcium/phopshate mediated by
PTH Vit D Calcitonin
26
Hypercalcemia
<12mg/dl From: Too much D or calcium Milk-alkali syndrome Increased bone resporption (hyperPTH, bone metasis from cancer, immobility) Decreased elim from thiazides or lithium Acidosis (decreases Ca binding to albumin)
27
Hypercalcemia clinical manifestations
Polyuria, dipsia, flank pain, renal failure, kidney stones Anorexia, N/V, constipation Muscle weakness, atrophy, ataxia, loss of tone Osteopenia (low density but not porosis low), osteoprosis Lethargy, personality and behaviour changes, stupor coma hypertension, QT shortening, AV block
28
Hypocalcemia
<8.5mg/dl HypoPTH, hypomag, resistance to PTH Decreased intake from vit d deficiency, liver or renal failure Abnormal loss from too much phosphate or renal failure
29
Hypocalcemia etiology
increased protein binding or chelation Increased pH increases serum albumin increases fatty acids or rapid transfusion of citrated blood Pancreatisi
30
Hypocalcemia clinical manifestations
Paraestehsia, cramps, gi spams, carpopedal spasm, tetany (intermittent spasm from PTH), laryngospasm Hypotension, arrythmias Osteomalacia, bone pain, fractures, deformities
31
Phosphate overview
Mainly in bone Serum it exists in phospholipids and inorganic compounds Acts as a buffer and role in high energy stores
32
Hyperphosphatemia
<4.5mg/dl Laxatives or enemas with phosphates Intracellular to extra shift from trauma, heat stroke, seziures, rhabdo, tumor Impaired elimination (renal failure or hyperthyroidism)
33
Clinical manifestations
same as low calcium
34
Hypophosphatemia
``` <2mg/dl Severe diarrhea Lack of D Antacids binding phosphates Increased renal secretion HyperPTH, DKA, alkalosis malnutrtion Total parental hyperalimentation, insulin from DKA ```
35
Hypophosphatemia manifestations
Reduced O2 capacity by RBC ATP issues 2,3 diphospho used to release oxygen, so decrese will shift to left (causing hypoxia) Hemorrhage from altere leukocyte and platelet function Irritability, confusion, numbness, weakness, chest pain, convulsions
36
Mg
Major intracellular cation | Cofactor in intracellular enzymatic reactions (ATP?)
37
Hypomag
``` <1.5 From absorption issues (ETOH, starvation, bowel bypass or increased losses (diuretics, hyperPT, hyperaldost, DKA) ```
38
Hypomag clinical manifestations
Similar to hypo calc and hypo K because they occur in conjucation Tachy, hypertensive, arrythmias
39
Hypermag
>2.5 Too much mag sulfate, or kidneys can't excrete N/V lethargy, HYPOreflexia, confusion, hypotension, brady, cardiac arrest, resp depression
40
Osmolality definition
Refers to concentration of solutes in soluction, term used in reference to extracellular space
41
Isotonic imbalance
Changes in body water equal with lytes. No cell shape changes
42
Isotonic volume depletion causes
Inadequate fluid | Excessive GI fluid loss, renal loss, skin loss, third space loss
43
Hypertonic imbalance
>0.9% Na+ causes ECF to attract water from intracellular space (ICF dehydration) cells shrink due to water loss
44
Hypotonic imbalance
Hypo-osmalar ECF less than 09% from sodium deficinecy or excess water causes edema and decreased plasma volume so symptoms of hypovolemia
45
Metabolic acidosis causes
Lactic acid build up from poor perfusion Kidney failure DKA Ingestion of ammounium chloride, salicylates Loss of bicarb from diarrhea or renal failure
46
Metabolic acidosis clinical
``` Neuro, resp, GI, CV issues Headache Kussmauls Anorexia dysrhythmias Resp increases CO2 exhalation to compensate ```
47
Metabolic alkalosis
Increases in bicarb or loss of acid from GI suctioning or vomiting Too much bicarb Diuretics Causes weakness cramps hyperactive reflexes and tetany CO2 retained to compensate
48
Resp acidosis
Hypercapnia (retained CO2) from depressed vent or decreased alveoli diffusion, chronic or acute Trauma or oversedation Resp muscle paraylsis Kyphoscoliosis, flail, pneumonia, pulmonary edmea, emphysema, asthma, bronchitis Kidneys compensate by retaining bicarb (HCO3-) and pissing out H+ but takes hours to days
49
Resp acidosis clinical
Restlessness, apprehension, lethargy, muscle twitching, tremors, convulsions, coma CO2 can cross blood brain and drop CSF pH and cause vasodilation
50
Resp alkolosis
Hypoxemia (pulmonary disease, CHF, high altitudes) fever, anemia, sepsis, salicyate OD (EARLY) hysteria, improper vent use Irritates CNS and PNS, dizziness, convulsions Carpopedal spasm

Pathology (24 decks)

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