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Patho > electrolytes > Flashcards

electrolytes Flashcards

1
Q

Hypernatremia

A

Na > 145 mEq/L

Causes

  • excess sodium intake
  • not enough water intake
  • too much water loss
  • 66666Disease: diabetes insipidus, primary hyperaldosteronism, Cushing, diabetes666666

Manifestations
-With low ECF: symptoms of low ECF as well as thirst,
changes in mental status
possible seizures and coma
-With normal or high ECF: twitching, weight gain, edema, flushed skin

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2
Q

Hyponatremia

A

NA <136 mEq/L

Causes:

  • sodium loss due to GI, Renal losees, or skin losses
  • not enogh sodium intake
  • too much water
  • 6666Disease: SIADH, heart failure, primary hypoaldosteronism, cirrhosis6666

Manifestations

  • mild: headache, irritability, difficulty concentrating
  • severe: confusion, vomitting, seizures, coma
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3
Q

How to deal with hyponatremia from fluid loss

A

replace fluid with isotonic sodium solution
encourage oral intake
withold diuretics

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4
Q

how to deal with hyponatremia from water excess

A

fluid restriction
possibly loop diuretics and demeclocycline

acute hyponatremia allows for small amts of IV hypertonic saline solution

vasopressor receptor antagonists if can’t deal with fluid restriction (vaprisol from water excess and samsca for SIADH or heart failure)

IMportant not to corret faster than 6-12 mEq/l per hour during first day to avoid demyelination syndrome

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5
Q

how to deal with hypernatremia in primary water defecit

A

replace fluid orally or with isotonic IV

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6
Q

how to deal with hypernatremia from excess sodium

how fast?

A

dilute with sodium free IVS (5% dextrose in water)
diuretics
restrict sodium intake

Should not decrease by more than 8-15 mEq/L in 8 hrs to avoid cerebral edema

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7
Q 
Potassium
-where is it?
why is it important?
-where do we get it?
-how do we lose it?
A
  • 98% of body potassium is in cells (sodium potassium pump)
  • regulates membrane potential of nerve and muscle cells. Also regulates osmolality and cell growth. Also needed for glycogen deposit. Also acid-base balance
  • diet (also IVs, transfusions, meds)
  • kidneys lose 90% of K intake (inverse relationship bt Na and K reabsorption)
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8
Q

Hyperkalemia causes

A

K > 5 mEq/L

Excess K intake

Shift of potassium out of cells

  • acidosis
  • tissue catabolism
  • intense exercise
  • tumor lysis syndrome

Failure to eliminate K

  • renal disease ——————-> most common
  • adrenal insufficiency
  • Meds: Angio II blockers, ACE inhibitors, heparin, K sparing diuretics, NSAIDs
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9
Q

Hyperkalemia manifestations

A 
Dysrhythmias
Fatigue, confusion
Tetany, muscle cramps
Weak or paralyzed skeletal muscles
Abdominal cramping or diarrhea
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10
Q

Hyperkalemia ECG changes

A
  • Tall peaked T wave
  • prolonged PR interval
  • ST segment depression
  • widening QRS
  • loss of P wave
  • Ventricular fibrillation
  • ventricular standstill
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11
Q

How to deal with hyperkalemia (Don’t really need to know this slide)

A

-stop potassium intake

Increase secretions
-loop or thiazide diuretics, dialysis, patiromer (Veltassa), Kayexalate

Force K from ECF to ICF

  • use IV with dextrose insulin and B-adrenergic agonists (stimulates Na/K pump)
  • can use IV sodium bicarb if patient is acidotic

Stabilize cardiac membranes
-IV CaCl2 or calcium gluconate (doesn’t lower K but reverses toxic effects on heart cell membrane –> protects from dysrhthmias

Monitor ECG and BP (Ca causes decrease)
Monitor for hypoglycemia if giving insulin

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12
Q

Veltassa and Kayexalate

A

Kayexalate binds K in bowel –> each gram removes 1 mEq of K

Veltassa does same thing, but takes hours to days and is used in chronic cases –> careful! It also binds to other drugs

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13
Q

Hypokalemia causes

A

K <3.5 mEq/L

K loss
-GI, Renal (hyperaldosteronism), skin (diaphoresis), dialysis

Shift of K into cells

  • increased insulin release
  • insulin therapy
  • alkalosis
  • increased epinephrine from stress

Lack of K intake

Renal loss from diuresis

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14
Q

Hypokalemia clinical manifestations

A 
-Cardiac most serious
Skeletal muscle weakness (legs)
Weakness of respiratory muscles
Decreased GI motility
Hyperglycemia

-hyperglycemia (from impaired insulin secretion)

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15
Q

Hypokalemia ECG changes

A
  • flattened T wave
  • U wave
  • ST segment depression
  • prolonged QRS
  • peaked P
  • ventricular dysrhythmias
  • first and second degree heart block
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16
Q

How to deal with Hypokalemia

A

-increase K intake via food, oral KCl supplements, or IV KCl

IV infusion shouldn’t be more than 10 mEq/hr unless critical and constant ECG monitor –> USE infusion pump –> careful! it irritates skin!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

only give KCL if urine is 0.5 ml/kg body weight per hr

Monitor for digitalis toxisity (confusion, lazy, GI issues, nausea, bad appetite, blurry vision)

don’t eat a bunch of licorish

17
Q

Calcium

  • why’s it important?
  • what is needed for its absorbance?
  • where is it?
  • serum Ca levels reflect what?
  • hormones that affect serum Ca levels?
A
  • bones, blood clotting, nerve impulses, muscle contraction
  • vit D
  • 99% in bones –> of the rest, 50% bound to plasma prots, 40% free, and the rest is bound to ions
  • all forms of plasma ca (including bound to albumin)
  • PTH moves Ca out of bones, causes GI and kidneys to retain it
  • calcitonin does the exact opposite
18
Q

Hypercalcemia causes

A

Ca> 10.5 mg/dL (2.62 mmol/L)

hyperparathyroidism
cancer

Acidosis

19
Q

Hypercalcemia manifestations

A 
Fatigue, lethargy, weakness, confusion
Hallucinations, seizures, coma
Dysrhythmias
Bone pain, fractures, nephrolithiasis
Polyuria, dehydration
20
Q

Hypercalcemia ECG (IGNORE)

A

short ST
short QT
ventricular dysrhythmias
increased digitalis effect

21
Q

How to deal with Hypercalcemia (Only kinda relevant)

A
  • stop taking meds related to hypercalcemia
  • lower Ca intake
  • weight bearing exercise
  • maintain hydration 3000-4000 mL fluid per day (esp cranberry or prune juice) to avoid kidney stones

If severe:

  • IV isotonic saline (beware fluid overload if kidneys cant excrete Na)
  • bisphosphonate (interfere with osteoclasts, but takes 2-4 days
  • calcitonin (quick Ca excretion, but temporary and risks tachycardia)
  • denosumab (Prolia)
22
Q

Hypocalcemia causes

A

Ca < 9 mg/dL (2.25 mmol/L)

Low serum Ca levels caused by
Decreased production of PTH
Multiple blood transfusions - discuss
Alkalosis
Increased calcium loss

tumor lysis syndrome

chronic alcohol use

Alkalosis

Excess citrated blood

23
Q

Hypocalcemia manifestations

A 
Positive Trousseau’s or Chvostek’s sign
Laryngeal stridor
Dysphagia
Numbness and tingling around the mouth or in the extremities 
Dysrhythmias
24
Q

hypocalcemia ECG (IGNORE)

A

elongation of ST
prolonged QT interval
ventricular tachycardia

25
Q

How to deal with hypocalcemia

A
  • eat more calcium and vit D and/or have supplements
  • IV calcium glutonate
  • breathe into paper bag to retain CO2 for muscle spasms or tetany
  • quit loop diuretics –> change to thiazide diuretics
  • make sure parathyroid gland isn’t damaged
  • make sure they’re not anxious
26
Q

Phosphorus
where?
what’s it for?
what regulates it?

A
  • most in bones as CaPO4; the rest metabollically active as salts
  • helps muscles, RBCs, and nerv syst to func –> acid-base buffer, ATP formation, glucose uptake, carb/prot/fat metabolism
  • PTH and kidneys –> if PTH low, kidneys reabsorb more —> reciprocal relationship bt phosphate and calcium
27
Q

Hyperphosphatemia causes

A

PO4 > 4.5 mg/dl (1.45 mmol/L)

Acute kidney injury or chronic kidney disease
Excess intake of phosphate or vitamin D
Hypoparathyroidism

28
Q

Hyperphosphatemia manifestations

A

Tetany, muscle cramps, paresthesias, hypotension, dysrhythmias, seizures (hypocalcemia)
Calcified deposition in soft tissue such as joints, arteries, skin, kidneys, and corneas (cause organ dysfunction)

29
Q

How to deal with hyperphosphatemia

A

restrict phosphorus foods
phosphate binding agents (CaCo3) limits abosorbtion and increases secretion

If serious
-hemodialysis
loop diuretics to increase secretion

Almost always happens with low Ca, so watch out for that

30
Q

Hypophosphotemia causes

A

PO4 < 3 mg/dL (0.97 mmol/L)

Malnourishment/malabsorption
Diarrhea
Use of phosphate-binding antacids
Inadequate replacement during parenteral nutrition

31
Q

Hypophosphatemia manifestations

A

CNS depression
Muscle weakness and pain
Respiratory and heart failure
Rickets and osteomalacia

Most of these due to low cellular energy and O2 delivery
Chronic hypophosphatemia alters bone metabolism

32
Q

How to deal with hypophosphatemia

A

eat more phosphorus and dairy or take supplements
-dairy supplements are better bc they won’t fuck up GI

If serious

  • IV sodium phosphate or potassium phosphate
  • watch for hypocalcemia, hyperkalemia, hypotension, dysrhythmias

Monitor serum calcium and phosphorus levels every 6 to 12 hours

33
Q 
Magensium
abundance?
what's it for?
where's it stored?
what regulates it?
A
  • 2nd most abundant intracellular cation
  • cofactor in enzyme systs (carb metabolism, DNA snth, blood glucose contr, BP regulation) —> ATP production, muscle contraction, neurologic func
  • 50-60% in muscle/bone; 30% in cells; 1% ECF
  • Kidneys and GI syst regulate through ascending loop and distal tubules
34
Q

Hypermagnesemia causes

A

Mg > 2.1 mEq/L (1.05 mmol/L)

Increased intake of products containing magnesium when renal insufficiency or failure is present
Excess IV magnesium administration

35
Q

Hypermagnesemia manifestations

A

Inhibits acytylcholine at myoneural junc and Ca movement into cells

Hypotension, facial flushing
Lethargy 
Nausea and vomiting
Impaired deep tendon reflexes
Muscle paralysis 
Respiratory and cardiac arrest

super severe: paralysis, coma, respiratory/cardiac arrest

36
Q

How to deal with Hypermagnesemia

A
  • avoid Mg drugs and limit intake
  • more fluids and diuretics if kidneys are ok
  • dialysis if kidneys aren’t ok

If serious
-IV calcium gluconate or CaCl to help cardiac muscles

37
Q

Hypomagnesemia causes

A

Mg <1.3 mEq/L (0.65 mmol/L)

Prolonged fasting or starvation
Chronic alcoholism
Fluid loss from GI tract
Prolonged parenteral nutrition without supplementation
Diuretics, proton-pump inhibitors
Hyperglycemic osmotic diuresis
38
Q

Hypomagnesemia manifestations

A

Resembles hypocalcemia

Muscle cramps, tremors
Hyperactive deep tendon reflexes
Chvostek’s and Trousseau’s signs
Confusion, vertigo, seizures 
Dysrhythmias
39
Q

How to deal with Hypomagnesemia

A

oral supplements and increased dietary intake

If severe or hypocalcemia

  • IV magnesium
  • CAREFUL: rapid infusion can lead to hypotension or cardiac/respiratory arrest

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