Exam 1 SG Flashcards
Fluid Volume Deficit Causes
-Fluid loss (diarrhea, vomiting, polyuria, hemorrhage)
-Inadequate intake (unconscious, not thirsty)
-Fluid shift (burns)
HYPOVOLEMIA
Fluid Volume Deficit Labs
Electrolytes are lost (elderly at risk)
Fluid Volume Deficit S/S-
-Confusion, restlessness/drowsy
-Thirst, dry mucous membranes*, decreased skin turgor & capillary refill
-Postural hypotension, increased HR, RR, low BP, low concentrated urine
-Weakness and weight loss
Fluid Volume Deficit Treatment
-Correct underlying causes and replace water and electrolytes (orally, blood products, balanced (isotonic) IV solutions
-Seizure precautions
Fluid Volume Excess Causes
-Excess fluid intake
-Renal failure
-Heart failure
-Burns (interstitial to plasma fluid shift)
-HYPERVOLEMIA
Fluid Volume Excess Labs
-Electrolytes aren’t necessarily unbalanced
-Monitor daily weights and I&O’s
1kg = 1L of fluid
Fluid Volume Excess S/S
-Weight Gain
-HA, confusion
-Peripheral edema, JVD, increased CVP
-S3 heart sounds, bounding pulse, increased BP
-Polyuria
-Dyspnea, crackles, pulmonary edema
-Muscle spasms, seizures, coma
Fluid Volume Excess Treatment
-Diuretics
-Na+ restriction
-Para/thoracentesis
-Monitor I&O’s
-Seizure Precautions
Hypertonic IV
-Too much can dehydrate cells, causing them to shrivel
-pulls fluid from cell
Hypotonic IV
-Too much can burst cells, cerebral edema
-Fluid moves into cells, plumps up the cells
- Risk for cells to explode!!
Isotonic IV
-Too much can cause fluid overload
-Hydrates the cells, expands vascular volume
-ISO = same
Hypernatremia Lab Value
> 145
Hyponatremia Lab Value
<136
Hyperkalemia Lab Value
> 5.0
Hypokalemia Lab Value
<3.5
Hypercalcemia Lab Value
> 10.5
Hypocalcemia Lab Value
<9.0
Hypermagnesemia Lab Value
> 2.1
Hypomagnesemia Lab Value
<3.1
Hyperphosphatemia Lab Value
> 4.5
Hypophosphatemia Lab Value
<3
Hypernatremia causes
“MODEL”
M-medications, meals (too much sodium intake)
O-osmotic diuretics
D-diabetes insipidus
E-excessive water loss
L-low water intake
> 145
Hypernatremia S/S
“FRIED & SALTED”
F-fever (low grade)
R-restlessness and agitation
I-increased fluid retention
E-edema: peripheral & pitting
D-dry mouth
S-skin flushed
A-altered LOC, confusion
L-low urinary output
T-thirst
E-elevated BP
D-decreased energy, weakness
Hypernatremia Treatment
Decreased ECF
-PO or IV isotonic fluid replacement
Normal/increased ICF
-Hypotonic IV (plumps up cells)
-Diuretics for Na+
-Na+ restriction
-Seizure precautions
-Fluid restriction
Hyponatremia Causes
“MOBS Fail”
M-medications (diuretics)
O-oral gastric tube suctioning
B-burns
S-SIADH
F-failure: heart, kidney, liver.
Hyponatremia S/S
“LOW SODIUM”
L-LOC altered (confusion*)
O-orthostatic hypotension
W-weak muscles
S-seizures*
O-osmolality low (serum)
D-diarrhea
I-increased ICP (difficulty concentrating*)
U-urine osmolality high
M-more bowel sounds
Hyponatremia Treatment
Fluid and Na+ loss
-Administer isotonic IV solutions
-Encourage oral fluid intake
-Stop diuretics
Dilutional hyponatremia
-Fluid restriction
-Diuretics
-Demeclocycline
Correct sodium level slowly (to prevent brain damage
Hyperkalemia Causes
“SIMM”
S- shift from ICF to ECF (acidosis)
I-impaired renal excretion (MOST COMMON)
M-massive intake of K+ (salt substitutes)
M-medications: digoxin, beta blockers, ACE inhibitors, potassium sparing diuretics
Hyperkalemia S/S
“MURDER”
M-muscle cramps
U-urine abnormalities
R-respiratory distress
D-decreased cardiac contractility
E-EKG changes (Peaked T waves and QRS waves, widened P wave)
R-reflexes (depressed/absent DTRs)
Hyperkalemia Treatment
-Stop oral or parenteral K+ intake
-Increase excretion
-Force into ICF with dextrose, insulin, bicarb, or albuterol (temporary)
Stabilize cardiac membranes using IV calcium
Hypokalemia Causes
“GRIM”
G- GI losses (diarrhea & vomiting)
R-renal losses (magnesium deficiency, diuretics)
I-inadequate K+ intake
M- metabolic alkalosis or insulin administration (shifts K+ into ICF)
Hypokalemia S/S
“7 L’s”
L-lethargic (N/V)
L-low shallow respirations (failure)
L-Lethal cardiac dysrhythmias (prominent U wave, ST depression, shallow T)
L-Leg cramps
L-Limp muscles
L-Low BP
L-Low GI motility
Hyperglycemia
Hypokalemia Treatment
1) Oral K+ first
2) Then IV
more K+ in diet
Hypercalcemia Causes
“CHIVE”
C-cancer
H-hyperparathyroidism
I-immobilization
V-vitamin D overdose
E-elevated vitamin D
Hypercalcemia S/S
“BACK ME”
B-bone pain
A-arrhythmias, HTN
C-cardiac arrest
K-kidney stones
M-muscle weakness
E-excessive urination (dehydration)
Hypercalcemia Treatment
Mild
-Stop meds
-low calcium diet
-exercise
-hydration
Severe
-Isotonic IV
-Calcitonin (inhibits Ca movement)
-Biphosphates (inhibit osteoclast activity, prevents Ca release)
-Dialysis (if life threatening)
Hypocalcemia Causes
“MAID”
M-multiple blood transfusions (6-10 per day)
A-alkalosis
I-increased calcium loss
D-decreased production of PTH
Hypocalcemia S/S
“CATS go Numb”
C-convulsions
A-arrhythmias
T-tetany
S-spasms and stridor
NUMB-numbness in the fingers and around mouth
*Trousseau’s (BP cuff, hand spasms)
*Chvostek’s (eye/lip twitch)
Hypocalcemia Treatment
-Treat underlying cause
-increase dietary calcium intake
-Vit D supplements
-IV calcium gluconate
-Change loop to thiazide
Hypermagnesemia Cause
-Increased intake of Maalox/milk of mag with renal insufficiency/failure
-Excess IV Mg administration
Hypermagnesemia S/S
-Hypotension, facial flushing
-Lethargy
-N/V
-Impaired DTR’s
-Muscle paralysis
-Resp and cardiac arrest
Hypermagnesemia Treatment
-Avoid Mg food/drugs
-Fluid administration to promote excretion
-Calcium gluconate IV to counteract the effects of the elevated Mg
Hypomagnesemia Causes
-Chronic alcoholism
-Prolonged fasting/starvation
-Fluid loss from GI tract
-Prolonged parenteral nutrition w/o supplementation
-Diuretics, PPI’s
-Hyperglycemic osmotic diuresis
Hypomagnesemia S/S
Resembles hypocalcemia
-Muscle cramps, tremors, hyperactive DTRs, Chvostek’s and Trousseau’s sign
-Confusion, vertigo and seizures
-Dysrhythmias
Hypomagnesemia Treatment
-Treat underlying cause
-Increase oral Mg intake
-Administer Mg IV if needed (monitor for hypotension and arrhythmias)
Hyperphosphatemia Causes
-Acute kidney injury
-Chronic kidney disease
-Excessive intake
-Excessive vitamin D
-Hypoparathyroidism
Hyperphosphatemia S/S
-Tetany, muscle cramps, paresthesia
-Hypotension, dysrhythmias
-Seizures
-Calcium deposition -> organ dysfunction
Hyperphosphatemia Treatment
-Treat underlying cause
-Restrict dietary intake of phosphate
-Calcium carbonate to bind
-Volume expansion & forced diuresis with loop diuretics
-Dialysis
Hypophosphatemia Causes
-Malnourishment/malabsorption
-Alcohol withdrawal
-Diarrhea
-Phosphate binding antacids
-Inadequate replacement from parenteral feeding
Hypophosphatemia S/S
-CNS depression
-Muscle weakness (including resp.) and pain
-Resp. and heart failure
-Rickets
-Osteomalacia (soft bones)
-Rhabdomyolysis (skeletal muscle breaks down rapidly)
Hypophosphatemia Treatment
-Increase oral intake (dairy)
-Supplements (can irritate GI tract)
-IV supplements (slow) (potassium phosphate, sodium phosphate)
pH Values
7.35-7.45
Carbon Dioxide (PaCO2) Values
35-45
Bicarb (HCO3) values
22-26
Partial Pressure of Arterial O2 (PaO2) Values
80-100
Saturation of Arterial O2 (SaO2) Values
95%-100%
Respiratory Acidosis Cause
-HYPOVENTILATION
-Respiratory depression from lungs
-Airway obstructions (COPD, pneumonia, PE)
-Ventilator hypoventilation
-Excess HCO3 (bicarb)
Respiratory Acidosis Labs
pH: <7.35
CO2: <45
Respiratory Acidosis Treatment
Stimulate them
Respiratory Alkalosis Cause
-HYPERVENTILATION
-Anxiety, stress
-Pain
-High ventilator settings
Respiratory Alkalosis Labs
pH: >7.45
CO2: <35
Respiratory Alkalosis Treatment
Calm them down
Metabolic Acidosis Causes
-Diarrhea
-Acid gain from hypoxia
-Renal Failure
-Drugs or toxins
-Bicarb loss from bile drainage
-Pancreatic fistulas
Metabolic Acidosis Labs
pH: <7.35
HCO3 (bicarb): <22
Metabolic Acidosis Treatment
-Encourage breathing
-Give bicarb
Metabolic Alkalosis Causes
Acid Loss
-Vomiting
-NG suctioning
-Diuretics
-Steroids
-Cushing’s
-Hyperaldosteronism
-Hepatic disease
-Hypokalemia
-Hypochloremia
Bicarbonate Gain
-Dosing with bicarb
-Excess infusion of lactated ringers’ solution
Metabolic Alkalosis Labs
pH: <7.45
HCO3 (bicarb): <26
Metabolic Alkalosis Treatment
Slow breathing
Daily amount of insulin secreted by an adult?
40-50 units
Type 1 Diabetes Mellitus Patho
-Autoimmune disease resulting in progressive destruction of pancreatic B cells
-80-90% of B cells are destroyed before S/S manifest
-Accounts for 5-10% of all diabetes cases
-Generally, affect those under 40 years
Type 1 Diabetes Mellitus Causes
-Genetic predisposition (human leukocyte antigen)
-Exposure to a virus or idiopathic
Type 1 Diabetes Mellitus Diagnostics
-A1C: >6.5
-Fasting glucose >126
-Random glucose >199
-2-hour OGTT >200
Type 1 Diabetes Mellitus S/S
-Polyuria, polydipsia, polyphagia
-Fatigue
-Weight loss
-No insulin produced
Type 1 Diabetes Mellitus Treatment-
-Will require insulin, should exercise
Type 2 Diabetes Mellitus Patho
-Most prevalent type 90-95%
-Pancreas continues to produce some insulin but not enough insulin is produced and the body does not use insulin effectively
Type 2 Diabetes Mellitus Cause
-Obese/overweight
-Old age
-Family history
Type 2 Diabetes Mellitus Diagnostics
-A1C >6.5
-Fasting glucose >126
-Random glucose >200
-2-hour OGTT >200
Type 2 Diabetes Mellitus S/S
-Recurrent infection (increase insulin needed)
-Fatigue
-Polyuria, polydipsia, polyphagia
-Prolonged wound healing, visual changes
Type 2 Diabetes Mellitus Treatment
-Emphasis on goals for glucose, lipids and BP
-Calorie reduction and weight loss to improve insulin sensitivity
-Needs exercise
Short Acting Insulin Examples
Regular Insulin
-Humulin R
-Novolin R
Short Acting Insulin Onset
30-60 minutes
Inject 30-45 minutes before meals
Short Acting Insulin Peak and Duration
Peak: 2-5 hours
Duration: 5-8 hours
Short Acting Insulin Uses/Administration Considerations
-Several hours after meal, may have hypoglycemia
-Insulin still present and glucose is falling post meal
-Abdomen is preferred site for all insulin-most rapid and consistent absorption
-The only insulin that can be given IV when immediate onset of action is desired
Rapid Acting Insulin Examples
Lispro (Humalog)
aspart (NovoLog)
Glulisine (Apidra)
Rapid Acting Insulin Onset
10-30 minutes
Inject 0-15 minutes before meals
Rapid Acting Insulin Peak/Duration
Peak: 30 minutes- 3 hours
Duration: 3-5 hours
Rapid Acting Insulin Uses/Administration Considerations
-Peak and duration more consistent with digestion and metabolism pattern postprandial.
-Better for meal coverage, but because of short duration of action a basal background insulin must be used in conjunction with it.
Intermediate Insulin Examples
NPH (cloudy)
Humulin N or Novolin N
Intermediate Insulin Onset
1.5-4 hours
Intermediate Insulin Peak and Duration
Peak: 4-12 hours
Duration: 12-18 hours
Intermediate Insulin Uses/Administration Considerations
-2 injections provide coverage for 24 hours
-Give at breakfast and dinner
-Hypoglycemia attacks most likely with peak of action, if food is not eaten at that time
-Mixed with zinc and protamine to prolong the action, therefore must be mixed (shaken) before administration
Long-Acting Insulin Examples
-Glargine (Lantus)
-Detemir (Levemir)
-Degludec (Thesiba)
Long-Acting Insulin Onset
0.8-4 hours
Administer at bedtime or in the morning (follow the regimen patients uses at home); important to give at the same time each day
Long-Acting Insulin Peak and Duration
Peak: no pronounced peak
Duration: 16-24 hours
Long-Acting Insulin Uses/Administration Considerations
-Mimics the basal cell level of insulin produced by the body in 24-hour period, low risk for hypoglycemia.
-DO NOT MIX WITH OTHER INSULINS
-Useful for people with nighttime rises in blood sugar
-Hold metformin for type 2 DM contrast procedures.
Hyperglycemia Glucose
> 126 mg/dl
Hyperglycemia Causes
Poorly controlled diabetes
Hyperglycemia Long Term
Can lead to neuropathy, kidney disease, vision loss, stoke, amputation.
Hypoglycemia Glucose
<70 mg/dl
Hypoglycemia Causes
-Too much insulin
-Exercise
-poor timing (r/t administration of insulin)
Hypoglycemia S/S
-Anxious, irritable, sweaty, cool clammy skin, hungry
-Confused, blurred/double vision
Hypoglycemia Treatment
-15g of carbs like fruit juice if below 70, recheck in 15 minutes, repeat if needed.
-IV D50 or IM glucagon if unresponsive/unconscious
-A set meal pattern with bedtime snacks is necessary to prevent this
Diabetic Ketoacidosis (DKA) Cause
-Profound lack of insulin
-Characterized by hyperglycemia, ketosis, acidosis, and dehydration (needs fluids)
-Occurs more with type 1 DM
Diabetic Ketoacidosis (DKA) Labs
Glucose >250
Blood pH <7.30, bicarb <16
High ketones in urine
Diabetic Ketoacidosis (DKA) S/S
-Hyperglycemia
-Ketosis (fruity breath), ketonuria
-Deep rapid breathing (Kussmaul)
-Metabolic acidosis, dehydration
-Hyperkalemia, tachycardia
Diabetic Ketoacidosis (DKA) Treatment
-Stat isotonic IV, then insulin
-Electrolyte replacement
-Only regular insulin can be used
-Potassium may need to be replaced when insulin is given
-If glucose is below 250 give dextrose in IV
Hyperglycemia Hyperosmolar Syndrome (HHS) Glucose
> 600
Hyperglycemia Hyperosmolar Syndrome (HHS) Causes
-Infections (UTI’s pneumonia, sepsis)
-New type 2 diabetes
-Impaired thirst/lack of fluids
Hyperglycemia Hyperosmolar Syndrome (HHS) S/S
->600
-Dry parched mouth, extreme thirst, polyuria
-Warm but not sweaty, fever
-Sleepiness, confusion, vision loss, hallucinations
Hyperglycemia Hyperosmolar Syndrome (HHS) Treatment
-Boat load of fluids
-IV NaCl and insulin
-More fluids and less insulin is needed compared to DKA
-Add dextrose to IV when glucose <250
-Monitor pt closely, especially K+ levels
Diabetic Retinopathy
-Diabetes is the most common cause of new cases of blindness
-Cataracts and glaucoma
-Control diabetes, surgery
Diabetic Nephropathy
-Kidney dysfunction
-Labs-elevated BUN and creatinine
-ACE inhibitors and angiotensin receptor 2 blockers with tight glucose control. Dialysis in late stages
Diabetic Foot Ulcer
-Staged ulcer resulting from poor lifestyle choices r/t diabetes. Common with sensory neuropathy and peripheral artery disease, smoking increases risk.
-Ulcer, risk for infection
-Wound care and debridement, pt must have meticulous foot care.
-Check water temperature with thermometer, not feet.
Diabetic Neuropathy
-Distal symmetric loss of sensation with uncontrolled diabetes (hands and feet), deformities may be present.
-Numbness, burning, tingling, shooting pain and cramps of extremities. Impaired balance, foot deformities, hot and cold sensitivity. Worse at night.
-Delayed gastric emptying CV problems, sexual dysfunction, neurogenic bladder
-Tight glucose control. Drugs- topical creams, tricyclic antidepressants, SSIs and NE reuptake inhibitors, antiseizures.
