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130 Cards in this Set
- Front
- Back
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Insulin receptors
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muscle, liver, fat
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Posterior pituitary
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- ADH
- oxytocin |
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Anterior pituitary
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everything else :)
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Neurohypophysis
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posterior pituitary
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ADH
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Colntrols water balance and restored volume
- does not directly affect sodium like aldosterone does - also known as vasopressin - regulates renal water excretion (plasma osmality) |
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Oxytocin
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- uterine contraction
- milk release during lactation |
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Suppressed ADH
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- promotes diuresis--> high urine output
- sodium increase in blood - diluted urine--> low specific gravity |
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ADH secreted
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- water retention
- increased fluid volume/hemodilution - low urine output - high specific gravity (concentrated) |
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V1 receptos for ADH
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promote vasoconstriction to assist in blood pressure regulation (ie: huge GI bleed)
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V2 receptors for ADH
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- promote renal tubular reabsorption of water to control fluid levels in body
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Thirst responsrs
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- a LATE response
- celullar dehydration sensed by osmoreceptors - volume depletion sensed by baroreceptors |
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RAA
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- vasoconstriction
- stimulates aldosterone release - stimulates thirst |
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Diabetes Insipidus
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- impaired ADH synthesis (don't make it)
- impaired ADH release (post pituitary doesn't release it) - Renal resistance to ADH (receptor problem) - kidney doesn't reuptake water - increased serum osmolality (hypernatremia) - excessive urine output- very diluted urine (hypotonic urine- urine Na down) - if thirst is intact, fluid volume may be maintained |
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Central/Neurogenic Diabetes Insipidus
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- absent or diminished ADH
- organic lesion of hypothalamus or posterior pituitary that interferes with ADH synthesis, transport, or release - inability to concentrate urine - excess fluid loss - transient or permanent |
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Central DI causes
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- hypothalamic injury, surgery, ischemia
- pituitary injury, surgery, or ischemia (stroke) - traumatic brain injury (pressure on hypothal or pituitary) - CNS infection (meningitis, encephalitis) - cerebrovascular disease - cerebral edema (this can happen when give to much glucose too fast or correct fluid too fast) - brain radiation - cranial neoplasms - intracranial hemorrhage - utoimmune - familial disease ** anything that affects CNS |
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#1 nursing management things when something going on with brain
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- urine output
- osmolality - also monitor serum sodium levels --> if any changes notify MD |
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Nephrogenic DI
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- renal collecting ducts ad distal tubules so not response to ADH
- adequate ADH levels - generally acquired - renal disease (chronic renal failure, chornic renal medullary disease, pyelonephritis, renal transplant - polycycstic kidney disease (#1 genetic disorder leading to kidney failure and common reason for transplant - Familial (x-linked trait) - sickle cell - chronic hypokalemia - chronic hypercalcemia - multiple myeloma - protein starvation - Meds (lithium, demeclorycline - Amphotericin - Methoxyflurane (anestatic) - loop diuretics - gentamicin - Colchicine (gout med) - may have a high ADH level if pull serum lab |
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Psychogenic DI
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- excessive fluif intake
- structural lesion in thirst - psychiatric issues |
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Lab presentation for diabetes insipius
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- polyuria (5-20 liters per day, hourly outputs may exceed 200mL)
- low uring specific gravity (dilute urine)- < 1.005 - low urine osmolality- < 1-- mOsm/kg - hypernatremia (hemoconcentration from losing all of the water) ** monitor I&O carefully |
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Water deprivation test
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- to distinguish central from nephrogenic
- fluids are held for 8-16 hours - BP< weight, and urine osmolality assessed before test and hourly - continues until osmolality normalizes or weight decreases by 3% or pt orthostatic--> then ADH adminstered--> - if nephrogenic, pt would not respond to ADH - if have central they were have a drop in urine output and and urine would become more concentrated |
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Clinical presentation of DI
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- hypovolemia/hemodynamic instability
- tachycardia - orthostatic hypotension - weight loss (more than 5% in a day is significant!) - poor skin turgor - sunken eyes - dry mucous membranes - extreme thirst - fatigue - nocturia (because they are always going to the bathroom) - Dehydration may be minimal if thirst drive intact, but its hard to drink enough and neurologic symptoms (see next card) |
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Neurologic clinical presentation of DI
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- altered mental status
- monitor neurological patient's carefully |
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Neurologic stages of DI
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Stage 1: acute stage--> polyuria (ADH impaired, ie: nerve shock)
Stage 2: interphase (day 2-14) --> water retention - urine volume normalizes Stage 3: return polyuria (10-14 days post event or surgery) - return of ADH impairment - may be permanent esp following cranial surgery ****As s nurse, need to know the pts urine output and what it has been trending and when it becomes a lot (stage 1)...etc. |
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Early identification of DI*******
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***********
- Intake and output--> this is how you find it!!! - daily weights - urine specific gravity - monitor electrolytes including plasma osmolality (Sodium electrolyte and osmolality are most important |
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DI treatment for central DI
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- fluid replacement (titrated to individual and selection of fluid based on electrolytes profile and clinical presentation)
**If volume is way down- isotonic first to restore volume, then may need hypotonic if cells have become dehydrated since it is pulling from it - Admin of central ADH (Desmopressin, vasopressin)--> for CENTRAL only - monitor hemodynamic and cardiovascular status (from pressure on brain stem) - monitor respiratory status (from pressure on brain stem) - monitor temperature (from pressure on brain stem) |
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Desmopressin/Vasopressin
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- duration is only 2-8hrs (individualized for pt) so need to monitor pt and may need to be give frequently
- intranasal is common route - this exogenous ADH will not impair release of endogenous ADH so monitor just in case body starts to produce its own ADH - may cause vasconstriction affecting cardiac perfusion (vasopressin affects V1 and can lead to increased BP) - may exacerbate renal and hepativ failure - monitor for signs of water intoxication (over treatment) |
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Signs of water intoxication/overtreatment
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- urine output down and becomes more diluted in serum
- Sodium down |
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Tx for nephrogenic DI
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- low sodium diet
- thiazide diuretics (promotes water reabsorption in renal tubule) - Indomethicin- NSAID |
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Syndrome of Inappropriate ADH secretion (SIADH)
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- aberrant production or sustained secretion of ADH
- failure in negative feedback system (like a primary issue) - excess water retention induced on renal tubules - leads to extreme water retention and potentially water intoxication |
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Primary vs secondary disease
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Primary- opposite
Secondary- same direction |
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Lithium
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the most common caused of nephrogenic DI
- hypokalemia and hypercalcemia may also cause it |
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Serum osmolality in DI
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> 295 mOsm/kg
- some people that still drink a lot of water so serum osmolality may not be that elevated |
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Di following intracranial surgery
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more likely to be permanent (head trauma is usually transient and improves with treatment of underlying problem)
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When is water restriction s test stopped?
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- when urinse osmolality stabalizes (< 30 mOsm/kg in 3 consecutive hours)
- 3% body weight decline - orthostatic hypotension - vasopressin is then given and urine osmolality is measured 1 hour later - central will have a rise of more than 9% |
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While pt is being treated with desmopressin...
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monitor I&O and urine specific gravity
- NOTIFY MD immediately if pt develops increased urine volume with low specific gravity. This could mean a need for increased Desmopressin |
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Causes of SIADH
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- malignancy (produce ADH)- lung, pancreas, duodenum, lymphoid tissue
- CNS disorders (brain tumor, brain hemorrhage, head trauma, CNS infection/injury) - Pulmonary (positive pressure ventilation, acute respiratory failure, infection, TB, COPD, lung abscess) - Drugs- tegretol, Diabenese, Barbituates (surgical and anesthetic), opioids, antineoplastic drugs/chemo, anesthetics, TCAs - postoperative |
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Laboratory presentation of SIADH
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- hyponatremia (< 134) hemodilution
- plasma hypoosmolality (<240) - high urinary sodium (>20mEq)- passing concentrated urine- this differentiates it from other volume expanding conditions - increased urine specific gravity (> 1.005) - decreased creatinine clearance - decreased H&H (hemodilution) |
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Clinical presentation of SIADH
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- related to water retention, hyponatremia, and hypoosmolalty
Early- thirst, dyspnea on exertion, fatigue - lethargy - muscle cramps - anorexia - N/V Later- (na < 120)- abdominal cramps, muscle twitching - cerebral edema - HA - coma - seizure Cardiovascular - increased ECF (fluid retention) - weight gain - increased BP - adventitious breath sounds Urinary - reduced urinary output - volume down - urine sodium up |
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Clinical management of SIADH
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- remove causative agent
- restrict fluids (no more than 500 (severe)- 1000 mL/day) - daily weights - neurologic assessment - head of bed flat or no more than twn degrees to help with venous return - hypertonic saline - Diuretic - Demeclocycline or lithium (both causes of DI, which is why they work) ---> evidence of tx working would be urine output increase |
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Give hypertonic saline in SIADH if-
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sodium < 120 mEq/L
yes this will increase sodium but it will also draw fluid and increase risk for fluid overload (caution!) |
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GFR in SIADH
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Increased GFR
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PTH
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- regulates calcium and phosphate levels
- stimulates bone resorption of calcium - renal reabsorption of calcium - Activation of Vit D --> increased serum calcium levels |
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Hyperparathyroidism primary v secondary
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primary- adenoma (age 4-50,, prior head/neck surgery)
secondary- response to hypocalcemia (chronic renal failure!) Tertiary - loss of negative feedback - hyperplasia of parathyroid gland |
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Signs of hypercalcemia/ hyperPTH
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- Dysrhythmias
- Shortened QT - HTN - Abdominal pain/N&V - Constipation, ileus - Pancreatitis - PUD - Cholethiasis - skeletal pain - isteoporosis - weakness - pathologic fracture of long bones and vertebrae - memory changes/psychoses - hyperactive reflexes - parasthesias - hypercalcuria- renal calculi - UTI - polyuria (slows everything down) |
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hyperPTH labs
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- parathyroid hromone hard to measure
- elevated calcium - decreased phosphorus - elevated urine calcium - elevated uric acid - elevated creatinine (lots of calcium is hard on kidneys) - elevated amylase (if pancreatitis) - bone density losses |
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Non surgical hyperPTH tx
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- avoid immobility
- high fluid intake - moderate calcium intake (bones still need it!) - phosphorus supplementation - Biphosphonates (Boniva, Fosamax) |
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Hypocalcemia symptoms
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- tetany
- parasthesias of hands or mouth - Dysphagia - laryngospasm (have laryngectomy tray in room) - Chyostek's and Trousseau's sign - Respiratory compromise (muscles need calcium in order to contract) - anxiety |
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Post op from PT removal (same as thryoid)
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- I&O
- monitor for hypocalcemia - mobilization - Electrolyte management |
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Hypoparathyroidism
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low PTH
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tx of hypoparathyroid
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- IV calcium gluconate
- ECG monitoring (careful esp with digoxin) - respiratory assessment - long term calcium replacement - Vitamin D - High calcium diet (dark greens, soybeans, tofu) |
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Pheochromocytoma
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Adrenal MEDULLA tumor that secretes:
- catecholamines (epi and nor epi, the METnephrines)--> vasoconstriction --> BP crisis, sweating, tachycardia, A fib, SVT - young, middle aged adults, less than 10% malignant |
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Potential pheocromocytoma physiologic responses
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- severe HTN (like 240/120)
- Tachydysrhythmias - Diabetes/ elevated glucose - cardiomyopathy (from stress on heart) - death |
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Adrenal medulla tumor may be precipitated by:
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- antihypertensives
- opioids - radiologic contrasts media - TCA |
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Clinical presentations of pheocromocytoma
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- flushing and sweating
- severe, episodic HTN (crisis!) - tachycardia - palpitations/arrythmias - glucose intolerance - heat intolerance - Anxiety- flight or flight - Abdominal pain (ischemia or tumor compression)/ chest pain (probably from ischemia) Classic triad: - severe pounding HA - tachycardia - profuse sweating |
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Diagnosis of Phechromocytoma
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- elevated plasma and urine catecholamine metabolites (24 hour urine for metanephrines)
- CT scan and MRI |
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Treatment of Pheochromocytoma
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- sta
- Stabalize BP and cardiac status durine and after surgery - calcium channel blockers to control BP - Sympathetic blockers - Alpha blockers (block sympathetic) - Beta blockers (block sympathetics, will help with tachy and BP)---prob want a systemic beta blocker (unless asthma pt) - Surgical removal- monitor BP (usually only need to remove from one kidney) - pt has to be stabile before removal/surgery |
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Thyroid storm (Thyrotoxicosis)
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- acute, rare, life threatening
**death is rare when treatment initiated but can occur within 48 hours!!** - Presumed causes are additional stressors in pt with pre-existing hyperthyroidism (Infection, trauma, surgery, catecholamines, sympathetic overstimulation) |
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Thyroid storm manifestations
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- severe tachy- a fib, tachy arrythmias
- HF - shock - hyperthermia (may go above 105 degrees F) - Restlessness- tremors, extremely agitated, nervous - Diaphoresis (heavy flushing) - agitation - seizures - abdominal pain - N/V - Diarrhea - Delirium - Coma |
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Tx of thyroid storm
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decrease hormone with drug therapy
- manage respiratory distress - fever reduction - fluid/electrolyte replacement (pt sweating like crazy! and cardio issues)- pt at risk for hemodynamic collapse - maintain airway and ensure oxygenation - monitor for dysrhythmias and decompensation - manage stressors (careful with who in room with them, keep away from nurses station, nice, quiet area, cool room, light bed coverings and change frequently) - eye exercises, artificial tears - tape eyelids shut - elevate bed and salt restriction for edema - meds - wear dark glasses to reduce glare and prevent environmental irritants - increased calories (4000-5000)- six meals - protein allowance 1-2 g/kg ideal body weight - avoid caffeine (stimulates heart), highly seasoned food, and high fiber foods |
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labs to diagnose hyperthyroidism
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decreased TSH and increased T4 (thyroxine) for PRIMARY
If SECONDARY then TSH and T4 would both be increased |
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Meds for thyroid storm
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- not curative
- antithyroid drugs (PTU- plythiouracil)- have to take like 3 x /day - Methimazole (Tapazole) *** Both of these cause agranulocytosis--> monitor neutrophils! - iodine, beta adrenergic blockers, Inderal, Atenolol |
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Radioactive iodine
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- delayed response (2-3 months to become hypothyroidism)
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Diabetic Ketoacidosis (DKA)
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- hyperglycemia--> fat breakdown --> ketones/ketosis--> Metabolic acidosis --> profound dehydration (as much as someone hemorrhaging!)
Can be caused by absolute deficiency (stop taking insulin) or a relative deficiency (insulin demands go up and unable to meet these demads) |
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Precipitating factors for DKA
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- undx Type 1 DM
- inadequate insulin dose (illness, pregnancy) - infection - physiological stressors (pneumonia, flu, gastrenteritis) - trauma - deliberate or accidental omission of insulin - pump ro infusion set failure - change in diet, insulin, or exercise - mismangement of sick days - psych issues |
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3 factors that add up to DKA
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- hyperglcemia
- acidosis - ketosis |
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Physiologic changes in DKA
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- hyperglycemia (liver keeps producing glucose and decreased utilization and stress response)
- osmotic diuresis and dehydration (polyuria, polydipsia) - hyperlipidemia (high triglycerides!) due to increased lipolysis - metabolic acidosis/ketosis |
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Clinical presentation of DKA
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- orthostasis
- polyuria - polydipsia - polyphagia (excessive hunger)- but eventually stop eating from nausea - hyperventilation/Kussmail respirations (metabolic acidosis) - flushed, dry skin - fruity odor to breath - lethargy/altered consciousness - abdominal pain/N/V - blood glucose greater than 250 mg/dL (in pregnancy may be 150-180)- monitor ketones if pregnant diabetic - ketonuria/glucosuria - weight loss (may be profound) - sunken eyes/dehydration signs - blood gas changes (metabolic acidosis) |
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Bicarb response to metabolic acidosis/DKA
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1) in seconds- bicarb goes down cause it grabs all free bicarb
2) in minutes- Kussmaul 3) days- biarb from kidney |
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Electrolyte disturbances in DKA
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- hyperglycemia
- hyperosmolarity - metabolic acidosis (< 7.35) - decreaed bicarb (renal loss) < 15 mEq - Decreased CO2 (respiratory loss) - **hypokalemia (even if serum K is normal or high!) because when insulin is given it will get worse!! - phosphate depletion (insulin makes worse) - Elevated BUN/creatinine (dehydration) (renal failure it stays normal) |
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First priority for DKA tx
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Ensure Patent Airway
- profound metabolic acidosis can cause respiratory complications - mental status changes and lack ability to protect airway leading to respiratory arrest and aspiration, etc...) |
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Second priority in DHA tx
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Correct Dehydration
- best degree of dehydration is degree of acute weight loss **Urine output is NOT a good indicator of hydration due to osmotic diuresis that accompanies this syndrome - Fluid replacement restores vascular volume and enhances renal excretion of glucose and dilutes glucose in serum * Isotonic (normal saline) ** Don't use lactated ringers because it has lactaid (sugar) in it!! |
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Goal of fluid therapy in DKA
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BP stabalization and urine output of 30-60 mL/hr
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Hour 1 of IV fluid therapy
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Initially isotonic saline in large bolus
- 15-20 ml/kg - restores vascular volume |
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Hour 2 of IV therapy
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May continue isotonic saline or convert to .45% saline when BP is stable
- .45 % will correct cellular dehydration |
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Hour 3 of IV therapy
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reduce fluid rate to 7.5mL/kg/hr in adults.
- Use .45% saline |
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Hour 4 of IV therapy
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Adjust rate to meet clinical needs
- when glucose is 250 mg/dL change to D5 1/2 NS until acidosis is corrected and tolerating fluids/foods (YES the IV will have glucose, calories are needed!! and you don't want blood glucose to drop too quickly or they will get cerebral edema!) |
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Third priority in DKA tx
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Insulin replacement
- suppresses ketone production and correct acidosis (needs insulin for this, bicarb will not stop ketone formation) * Only short acting insulin initially by IV - Initial mix is 100mL NS with 100 Units regular insulin (1.0 units per ml) - 0.15 units per kg bolus intitially - May initially bolus then start insulin infusion at 0.1 U/kg/hr - then adjusted per slide scale to maintain glucose at about 200mg/dL for first 24-48 hours (not a regular scale, one individualized by endocrinologist) ***DO NOT lower blood glucose too rapidly --> cerebral edema and brain damage - glucose drop of 36-54 mg/dL is ideal*** - monitor glucose and adjust infusion q 1 hr with q 1 h infusion sticks - when tolerating fluids and glucose control improved, may discontinue IV insulin (may still have ketones in urine but they are old ones, look at blood gasses to determine!) ******NEVER, EVER bolus insulin in children, this will result in too fast a glucose drop and cause cerebral edema!!!***** |
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Starting subcu insulin regimen
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- give first subcu prior to discontinuing drip
- based on pt - if use a rapid acting (5 min) liek Novolog, humalog, or Aprida then can stop drip quicker, Regular insulin would be slightly slower and would have to give it earlier. NPH for basal will need to be monitored more |
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When is the pt ready to be switched to subcu insulin?
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- clinically stable vital signs
- blood gassess normalized (keotis sprocess is over, old ketones may still be in urine) - drinking fluids without N/V - Precipitating stress is relieved (infection, etc.) - insulin regimen should reflect what will be used at home - continue to monitor urine for ketones for reoccurance of acidosis. - will require frequent adjustment (be aware of honeymoon period) |
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Honeymoon period
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especially new dx pts
- come beta cells still working and may start producing insulin - if mixed with insulin being given, then pt may have hypoglycemia - monitor closely for when honeymoon phase ends also |
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Rapid acting insulins
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Novolog, Humulog, Aprida
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Onset, Peak, and Duration of rapid acting insulins
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O: 5-15 min
P: 60-90 min D: 3-4 hours |
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Short acting insulins
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Humulin R
Novolin R |
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Onset, Peak and Duration of short acting/regular insulins
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O: 30-60 min
P: 2-3 hours D: 3-6 hours |
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Intermediate insulins
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Humulin N
Novolin N |
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Onset, Peak, and Duration of NPH insulins
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O: 2-4 hours
P: 6-8 hours D: 12-16 hours |
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Long acting insulins
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Lantus
Levemir |
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Onset, Peak and Duration of Lantus
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O: gradual
P: none D: 24 hours |
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Onset, Peak, and Duration of Levemir
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O: 1-2 hours
P: 2-12 hours (dose dependant) D: varies by dose |
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Split combinations of insulins
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Humulog 75/25
Novolog 70/30 Humulin 70/30 Novolin 70/30 |
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Important notes with Insulin
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- activity varies by individual
- renal insufficiency/failure may have erractic glucose control - diabetic neuropathy (gastroparesis) may have difficult matching intake to insulin action. Autonomic neuropathy too. Pt will bottom out before food is actually digested from insulin given |
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S/S of gastroparesis
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N/V
- diarrhea - constipation - bloating after meal - erratic glucose |
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Only insulin given IV
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Regular/short acting insulins
- Humulin R and Novolin R * never push/bolus in children |
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in mixed combinations what do each number mean (ie: 70/30)
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70= NPH
30= other insulin ** high risk for hypo with these! two peaks! |
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Basal insulin
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background insulin, generally taken before bed
- meets metabolic body needs - suppresses hepatic glucose production - longer acting, once daily - NPH ILantus, Levemir) - will generally control dawn phenomena * Inadequate basal insulin is what puts people in DKA! |
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Dawn phenomenon
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glucose goes up when rising in morning- from inadequate basal insulin
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Bolus insulin
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meal bolus OR Correction bolus
mean (carb/insulin ratio) correction (given for high blood sugar) |
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When pt discharged on pen...
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- make sure have rx for pen and needles
- always write insulin name first then type of delivery device (Novolog flex pen) |
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pen priming
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- must prime pen every time use it (air shot). Dial to 2 then push air out, then dial dose
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Advantages to Insulin pump therapy
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- most physiologic method of subcu insulin delivery
- can adjust for physciologic concerns or gastreparesis - can adjust to intake and also food characteristics ( high fat/high fiber) - Immediate ability to manage hypo - Newer pumps include continuous glucose monitoring systems that relay real time infor to pump |
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Disadvantages of Insulin pump
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- cost (thousands!)
- dexterity, learning curve - they do fail--> DKA (1-800 number on them) - have to have ability to critically think - need for glucose testing does not go away (it usually increases!) |
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Fourth priority for DKA treatment
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Electrolyte Replacement
- Potassium, Phosphate, Bicarb |
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Potassium replacement in DKA
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- total body potassium is depleted even if serum levels are normal!
- establish renal status before replacing - cardiac monitoring - potassium replacement is based upon plasma K+ - recheck K+ q 2 hours and adjust replacement accordingly - May be admisnterd as KCl or K phosphate - monitor potassium carefully (insulin causes drop) |
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Bicarb replacement for DKA
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- benefits in correcting acidosis but may bring risk (only used with severe cases)
- not recommended in most cases when pH is > or equal to 7.1. due to acceleration in K reduction, sodium overload, and exacerbating intracellular acidosis - If bicarb is required then should NOT be given as a bolus and should not exceed 5 mEq/kg/12 hours |
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Phosphate replacement in DKA
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- generally phosphate depleted
- phosphate also shifts into cell with K when insulin given - giving to much phosphate can result in hypocalcemia - routine replacement may not help DKA but conservtive replacement not to exceed 1.5 mEq/kg/24hours may be recommended |
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Cautions with DKA tx
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- glucose normalizes before acidosis so don't discontinue insulin too soon.
- hypoclycemia may occur if insulin is not supplemented with glucose (risk for cerebral edema!) - monitor neurologic status and avoid over aggressive correction of glucose level (cerebral edema) - high risk for aspiration so introduce solids slowly - aggressive fluid replacement may lead to HF |
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Prevention of future DKA
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- determine cause
- complete physical and psychosocial assessment is needed - may come with a "story" and requires counseling referral Educate pt: - insulin admin (dosing times, peak activity, etc.) - meal planning - home glucose monitoring and pattern detection, target glucose - watch pt draw up insulin, even if they've had DM for a long time - hypoglycemia management - sick day rules |
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Sick day rules
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- Increased testing if glucose > 240 mg/dL (will require supplemental insulin)
- Testing urine ketones if glucose > 240 (if pregnant, everyday!) - Ketonuria indicates relative insulin deficiency - No exercise of glucose > 240 and ketones present (Type 1 Dm only) - increase fluid intake and alternate glucose containing with non-glucose containing fluids when ill - notify MD if doesn't improve - glucose is labile during stress, adolescence, and pregnancy |
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Hypoglycemia
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- generally is glucose < 70 mg.dL (may be dif in some pts). If have unawareness may not want them under 100.
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Causes of hypoglycemia
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- honeymoon period
- too little food or delayed or missed meals - a lot of alcohol - extra activity/ exercise - medications (insulin, glipizides, gliptins, jenuvia, Byetta, Symlin) |
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Hypoglycemia S/S
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- shakes
- sweats - craving food - fast heart beat - HA - poor concentration - confusion - changes in mood - seizures |
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Autonomic neuropathy
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may have NO sx of hypoglycemia!
Hypoglycemia unawareness * Pts with this and hastroparesis and renal insufficiency (monitor creatinine) are at high risk for hypoglycemia |
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Treatment of hypoglycemia
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- check sugar
- if have no meter, assume it is low and replace glucose with foods to raise - recheck glucose in 15 min - if not above 70, retreat - provide meal or snack ** These calories are in addition to those on meal plan - encourage use of medical identification - lab may have "critical values" requiring draw of plasma specimen |
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Foods that will raise sugar quickly
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- 3-4 glucose tablets
- 1/3 roll of life savers/gummies savers - 6-7 hard candies - 1.2 cup of juice (apple is best) - 1 cup of milk - 1/2 can sugared soda - small box of raisins - 15 grams of glucose jelly (usually one tube)- can squirt under tongue |
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Hypoglycemia pt education
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- know S/S of hypoglycemia
- never skips meals or snacks test frequently if: - hx of low blood sugar - exercising - change in tx plan (diet, exercise, new med) - ALWAYS carry sugar source or treatment for low blood sugar - use medical alert - instruct family and friends |
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Tx for severe hypoglycemia/ unconscious pt
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- pt unable to take glucose or unconscious
- Glucagon 1mg subcu or IM (child may only get .5) - Position pt on side after, high risk for vomiting and aspiration in unconscious pt - short shelf life and may require refill - educate family/friends how to use |
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Thyroid function tests...
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recommended at DM dx in older pts
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EKG testing an cardiac stress test in pts over...
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45 yo
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Preferred agents for HTN
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Ace inhibitors- because they provide renal protection
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Aspirin therapy
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recommended after age 21 for CAD protection
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pts are at high risk for hypoglycemia if on...
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sulfonylureas and insulin
* educate pts on which meds cause hypo and which don't |
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Beta Blockers may...
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obscure symptoms of hypoglycemia
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glucose targets may be higher if pt has hx of
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stroke, MI, or autonomic neuropathy
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Hyperosmolar Hyperglycemic Syndrome (HHS) (also caled NIDHS, non insulin dependent...)
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- Complication of Type 2 DM
- HIGH MORTALITY, life threatening - produce adequate insulin to prevent ketosis but will have VERY high blood glucose (1000s +) - undx DM or those who have had hyperglycemia for a long period of time - abnormal thirst response or limited access to water may precipitate conidtion (seen in elderly) |
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Preceipitating factors of HHS
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- glucorticoids, Diuretics, Alpha blockers
- dialysis, TPN, surgical stress - chronic disease (renal, old stroke, dementia, alcoholism, loss of thirst) - Acute health problems (Infection, foot ulcers, GI hemorrhage, CVA, MI, Pancreatitis) |
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Clinical presentation of HHS
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- severe hyperglycemia (even > 1000 mg/dL)
- altered mental status/coma - no or slight ketones, normal blood gasses - plasma hyperosmolarity - profound dehydration |
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Tx for HHS
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- correct precipitating event
- Rehydration (use caution as they are typically elderly and have other problems) - Coorect electrolyte imbalances (K, Phosphorus, Sodium) - Insulin replacment - Vital sign monitoring - I&O - Assessment of cardiovascular status - High mortality rate because pts usually have co morbidities and fluids can make worse |
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Symptoms of this may resemble a stroke
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HHS
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DKA or HHS requires greater fluid replacement?
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HHS
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SKA or HHS has more potassium loss?
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DKA
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