Endocrine Part 1

Endocrine SIADH, Diabetes Insipidus DKA/HHNK, Hypoglycemia SIADH (Syndrome of Inappropriate ADH) = too much ADH ADH – made in hypothalamus and stored in posterior pituitary -when it goes down to the kidneys, makes kidneys hold on to water -ADH = WATER! (kidneys hold on to water) -ADH goes down to the distal convoluted and collecting tubule of the kidney- causing kidney to hold on to water -when you hold on to water, decreased sodium level = DILUTIONAL HYPONATREMIA -DILUTIONAL HYPONATREMIA = THINK SIADH! -decreased osmolarity-- osmolarity = 2x sodium level (ex. Sodium = 140, osmolarity = 280) ex. Sodium = 160, osmolarity = 340 (concentrated) -SIADH = osmolarity less than 275 -decreased urine output because holding on to water CAUSES: OAT CELL CARCINOMA (tumor in apical portion of lung), viral pneumonia, head problems (think neuro) -also caused by increased serum osmolarity, anesthesia (get a lot of fluids in the OR then aren't putting out a lot of urine), analgesia, and stress SIADH = high ADH, low sodium levels, low serum osmolarity, low urine output -if one arrow goes up, the other arrows go down *complication = SEIZURE ACTIVITY! -due to dilutional hyponatremia ex. pt comes in with viral pneumonia and dehydration, Na level = 120 (osmolarity = 240), dilutional hyponatremia causes water to go into the cell because it is more concentrated in the cell than out of the cell- goes into brain cells (causes confusion, restlessness, seizure activity) Treatment = get rid of oat cell carcinoma, viral PNA, head problems and... -fluid restriction (because SIADH makes you hold on to water) -hypertonic 3% saline (concentration of 1,500)- only run at small rate like 25 mL/hr for 3-4 hours, pulls water out of the cell and stops seizures, monitor pt **DO NOT GIVE HYPOTONIC SOLUTIONS (0.33 NS, 0.45 NS, D5W) -D5W is isotonic in the bag, but hypotonic in the body -hypotonic solutions cause water to go into the cell (water flows to higher concentration) **GIVE HYPERTONIC SOLUTIONS (3% NS, D5NS, D51/2NS) -keep an eye for fluid overload and CHF after giving hypertonic solution because pulls fluid out of cell Diabetes Insipidus (DI) -opposite of SIADH -NO ADH -losing all your water (not reabsorbing water at kidney site) -output 6-24 liters in 24 hours, too much urination- VERY CLEAR (looks like water) -increase in serum sodium because peeing out all the water -hyperosmolar (concentrated) Causes: head problems #1 !, Dilantin (DI – DI-lantin) -Low ADH, increased sodium levels, increased serum osmolarity, large increase in urine output -dilute urine, 1.001-1.005 specific gravity (looks like water) -complication = severe HYPOVOLEMIA → HYPOVOLEMIC SHOCK! Ex. 16 yr old head trauma putting out very large amounts of urine, sodium level is 174, do not give D5W, sodium of 174 means you are intravascularly depleted, so NS would replete his volume, if you gave D5W it would go into the cell, not the intravascular space- helps tachy, etc *TREATMENT = GIVE ADH (Pitressin), IV, IM, SubQ -remember = spray ADH to kids on a trip in the car so they retain urine so they dont have to pee -give fluids to increase intravascular volume -monitor urine specific gravity -monitor EKG for ischemia- ADH medication is a vasoconstricter Hypoglycemia -Signs and symptoms = initially cardiac, then nervous system -CV signs = tachycardia, palpitations, diaphoresis, irritable, restlessness -CNS signs = confusion, lethargy, slurred speech, seizure, coma, dead -WHY do you get these signs? Your adrenal medulla knows when you are low in glucose, adrenal medulla releases adrenaline, goes to liver to turn glycogen into glucose -so when you are low in glucose, adrenaline is released (anxious, tachy, irritable, diaphoretic) -if you are on a beta blocker (inderil, lopressor, etc), there wont be that adrenaline release, so you wont increase your sugar so you will get lethargy, slurred speech, your glucose wont come up, coma -if you are a drinker (alcoholic), you dont have enough glycogen stored in your liver so when the adrenaline is released, cant convert glycogen into glucose because liver is too busy converting alcohol to store glycogen an you get hypoglycemic -SO initial signs of hypoglycemia are of adrenaline release- irritable, tachy, etc. *IF you are on a beta blocker → blocks the release of adrenaline – no CV signs (tachy, palpitations, etc), goes right to showing CNS signs –> confusion, lethargy, slurred speech, seizures, coma ex. 70 yo F on a beta blocker (to prevent sudden cardiac death), gets the flu on monday, doesnt eat for a three days, wednesday afternoon because hypoglycemic because not eating due to illness, immediately shows confusion, lethergy, slurred speech (no CV signs because on a beta blocker)-- looks like a stroke! But is actually just hypoglycemia (CONSIDER THIS IN THE ELDERLY!) -initial CV symptoms are due to adrenaline release DKA vs HHNK DKA: Diabetic Ketoacidosis HHNK: Hyperglycemic Hyperosmolar Non-Ketotic Coma WHO GETS HHNK? Elderly (because pancreas gets tired when youre old, dont put out right amount of insulin and get hyperglycemic), DIET controlled Diabetics, pts on TPN, pancreatitis (eats itself)auto digestion of the pancreas by itself, doesnt put out enough insulin so glucose goes up, pts on thiazides (kidneys hold on to glucose) and steroids (make your body resistant to own insulin- glucose increased) ex. 20 yo F with Crohn's on TPN, TPN causes hyperglycemia, TPN makes your pancreas tired and you dont put out enough insulin so you get HHNK WHO GETS DKA? Insulin Dependent Diabetics DKA Blood Sugar = 400-900 Dehydration (-4-6 L fluid) No Insulin (people with DKA have no insulin) After about 5 days, coma- caught earlier because of severe changes, so blood sugar only goes to about 900 because it is detected earlier (family members catch it earlier) *State of acidosis- need to break down fats for energy → release ketones → state of acidosis **Kussmal breathing- increase in rate and depth to BLOW OFF CO2 TREATMENT = insulin drip**, fluids -large doses of insulin to get glucose down because pt has no insulin -start with NS, switch to 0.45 Saline once good UOP, BP and good pulse because fluid goes into the cell and corrects dehydration, then switch to D51/2NS (prevent hypoglycemia after giving so much insulin, and decreases cellular edema if too much fluid from the hypotonic solution went into the cell), so give isotonic, hypotonic, then hypertonic solution **WHEN PEOPLE COME IN WITH DKA → MUST HAVE A NORMAL OR HIGH K LEVEL **IF THEY HAVE A LOW K → THEY WILL DIE! **YOU WANT THEM TO HAVE A VERY HIGH K LEVEL *K and PH works in a reciprocal way, for any change in pH by 0.1, K changes by 0.6 -K lives in cells, level in cell = 150, serum = 4.5, most K is in cell (postiviely charged) -when body is in a state of acidosis, thinks you have extra acids and you need to get rid of the acidosishyperventilate to get rid of acid, and on a cellular level, hide the hydrogen from the serum into the cellthe positively charged ion goes into the cell with the positively charged potassium, so when hydrogen ion goes in, K comes out of the cell → this is why in a state of acidosis, you should have a high K level -in a state of acidosis, hydrogen goes into the cell, K goes out of the cell Ex. pt has pH = 7.45, K = 4.5, if pH drops to 7.35, K = 5.1, if pH drops to 7.25, K = 5.7, pH = 7.15, K = 6.3, pH= 7.05, K = 6.9 **IF PT IS ACIDODIC = THINK HIGH K! -whenever someone comes in with acidosis, keep their K high, if K drops causes CV arrythmias ex. police officer comes into the ER, 35 yo, pH = 7.05, glucose = 660, no hx of diabetes, K =4.0, CO2 = 6 → DEAD, caused by a benign pancreatic tumor that caused DKA, was previously home, drinking a lot of water and putting out a lot of urine -would not give bicarb to correct the PH, because it causes the K to drop! Insulin further drops K and causes cardiac arrythmias (vfib) HHNK Blood Sugar = 1000-2000 Severe dehydration (-6-8 L fluid) Insulin (people with HHNK have insulin) Slow, progressive, can live with this for a long time- thats why such a high glucose, because it develops over time- people dont catch it for weeks to months sometimes ex. story about visiting the nursing home, lady urinates sticky pee on the floor (glucose in the urine), has blurry vision, very dehydrated because of osmostic diuresis (also brain cells dehydrated) -95% mortality rate -brain is dehydrated, neuro symptoms- one sided weakness, etc., often misdiagnosed as a neuro event ** No Acidosis- they do have insulin which prevents the breakdown of fats, no ketosis, no acidosis *LTBB = lucky to be breathing! (because brain is all dried up due to dehydration)! *LTBB = little tiny baby breaths TREATMENT = fluids, then insulin, only takes a small amount of insulin to correct their glucose because they do already have insulin, unlike DKA which has none Practice Questions 1) What is the effect of ADH on urine formation? -Retention of water, concentration of urine 2) The releasing stimulus for ADH is normally: -Increased serum osmolarity (dehydration) 3) The normal range for serum osmolarity is: -275-295 mOsm/L -concentration greater than 295 = dehydrated, lower than 275 = dilute, fluid overloaded 4) SIADH is manifested clinically as: -water intoxication state 5) In addition to its affect on body water equilibrium, ADH is also a: -vasopressor (keep your eye on EKG- observe for ST depression for myocardial ischemia) 6) The symptomatology you would assess in the patient with SIADH results from: -water intoxication 7) The “cardinal sign” of inappropriate ADH secretion is: -dilutional hyponatremia 8) Which of the following laboratory findings would be present in a patient with SIADH? -low serum sodium 9) The patient with SIADH may present with: -seizures 10) As a staff nurse in ICU, you are assigned to a patient recently admitted with diabetes insipidus (DI), which of the following would likely develop DI? -A head trauma pt with a skull fracture 11) Who would develop SIADH? -an elderly pt receiving thiazides, a young woman with severe pneumonia, 50 yo man with esophageal varices on Pitressin 12) During your assessment, which of the following findings would be present in a pt with DI? -serum sodium level of 165 13) The nurse understands a major complication of DI is: -Hypovolemic shock 14) Evaluation of laboratory findings in a patient with DI would show: -Urine specific gravity between 1.001 to 1.005 15) The most dangerous complication of Diabetes Insipidus is: -Hypovolemia 16) Diabetes Insipidus is characterized by the following: - Tachycardia, urinary output of 2000 cc in three hours, BP 90/40 17) Which of the following is characterisic of Diabetes Insipidus? - low urine osmolarity, serium osmolarity increased, increased serum sodium 18) A 68 year old is admitted with a blood sugar of 1200 mg, she is severely dehydrated, respirations are 18 per minute and shallow. You would first suspect? -Hyperosmolar coma (HHNK) 19) Which condition would NOT predispose a patient to develop HHNK? -Cerebrovascular accidnet (CVA) -could cause HHNK = pancreatitis, thiazide of steroid therapy, TPN therapy 20) Nonketotic hyperosmolar coma (HHNK) is NOT usually associated with: -defects in ADH secretion -is associated with diabetes of recent mild onset (diet controlled diabetes), old age, use of diuretics, steroids, TPN/hypertonic solutions 21) The nurse undersands that the primary cause of the classical manifestations of HHNK is: -markedly elevated serum glucose (causes cellular dehydration, not intravascular dehydration) -very high glucoses causes dehydration in the serum, but also in the cell- brain, causes seizures and altered mental status which often caues misdiagnosis 22) The altered mental status in a patient in HHNK results from: -Intracellular dehydration 23) Which of the following findings would NOT be presenet in HHNK? -Kussmal's respiraration of 28/minute- this is with DKA, HHNK is LTBB -present = severe dehydration, absence of ketosis, serum osmo above 350, serum glucose above 650 up to 1000 24) Evaluation of a patient's laboratory values with HHNK would include: -A serum osmolarity of 340 mOsmo/L (hyperosmolar → serum osmo >295) 25) Further asssessment of diagnostic data in a patient with HHNK would reflect: -Azotemia (temporary increase in BUN and Cr due to dehydration) 26) Which of the following laboratory findings is NOT likely to be seen in patients with DKA? -pCO2 = 45 (this is normal), with DKA, you are Kussmaul's breathing to blow off CO2 to it should be around 35 (lower than normal)