CCRN Review #1: Endocrine #2: Neuro #3: GI, Renal, Hematology #4: Cardiovascular #5: Cardiovascular cont. #6: ABG, Pulmonary (complete 2021 A+ Guide)
CCRN Review #1: Endocrine #2: Neuro #3: GI, Renal, Hematology #4: Cardiovascular #5: Cardiovascular cont. #6: ABG, Pulmonary Endocrine • SIADH Syndrome of Inappropriate ADH and DI • SIADH—means too much ADH • You know that ADH is made in your hypothalamus and stored in your posterior pituitary sent to kidneys causing the distal convoluted and collecting tubule hold on to water • ADH makes you hold on to water • ADH WATER ADH WATER ADH • ADH makes your kidneys and makes you hold on to water • ADH goes down to you distal convoluted and collecting tubule • When you hold onto water you’re gonna decrese your sodium level… you get DILUTIONAL HYPONATREMIA=SIADH • DILUTIONAL HYPONATREMIA=SIADH • Hypo-osmolar—DECREASED SERUM Osmolarity…osmolarity less than 275 • A cheat to determine SERUM osmolarity is doubling the sodium content…say someone comes in with a sodium of 150…double that and it makes 300….this person is hyperosmolar Normal sodium concentration (hypo-osmolar =decreased unrine output -275-295 -hyperosmolar • Say someone comes in with sodium of 120…double that and that makes 240 and someone is hypo-osmolar • Normal concentration of your body is 280 • Decreased urinary output • CAUSES • Oat cell carcinoma-tumor in apical portion of your lung… makes ADH which goes down to your kidneys and casues your kidneys to hold on to water • Viral Pneumonia-they’re not too sure why…hypoxic areas in your lung which causes your posterior pituitary to release ADH which goes down to your kidneys and casues your kidneys to hold on to water • Structural Head Problem can give you SIADH • Increase SERUM osmolarity CAUSED BY {anesthesia (pt given fluids during the OR), analgesic]s, and stress causes hypothalamus to produce ADH and stores in the posterior Pituitary gland and releases to kidney (distal convoluted tubules and collecting yubules) • Increase ADH = low SODIUM, low serum osmolarity, lower urinary output SIDE NOTE – PH is up Alkalosis = ICP goes down, decreased potassium level Liver disease =(low protein and acids and high potassium level) – never have increase in protein and acids, never have low potassium level because kidneys hold on to potassium which makes you hold on to ammonium ion which is not good for liver disease (hepatic encephalopathy) DILUTIONAL HYPONATREMIA = SIADH • DILUTIONAL HYPONATREMIA=SIADH • COMPLICATION • Monitor for SEIZURE ACTIVITY—because if you have SIADH…you get a dilutional hyponatremia (LOW SODIUM CONCENTRATION EXTRACELLULARLY{SERUM}) • Dilutional hyponatremia causes water to go into the brain cell….level of consciousness decreases…eventually resulting in SEIZURE • TREATMENT FOR SIADH • Get rid of the oat cell carcinoma, viral pneumonia, or head problems • FLUID RESTRICTION • Hypertonic Solutions 3% Sodium Chloride—has osmolarity of 1500…causes water to go back into intravascular space… only 25 cc’s per hour for about 4 hours • NO HYPOTONIC SOLUTIONS WITH SIADH—like D50/ ½ NS (has bag concentration/osmolarity of 155), . 33% SALINE has bag concentration/osmolarity of 100), 2.5 DEXTROSE (has bag concentration/osmolarity of 130) D5W, A ISOTONIC SOLUTION (has bag concentration/osmolarity of 275 but when given and metabolized concentration/osmolarity = 245) SIDE NOTE D5W IS ISOTONIC, but when given and metabolized by the body, concentration decrease by 40 points because glucose utilized by body and decreases osmolarity by 40 points. For example d5w has bag concentration/osmolarity of 275 but when glucose is metabolized, concentration/osmolarity of d5w decreases to 245 which becomes an hypotonic solution. normal serum osmolarity 275-295. Normal Saline 9% saline Isotonic solution – osmolality 308 • Hypertonic solutions to give— TO MOVE FLUID FROM INTRACELLULAR TO SERUM (EXTRACELLULAR) THROUGH OSMOSIS (WATER MOVES FROM HIGHGER CONCENTRATION SOLUTION TO A LOWER CONCENTRATION SOULUTION) TO GET RID OF THE SEIZURE, A COMPLICATION OF SIADH! 3% sodium chloride, (has bag concentration/osmolarity of 1500) D5NS%, (has bag concentration/osmolarity of 565) D5 1/2 NS (has bag concentration/osmolarity of 406) WATCH OUT FOR CHF AND FLUID OVERLOAD WHEN GIVING HYPERTONIC SOLUTIONS D5 1/2 NS, D5NS%,3% sodium chloride, CONCLUSION OF siadh AT 24.00 MIN OF DISC ONE • DIABETES INSIPIDUS • NO ADH Will loose water( 6-24 liters per day )by diuresis because antidiuretic hormone is not sufficient or present to reabsorb water in the distal convoluted and collecting tubule. Will lead to- increase sodium level • INCREASE IN SODIUM LEVEL = serum osmolarity will increase (hyperosmolar) • HYPEROSMOLAR—increase in OSMOLARITY • INCREASED URINARY OUTPUT (6-24L/day) • CAUSES • Head Problems • DILANTIN—diabetes insipidus is DI…dilantin is DI • Low adh=increase in sodium level, increase in serum osmolarity, increase in urinary output dilute urine (specific gravity is low 1.001-1.005 dilute urine) NORMAL urine specific gravity = 1.010 – 1.030 • Complications—hypovolemia that leads to SHOCK • TREATMENT • Give ADH (Pitressin)…or vasopressin • Give Fluids to increase Intravascular Volume • Monitor Urine Specific Gravity • Monitor EKG for Ischemia because vasopressin is a vasoconstrictor and may cause an Myocardial ischemic attack since it will constrict arteries and will look like an ST-depression on the EKG • HYPOGLYCEMIA Sugns and symptoms (cardiovascular signs first then neurological due to compensatory mechanisms) if on beta blocker, cardiovascular signs may not occur. CARDIOVASCULAR (caused by adrenaline release for hypoglycemia compensatory mechanism) – Tachycardia, palpitation ,diaphoresis restlessness, irritability NEUROLOGICAL (caused by brain cell death due to hypoglycemia) - confusion, lethargy, slurred speech, seizure, coma, death • Whenever you’re hypoglycemic, your adrenal medulla knows this and will release adrenaline, and adrenaline goes to your liver and makes you convert glycogen to glucose to get you out of this predicament, so whenever you’re low on glucose…ADRENALINE IS RELEASED Adrenaline causes tachycardia, palpitation, restlessness, diaphoresis, irritation • However, if you’re on a betablocker like Lopressor, or Inderal, tenormin, there won’t be as much or any adrenaline release, and adrenaline won’t be as effective or wont be released into the liver and won’t cause the liver to convert glycogen to glucose. Glucagon is secreted by the pancreas to the liver to convert glycogen into glucose when hypoglycemic. • Let’s say you do have adrenaline release, and when the adrenaline went to your liver to convert glycogen into glucose…because you were drinking all weekend…when you drink your liver works to convert alcohol that it really doesn’t have time to store glycogen…so this person would go hypoglycemic • CARDIOVASCULAR SYMPTOMS • Tachycardia, palpitations, diaphoresis, irritable, restlessness • CENTRAL NERVOUS SYSTEM SYMPTOMS • Confusion, Lethargy, Slurred speech, seizure, coma • Means your brain cells are dying • IF YOU ARE ON A BETA ADRENERGIC BLOCKER…. It blocks the cardiovascular symptoms…. The only thing you’re gonna get is the confusion, lethargy, slurred speech, seizure, and eventually coma • DKA and HHNK/hyperglycemic hyperosmolar non-ketotic coma • HHNK—(blood sugar can be as high as (-6-8 liters of fluid dehydrated) • have insulin. • No acidosis beause they have insulin Circulating insulin prevent breakdown of fat = no ketone production that causes acidosis. Breathing pattern = little tiny baby breaths. because brain is dried up, the person lucky to be breathing • People don’t go to a coma and can hang out with a high blood sugar for more than 4-5 days(weeks and months) and can accumulate blood sugars as high as . • old people/old age get hhnk because pancreas does not secrete as much insulin as when young, diet controlled diabetic gets HHNK, people on TPN because when you’re on tpn you’re getting high concentrations of glucose and it will make your pancrease tired and wont put out the right amounts of insulin = blood sugar goes up Population of people who have hyperglycemic hyperosmolar non ketotic coma • Old age • Diet controlled diabetics • People on TPN • Pancreatitis – pancreas eat itself (autodigestion) therefore wont secrete as much insulin • People on thiazides – Thiazides cause kidneys cause kidneys to hold on to glucose • and steroids can get HHNK – steroids make people resistant to their own insulin 95% mortality rate from misdiagnosis- osmotic diuresis causes dehydration and cerebral dehydration – neurological symptoms such as one sided weakness and focal seizures. People think diagnose with neurological cause (wrong) Treatment- give fluids first then insulin Fluids give 9% NS normal saline (Isotonic solution) because it stays in the intravascular space to maintain hemodynamic stability (good blood pressure, good pulse and good UOP. When hemodynamically stable switch to .45% NS (hypotonic solution) because fluid goes into the cell. Good because they are dehydrated. Watch out for cerebral edema due to excess water in the cell *************************CONTINUED**************************
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Subjects
- nur 450
- renal
- pulmonary
- ccrn dvd review notes
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ccrn review 1 endocrine 2 neuro 3 gi
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hematology 4 cardiovascular 5 cardiovascular cont 6 abg
