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Laura Gasparis CCRN Review Medical Surgical 1 (Chamberlain University) CCRN Review- Laura Gasparis DISK 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, an
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CCRN Review- Laura Gasparis DISK 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- 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
WHO GETS DKA? Insulin Dependent Diabetics DKA Blood Sugar = 400- 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 CO 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. -K lives in cells, level in cell = 150, serum = 4.5, most K is in cell (postiviely charged)
-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
Disc 2 Neurological Cerebral Vascuar Accident DUE TO: iscehmic or hemorrhagic event -can wind up being a TIA, RIND, or CI → Basilar Vertebral Artery, Carotid Artery -TIA: all better after 24 hours -RIND: reversible ischemic neurological deficit -long TIA, longer than 24 hours, lasts for about 3 months -ex. Guy has a stroke, can't move one side, weeks and months go by, start to move that side, in a wheelchair, then a cane, then resolves (in the hospital longer) -CI: Cerebral Infarct, dead tissue forever *2 blood supply systems to brain: Basilar Verterbral Artery, Carotid Artery *Carotid- would rather have a stroke here (infarct affects one side of body, etc) -one sided weakness, one sided paraesthesias, hemiplegia, etc. *Basilar Verterbral- supplies brain stem (stroke would infarct somewhere in brain stem) *Hemonymous Hemoniopia: caused by a carotid ischemic event or hemorrhage, blindness in one half of both eyes (ex. If right side was infarcted, you would have right sided hemonymous hemoniopia) **if you have an infarct on the left side, eyes always look left (EYES LOOK TO THE BOO BOO.. HEY! WHAT'S GOING ON OVER HERE?!) *ex. Right side infarct or hemorrhage-- right sided weakness, ride sided plegia, right sided hemonymous hemoniopia, BUT LEFT eye deviation (eyes look to left side) Neuro Anatomy Cortex: problem= decorticate (hands flexed up to core) Brainstem: midbrain, pons, medulla = decerebrate (hands extended down and out) 2 holes in head: Tentorial notch, foramen magnum (down at the bottom below brain stem) -If herniating down foramen magnum → brian is leaving your head -holes decrease ICP to allow swollen brain to expand Pyramidal tracts: start on one side of the brain, cross over and go on other side of cord, motor tracts → they make you move! -if you have an injury to the pyramidal tract, you get a babinski -injury opposite of babinski → left injury = right babinski, right injury = left babinksi, bilateral injury = bilateral babinski Pupils: innervated by CN 3, parasympathetic innervation (pinpoint), sympathetic inneration (dilate) -where parietal and temporal meet is the weakest part of your head, this is where meningeal artery is, drunk people often fall and hit this part of the head (fall to the side- staggering sideways) → epidural bleed *Epidural bleed → head shifts LATERALLY **Uncal herniation = lateral shifting of brain in the head -expanding mass knocks off parasympathetic innervation of pupil, leaves only sympathetic innervation → DILATED PUPIL ON SIDE OF INJURY! **Uncal herniation = IPSILATERAL DILATED PUPIL! NO CHANGE IN LOC!
*Supratentorial Herniation- whole brain is coming on down -diffuse edema **CHANGE IN LOC (early sign), then → DILATED PUPILS (late sign)
***Cushing's Triad- INCREASED systolic BP, WIDENING pulse pressure, DECREASED HR and RR -widening pulse pressure due to increased systolic BP (ex. 200/70, then 250/70) -CUSHING'S = SIGN OF HERNIATION! **WITH ANY DOWNWARD SHIFT = CHANGE IN LOC (SUPRATENTORIAL HERNATION), AS BRAIN CONTINUES TO GO DOWN, KNOCKS OF PARASYMPATHETIC INNERVATION OF PUPILS, THEN → PUPIL CHANGE, DOWN THRU FORAMEN MAGNUM = DEATH **WITH LATERAL SHIFT = NO CHANGE IN LOC, PUPIL CHANGE ONLY (UNCAL HERNATION) Glasgow Coma Scale (GCS) Eyes Open → 4- Spontaneous 3- To Commands 2- To Pain 1- No Response Motor → 6- Obeys Commands 5- Localizes Pain 4- Withdraws from pain 3- Abnormal Flexion (Decorticate posturing) 2- Abnormal Extension (Decerebrate posturing) 1- No response (No movement) Verbal → 5- Oriented 4- Confused 3- Inappropriate Words 2- Incomprehensible Sounds 1- No Response Increased ICP AVOID:
Bacterial vs Viral Meningitis Bacterial -usually due to staphylococcus aureus -very elevated protein -low glucose! -purulent (cloudy) CSF -leukocytes (WBCs) Viral -usually due to enterovirus or herpes virus -elevated protein -normal glucose! -clear -lymphocytes *S/S of bacterial and viral meningitis: headache, nuchal rigidity, brudzinski's sign, kernig's sign -nuchal rigidity = stiff neck -brudzinski= take chin and put to chest, legs fly up -kernig- extend their leg out, pain in hamstring and neck Dolls Eyes Reflex: lift eyelids of unconscious person, eyes always return to midline when head turned side to side, oculocephalic reflex = brain stem integrity (eyes are always looking at you) **contraindicated with cervical neck injury (c-spine) Practice Questions
Gastrointestinal Pancreatitis Causes: obstruction of pancreatic ducts (gallstones, infections), alcoholism, drug toxicity (cyclosporine, steroids, thiazides, tetracyclines), trauma *auto-digestion of the pancreas- pancreas eats itself, the pancreas is fatty, needs calcium → uses up calcium to eat itself so pts with pancreatitis have hypocalcemia, also doesn't have the time to put out the right amount of insulin pts also get HHNK -when pancreas is eating itself, lifts the diaphragm up → left sided atelectasis, left sided pleaural effusions (left sided lung mess), BILATERAL rales (sympathetic rales → right side feels bad for the left and gets rales too) -complications of pancreatitis = HHNK, hypocalcemia, bilateral rales, left lung affected, ARDS -bleeding → Cullen's sign = black and blue umbilicus (belly button) Grey-Turner's sign = black and blue flank and groin ex. what is the electrolyte abnormality found in people with pancreatitis? Hypocalcemia (NOT hyperglycemia because glucose is NOT an electrolyte), but people with pancreatitis are very hyperglycemic *ARDS is the most common cause of death resulting from pancreatitis! -pancreas releases an enzyme phospholipase A → travels to lungs and kills type 2 alveolar cells that make surfactant, alveoli cannot open, no gas exchange → ARDS -elevated amylase levels **NO morphine because causes sphincter of odi to spasm (give demerol instead) Bowel Obstruction Large bowel = large distention -nothing is coming out! Small bowel = small distention, diarrhea, vomiting -small distention because everything is coming up and out! *I'll take the large bowel! Disc 3 Liver Kupper cells- detoxify blood Makes Bile Synthesizes amino acids makes albumin, prothrombin and fibrinogen (clotting) → people with liver disease don't clot well (bleed easily), people with liver disease have low albumin levels so they get ascites -blood drains from the esophagus and stomach, spleen, intestines and goes to liver to be detoxified -1500 cc goes to liver each minute to detoxify -if liver is diseased, unable to accept blood coming in → back pressure of blood to esophagus causes varices, back pressure to stomach causes gastritis, back pressure to spleen causes splenomegaly, back flow to intestines causes hemorrhoids → it doesn't pay to drink! -Liver converts glycogen to glucose
-Liver converts ammonia into urea -if your liver doesn't work, you can't detoxify blood, can't clot, hypoglycemic because can't convert glycogen into glucose, high ammonia levels → hepatic encephalopathy **NEVER WANT ANYONE WITH LIVER DISEASE TO HAVE A LOW K LEVEL -when you have a low K, your kidneys hold on to K → when kidneys hold on to K, they hold on to ammonia → puts you into a worse state of liver disease **always give aldactone = K sparing diuretic **NO lasix! Because decreases K **NEVER want anyone with liver disease to become dehydrated (have a high BUN/Cr), never want them to have a high fever *NO protein → NO food OR blood! -blood is a protein (difficult if they have a GI bleed because they need blood- but blood is a protein and breaks down which increases ammonia which worsens their condition and eventually causes hepatic encephalopathy) *DO NOT want them to have high acids (ex. Prevent hypotension because do not want them to develop lactic acidosis), never give ringer's lactate (LR) because lactate converts into bicarb by liver -LR is converted to bicarb by a healthy liver, but a diseased liver is unable to convert it to bicarb so it stays in your body as lactate, which kidneys convert to lactic acid → hepatic encephalopathy *Causes of hepatic encephalopathy: things that increase ammonia level (low K, increased BUN/dehydration, increased protein, increased acids) ex. think of the story with the post-op pt getting LR for 5 days in a coma (it wasn't anesthesia, it was the LR!), as soon as they switched LR to NS, clinical picture improved and mental status improved → very high ammonia level when labs drawn (480) → tx. Lactulose – loose stools *Complication of Neomycin therapy?? stays in the gut, affects gut bacteria, bacteria in the bowels make vitamins like folic acid and riboflavin, synthesizes vitamin K → neomycin stays in the bowel and kills all the bacteria -bacteria normally make vitamins which produce ammonia → hepatic encephalopathy -so give neomycin to people with liver disease because it kills the bacteria that make the vitamins so that they don't get hepatic encephalopathy -NOT ototoxicity, or nephrotoxicity -SO a complication of neomycin therapy is??? VITAMIN DEFICIENCY! Bowel Sounds 5-34 rumbles per minute Listen in each quadrant for 5 minutes (20 minutes total) Jaundice Your patient is jaundiced... is it hepatic (liver) failure or gallbladder disease (biliary tract disease)? -jaundice is either a problem with liver or gallbladder -bilirubin and albumin are unconjugated through blood (indirect, not married), when they get to the liver they become conjugated (married), once conjugated, go to the gallbladder to live happily ever after -so, if high levels of indirect, or unconjugated bilirubin → problem is liver (hepatic disease) -if high levels of direct, or conjugated → problem is gallbladder (gallbladder/biliary tract disease)
Renal Kidney Anatomy Proximal Tubule: reabsorption of Na, Cl, HCO3, glucose, hydrogen, phosphates, calcium, etc. -resabsorbs everything (all electrolytes), including the kitchen sink -if you body thinks you're low in K, Na, Cl, etc., your body will reabsorb it Loop of Henle: concentration and diluation of urine Distal Convoluted Tubule: site of ADH control (where ADH works to make your kidneys hold on to water) Acute Renal Failure -decrease in urine output less than 400 cc in 24 hours -3 stages of ARF: Pre-renal vs Renal Failure vs Post Renal stage of Acute Renal Failure Post-Renal Stage -you make urine, but it doesn't come out -ex. Benign prostatic hypertrophy -not a kidney problem, more of a urological problem Pre-Renal Stage -decrease in urine output (less than 400 cc/24 hours) due to decreased blood supply to kidneys -hypovolemia, CHF Renal Stage -decrease in urine output (less than 400 cc/24 hours) due to kidney damage (damaged tissues or nephrons) -acute tubular necrosis (ATN) = damage to nephron -50% mortality rate, 25% of those 50 need HD, only 25% unaffected without being dialysis dependent -caused by ischemia, nephrotoxicity (aminoglycosides, contrast, heavy metals, cephalosporins) -if caused by ischemia: hemorrhage, burns, sepsis, heart failure, transfusion reactions) -if caused by nephrotoxicity: heavy metals, medications, street drugs, rhabdomyolosis (breakdown of muscle), contrast dye -SO correct hypotension right away, before it develops from pre-renal to renal stage
Pre-Renal: BUN:Creatinine is 20: Renal (ATN): BUN:Cr is 10: OR.... Lasix or Fluid Challenge Pre-Renal failure- responds to lasix or fluids, puts out urine Renal- does not respond to lasix or fluids, does not put out urine Hyperkalemia -muscle weakness and EKG changes -peaked T wave (6.5-6.8) -prolonged P-R interval (7.0) -lose your P wave → >7. -then, widened QRS -biphasic (about 8.0) -sine wave (>8.0)= signing off -stopping steroids can cause adrenal insufficiency which causes hyperkalemia and hyponatremia *Treatment = Calcium Chloride (ONLY if there is EKG involvement → does not lower K level, but allows electricity to go through the heart normally- protects your heart) -Insulin + Glucose = pushes and hides K in cell, need to give glucose with the insulin so you don't become more hypoglycemic -Sodium Bicarb K-Excelate = antidote Calcium and Phosphate -reciprocal relationship (when Ca is low, Phos is high, etc.) -people with kidney disease always have a low calcium level -kidneys make vitamin D → you need vitamin D to reabsorb calcium from your gut -people with kidney disease don't make vitamin D and can't absorb calcium from the gut, so... -kidney disease → hypocalcemia, hyperphosphatemia -if you give amphogel or vasogel (antacid) to coat stomach, it binds with phosphate and brings phosphate level down, so calcium level will increase -clinical manifestations of hyperphosphatemia: chvostek's sign (because hyperphosphatemia is the same as hypocalcemia), the signs of hyperphosphatemia are the same signs as hypocalcemia (twitch, twitch, seize, seize, chvostek and trousseau) -hypercalcemia/hypophosphatemia = severe muscle weakness ex. her brother in law with tums → became very week and lethargic, weight loss from high calcium levels of overingestion of calcium/ low phosphate (antacid binds with phosphate)
Practice Questions