Laura Gasparis CCRN Review, Exams of Health sciences

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Laura Gasparis CCRN Review

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)

• when body is in a state of acidosis, thinks you have extra acids and you need to get rid of the acidosis- hyperventilate to get rid of acid, and on a cellular level, hide the hydrogen from the serum into the cell- the 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. **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, CO = 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- 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:

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:

• Acidosis: acidosis vasodilates blood vessels and increases ICP, keep pt alkalotic with high ICP -Hypotonic Solutions: they go in the cell, give hypertonic solutions to draw water out of the cell -Hyperextension/Flexion: do not flex neck and head, log roll in bed -Decreased Protein: feed them (when protein levels drop, lose oncotic pressure and fluid goes into cell and causes more cerebral edema), ensure adequate caloric pressure -Wrist Restraints: increases ICP up to 50 pts -Stroke: most s/s are due to TEMPORARY cerebral edema (increased ICP) -NPO, restraints, turning, hypotonic solution (D5W since NPO) all cause worsening cerebral edema and woresning s/s

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

1. The single most important index of neurological state is the: -Level of consciousness
2. Quick rotation of the head back and forth while holding the eyes open causing the eyes of the comatose patient to rotate opposite the side toward which the head is turned is a positive response known as: -Oculocephalic Reflex (Dolls Eyes Reflex)
3. The response elicited when the neck is flexed, producing flexion of both thighs at the hips, as well as flexion movements of the ankles and knees is called: -Brudzinski's Sign
4. The respiratory pattern seen in upper brainstem lesion (midbrain) is: -Hyperventilation *Midbrain problems = hyperventilate (blow off CO2 and put yourself in alkalotic state) *Apneustic breathing = pontene problem (Pontene has P, apneustic has P)
5. A 26 year old male is complaining of a severe headache. On assessmnet, he has a nuchal rigidity, and a positive Kernig's sign. Which of the following is most likely present? -Subarachnoid Hemorrhage

6. The classic CV signs of increasing ICP known as Cushing's triad include? -Decreased pulse, increased systolic BP, widening pulse pressure
7. Ventricular fluid pressure is the most sensitive indicator of increased ICP. The normal ventricular fluid pressure is: -0-10 mmHg
8. A patient has a subarachnoid screw inserted to monitor his ICP and cerebral perfusion pressure (CPP). The ICP and CPP are both 35 mmHg. This means that this patient's: -Cerebral blood flow has markedly decreased to the brain -problem = CPP is low, ICP is high (no perfusion)
9. Which of the following parameters are graded when using the Glasgow Coma Scale in the assessment of the patient with an altered state of consciousness? -eye opening, motor response, and verbal response
10. Blindness in one hald of both visual fields following a CVA is referred to as: -Hemonymous Hemianopia
11. Patients with injury to the left cerebral hemisphere may exhibit: -Deviation of the eye to the left
12. Pinpoint pupils that react to light if viewed with a magnifying glass are indicative of: -A lesion in the pons (pintpoint pupils = pontene infarct) -sympathetic innervation goes up through the pons -parasympathetic innervation goes up through the midbrain -pontene infarct is dead tissue, so you lose the sympathetic innervation and you only have the parasympathetic innervation of the pupil, so it becomes pinpoint -pontene infart also = apneustic breathing (prolonged pauses between exhaling and inhaling), they take a long inhale and you're waiting for them to exhale (call a code.. no nevermind!)
13. The nurse caring for a patient with a supratentorial herniation understands that the earliest sign would be:

• Lethargy and Stupor

14. Which of the following treatment modalities would the nurse consider to be inappropriate for the ventilator patient with increased ICP? -Administering D5W at 75 cc/hr (hypotonic solution increases brain swelling) -would want to keep the pt acidodic (CO2 between 29-33) ex. kid with head trauma and DKA (do not give hypotonic even though DKA because head comes first)
15. While assessing the laboratory data of a patient with head trauma, which finding necessitates notification of the physician? -A urine specific gravity of 1.005 → indicates DI, head trauma is the number 1 cause!
16. A Basal Skull fracture affecting the middle fossa may cause which of the following? -Cranial Nerve Injuries (1) -Battle's Sign -CSF Otorrhea and Rhinorrhea

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)

11. Which of the following may contribute to the preciptation of encephalopathy in the patient with liver failure? -GI bleeding (blood = protein), hypokalemia (low K- kidneys hold on to K and ammonia), hypotension (build up of lactic acid causes hepatic encephalopathy)
12. Ecchymosis around the umbilicus indicative of peritoneal bleeding is called: -Cullen's sign FYI: Chvostek = cheek twitching, hypocalcemia Trousseau's sign = hypocalcemia, inflate BP cuff
13. Pulmonary complications of acute pancreatitis may include: -ARDS, elevation of diaphragm and bilateral basilar rales, atelectasis (especially left base)
14. A bluish-green, brown discoloration in the flank and groin due to retroperitoneal bleeding is called: -Grey-Turners sign
15. Patient assessment findings indicative of a bowel infarction would include: -Hypoactive bowel sounds and leukocytosis, hyperresonance and abdominal tenderness, absense of dullness in the liver area

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

OR...

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

1. A weight gain of one kilogram in 24 hours may indicate fluid retention of at least: -1,000 mL
2. Signs of rapidly developing alkalosis include ALL BUT WHICH of the following: -obtundation -alkalosis = low calcium level -hypocalcemia = nervous irritability, muscle tremors, seizures
3. Which of the following drugs actually removes potassium from the body in hyperkalemic patients in acute renal failure? -Kayexalate and sorbital
4. The electrolyte abnormality that produces a U wave, depressed ST segment, and ventricular irriability is: -Hypokalemia
5. Which EKG finding would NOT be observed in the presence of hyperkalemia? -Ventricular irritability -hyperkalemia = prolonged PR interval, absence of P waves, widened QRS complexes
6. The glomerular filtration rate (GFR) can be best measured by evaluating the patient's: -Creatinine clearance
7. Approximately 60-80% of sodium and water is reabsorbed from the glomerular filtrate at the: -proximal tubule
8. The major function of the loop of Henle is: -Concentration or dilution of urine
9. What activity is performed at the distal convoluted tubule? -water reabsorption under ADH control
10. A patient has a urinary output of 1000 cc in 24 hours with a urine sodium of 25 mEq/liter. These findings indicate: -the patient is on a salt-free diet
11. Ischemic injury to the kidney will usually commence when the mean arterial blood pressure (MAP) falls below: -60 mmHg for 40 minutes
12. The two most common causes of acute renal failure or ATN are: -nephrotoxic substances and ischemia
13. The patient with acute tubular necrosis is differentiated from a patient with decreased renal perfusion because ONLY in decreased renal perfusion: -the BUN to creatinine ratio is 20: