NGN bow tie practice questions.

Answer

The key, and why

Warfarin blocks the recycling of vitamin K in the liver, and without active vitamin K the liver cannot finish making clotting factors II, VII, IX, and X. The dose that kept this client's INR at 2.2 to 2.8 for a year was matched to the vitamin K in the usual diet. A daily smoothie of kale and spinach delivers several times the vitamin K the client was eating before, so the liver has enough to keep making clotting factors despite the drug, and the INR falls. An INR of 1.4 means the blood clots almost normally, which is subtherapeutic anticoagulation. In atrial fibrillation, blood pools in the quivering left atrium and can form a clot that travels to the brain. With the INR this low, that protection is gone. The nurse reports the result and the cause so the provider can decide how to adjust the dose, and teaches the client that greens are allowed but the amount should stay about the same each day. The INR is rechecked to see whether the plan has worked, and the client and family are taught to watch for signs of stroke and to call emergency services if they appear.

Each distractor

Phytonadione is vitamin K. It is given to reverse warfarin when the INR is too high, and here it would push the INR even lower. Stopping all green vegetables trades one change for another. If the client stops the smoothie and the greens at once, the INR can rise above range and cause bleeding, and the client loses healthy foods. Taking an extra dose of warfarin without a prescription is unsafe. The dose is changed by the provider, based on the INR, and a doubled dose can overshoot. Warfarin toxicity causes a high INR with bruising or bleeding, the opposite of this result. Vitamin K deficiency from poor intake also raises the INR. This client is eating more vitamin K, not less. Liver disease lowers the production of clotting factors and raises the INR. Nothing suggests liver disease, and the INR is low. The serum potassium has no link to warfarin or vitamin K. The platelet count is monitored with heparin, because of heparin-induced thrombocytopenia. Warfarin does not lower platelets. Stool for occult blood screens for bleeding, which is the risk when the INR is too high. With an INR of 1.4, the risk is a clot.

The teaching point

MORE vitamin K = INR DOWN = CLOT and STROKE risk. LESS vitamin K = INR UP = BLEEDING risk. The fix = CONSISTENT vitamin K, REPORT, recheck the INR. Never self-adjust the dose. Phytonadione = vitamin K = reverses a HIGH INR.

Answer

The key, and why

Myxedema coma is severe hypothyroidism that has decompensated, and this client has every sign of it after 3 months without levothyroxine. The body is slowed and cold. The temperature is 93° F (33.9° C), the heart rate is 44, the breathing is so slow that the carbon dioxide has climbed to 68 mm Hg and the pH has fallen, and the sodium and glucose are low. The two actions treat the cause and protect the airway. IV levothyroxine replaces the missing hormone; the IV route is used because the gut is sluggish and absorbs tablets poorly. A respiratory rate of 8 with a PaCO2 of 68 and an SpO2 of 89% is respiratory failure, and the nurse prepares for intubation and mechanical ventilation. The two parameters show whether the plan is working and whether it is causing harm. A core temperature that rises slowly with passive rewarming shows the metabolism coming back. Continuous cardiac monitoring matters because the client starts bradycardic and hypotensive, and thyroid hormone in an older heart can bring on ischemia and dysrhythmias as the metabolic rate rises.

Each distractor

An electric heating pad is active external rewarming. It dilates the skin vessels and can drop the BP into collapse in a client whose circulation is already failing, and it burns poorly perfused skin. Warm blankets and a warm room are used instead. The Trendelenburg position is no longer used for hypotension. It pushes the abdominal organs against the diaphragm and makes breathing harder in a client who is already hypoventilating. An oral levothyroxine tablet is poorly absorbed in myxedema coma, and a client who opens the eyes only to a loud voice cannot swallow safely. Thyroid storm is the opposite state, with fever, tachycardia, and agitation. Adrenal crisis causes hypotension, hyponatremia, and hypoglycemia, but not hypothermia with this degree of hypoventilation, and it does not follow stopping levothyroxine. Hyperosmolar hyperglycemic state needs a very high glucose. This glucose is 68 mg/dL. Hemoglobin A1C reflects glucose control over 3 months and tells the nurse nothing about this crisis. Serum calcium is watched after thyroid surgery, when the parathyroid glands may be injured. This client has had no surgery, and calcium does not track the course of myxedema coma. Urine ketones are watched in diabetic ketoacidosis. Nothing in this client points to ketosis, and they would not show whether the metabolic rate is recovering.

The teaching point

MYXEDEMA COMA = cold, slow, sleepy, HYPOVENTILATING, low sodium, low glucose. IV LEVOTHYROXINE + AIRWAY support + PASSIVE rewarming. NO heating pads, NO sedatives, NO Trendelenburg. Monitor TEMPERATURE coming up and the cardiac RHYTHM as the hormone kicks in.

Answer

The key, and why

Neurogenic shock is a distributive shock that follows a spinal cord injury at T6 or above. The injury cuts the sympathetic nerves that leave the cord below it, so the blood vessels lose their tone and dilate, and the heart loses the nerves that speed it up while the vagus nerve still slows it. The result is the combination that gives it away, hypotension with bradycardia and warm, dry, pink skin below the injury. The cues fit exactly. A C5 injury 3 hours ago, a heart rate of 46, a pressure of 78/42, warm skin, and no sign of bleeding, with a normal hemoglobin and no free fluid in the abdomen. Treatment starts with an isotonic crystalloid bolus to fill the dilated vessels, then a vasopressor such as norepinephrine if the pressure stays low. Symptomatic bradycardia is treated with IV atropine, and some clients need a pacemaker. The usual goal is a MAP of about 85 to 90 mm Hg (at least 75 to 80 under newer guidance) for the first 3 to 7 days, to keep blood flowing to the injured cord. The heart rate and rhythm and the MAP are the measures that show whether this is working.

Each distractor

Trendelenburg position with the head down is no longer recommended for shock. It shifts the abdominal organs against the diaphragm and makes breathing harder, which matters in a C5 injury that already weakens the breathing muscles. Furosemide removes fluid from a client whose problem is too little filling of dilated vessels. It would drop the pressure further. A hypothermia blanket is wrong for this client, even though cooling is sometimes described as protecting the cord. After a high cord injury the client cannot shiver or constrict skin vessels below the injury, so body temperature drifts toward the room temperature. The nurse keeps the client normothermic and warm, not cooled. Hypovolemic shock would bring a fast heart rate, cool, pale skin and signs of bleeding, and the hemoglobin and ultrasound show none. Septic shock would need an infection, and it is far too early after the injury for one. Autonomic dysreflexia causes severe hypertension, not hypotension, and appears weeks to months after the injury, once spinal shock has resolved. Pupil size and reactivity belong to the neurologic examination of a head injury. They do not show whether the shock is responding. Deep tendon reflexes in the legs track the end of spinal shock over days to weeks. They do not change with fluids or atropine. Bowel sounds are checked for paralytic ileus, which is common after a cord injury, but they say nothing about perfusion.

The teaching point

NEUROGENIC shock = injury at T6 or ABOVE → LOW BP + SLOW HR + WARM, DRY skin. HYPOVOLEMIC shock = low BP + FAST HR + COOL, PALE skin. Treat = FLUIDS, then VASOPRESSOR; ATROPINE for symptomatic bradycardia. MAP goal about 85 to 90 (at least 75 to 80 under newer guidance) for 3 to 7 days. Keep the client WARM. No shivering below the injury.

Answer

The key, and why

Spontaneous bacterial peritonitis is an infection of ascitic fluid with no surgical source, such as a hole in the bowel. Bacteria cross the wall of a congested gut and seed the fluid. It is diagnosed when the ascitic fluid has 250 neutrophils/mm3 or more. Fever, abdominal tenderness and new confusion are typical, although some clients have very few signs and the only change is worsening encephalopathy or kidney function. The treatment is an IV third-generation cephalosporin, such as ceftriaxone or cefotaxime, started as soon as the fluid has been sampled. IV albumin is given on the first and third days, especially when the creatinine or bilirubin is raised, because it supports the circulation and cuts the risk of kidney failure and death. Kidney injury is the complication that kills these clients, so the creatinine and hourly urine output show whether the albumin is protecting the kidneys. The temperature and mental status show whether the infection is clearing.

Each distractor

An emergency laparotomy is for secondary peritonitis, when a perforation or abscess needs surgery. Operating on a client with spontaneous bacterial peritonitis adds risk with no benefit. Restricting protein to 20 g a day is outdated and worsens the muscle wasting that raises ammonia. Giving the diuretics would remove volume from a client at high risk for kidney failure. They are held during the infection. Secondary peritonitis comes from a perforated or inflamed organ, usually with very high neutrophil counts, several organisms on culture, free air or a recent abdominal injury or surgery. This client has none of these. Hepatorenal syndrome is kidney failure in advanced liver disease. Spontaneous bacterial peritonitis is one of its triggers, but the cues here describe an infection. Acute pancreatitis causes epigastric pain radiating to the back with a high lipase, not cloudy ascites with high neutrophils. Serum lipase follows pancreatitis and tells the nurse nothing about this infection. Hemoglobin A1C reflects glucose control over about 3 months. A stool test for occult blood looks for gastrointestinal bleeding, which is not the problem being treated.

The teaching point

SPONTANEOUS BACTERIAL PERITONITIS = ascitic fluid neutrophils 250/mm3 or more, NO surgical source. Treat = IV CEFTRIAXONE or cefotaxime + IV ALBUMIN. HOLD diuretics. Watch = CREATININE and URINE OUTPUT, temperature, mental status.

Answer

The key, and why

SIADH is the release of antidiuretic hormone when the body does not need it, so the kidneys keep holding water. Small cell lung cancer is a classic cause, because the tumor can make the hormone itself. The client has a low sodium and a low serum osmolality, which show the blood is diluted, yet the urine is concentrated with a specific gravity of 1.028. The kidneys are holding water they should be releasing. The weight gain without edema and the moist mucous membranes fit, and drinking extra water makes it worse. The water has to go. Fluid restriction lets the sodium rise as the kidneys slowly clear the excess. A sodium of 122 mEq/L with confusion places the client at risk for seizures, so seizure precautions are in place while the sodium is corrected. The serum sodium shows whether the restriction is working and whether it is rising at a safe pace, about 8 mEq/L or less in 24 hours. The level of consciousness shows how the brain is responding, since swelling of brain cells from the dilute blood causes the confusion and headache.

Each distractor

Encouraging 3 L of fluid adds the very water the kidneys cannot clear and drops the sodium further. 5% dextrose in water is free water once the glucose is used, so it lowers the sodium more. A 2,000-mg sodium diet restricts sodium in a client whose sodium is already too low. Diabetes insipidus causes the opposite picture, with a high sodium and large volumes of very dilute urine. Hypovolemic hyponatremia from vomiting would bring dry mucous membranes, a low BP, weight loss, and a low urine sodium. Heart failure with fluid overload would cause edema, crackles, and distended neck veins, and the client has no edema. Capillary glucose matters during chemotherapy but does not show whether the hyponatremia is improving. Serum potassium is not the problem in SIADH and is not the measure of response. White blood cell count tracks chemotherapy effects and infection risk, not the water balance.

The teaching point

SIADH = LOW sodium, LOW serum osmolality, CONCENTRATED urine, weight UP, NO edema. Treat = FLUID RESTRICTION, SEIZURE precautions. Monitor = SODIUM and LEVEL OF CONSCIOUSNESS. SMALL CELL lung cancer = classic cause.

Answer

The key, and why

Aspiration pneumonia is a lung infection that follows the entry of food, liquid, or oral secretions into the airway. Parkinson's disease weakens and slows the muscles of swallowing and dulls the cough, so dysphagia and aspiration are common in its later stages and are a leading cause of death. A week of coughing at meals and a wet voice after drinking thin liquids shows the client has been aspirating, and fever, tachypnea, low SpO2, and crackles in the right lower lobe show pneumonia has followed. The right lower lobe is the usual site, because the right main bronchus is wider and more vertical. The nurse treats the hypoxemia first with oxygen to keep the SpO2 at 92% or higher, and stops all oral intake until the speech-language pathologist decides what, if anything, the client can swallow safely. The SpO2 with the respiratory rate shows whether oxygenation is improving, and the temperature with the breath sounds shows whether the infection is responding to treatment.

Each distractor

Thin liquids through a straw are the consistency and the delivery most likely to be aspirated. Hydration is maintained intravenously until the swallow is evaluated. Lying flat lets secretions and any refluxed stomach contents pool in the airway. The client sits upright, at least 30 to 45 degrees, and higher for meals. An antitussive suppresses the cough, which is the client's only protection against aspirated material. Pulmonary embolism causes sudden dyspnea and pleuritic chest pain, not a week of coughing at meals with fever and localized crackles. Acute heart failure causes crackles in both bases, edema, and orthopnea, not a fever with crackles in one lobe. A spontaneous pneumothorax causes sudden chest pain with absent breath sounds on one side, not crackles. Serum potassium does not reflect the course of pneumonia. Capillary glucose may rise with infection, but it does not show whether the lung is improving. Bowel sounds tell the nurse nothing about oxygenation or the infection.

The teaching point

Parkinson's + COUGHING at meals + WET voice + FEVER + RIGHT lower lobe crackles = ASPIRATION PNEUMONIA. OXYGEN, NPO until swallow evaluation, UPRIGHT. Never suppress the COUGH. Monitor SpO2, RESPIRATORY rate, TEMPERATURE, BREATH sounds.

Answer

The key, and why

Iron deficiency anemia is a shortage of iron to build hemoglobin, so the red cells come out small and pale. A mean corpuscular volume of 62 fL is well below the normal range of about 70 to 86 fL for a toddler, and a hemoglobin of 8.4 g/dL is below the 11 g/dL cutoff. The cause is in the history. A toddler who drinks 40 oz of milk a day fills up on a food that has almost no iron and blocks iron absorption, so there is no room for iron-rich foods. The pallor, fatigue, poor appetite, and fast heart rate all follow from the low hemoglobin. Treatment has two parts. Cutting milk to 16 to 24 oz a day, in a cup and with meals, lets hunger return for iron-rich foods. The prescribed iron is given between meals with a little vitamin C, which keeps iron in the form the gut absorbs best. The hemoglobin is rechecked after about 4 weeks. A rise of at least 1 g/dL confirms the diagnosis and shows the treatment is working, and the iron is continued for several months after it normalizes to refill the stores. The parent's daily record of milk and food shows whether the change that caused the anemia has actually been made.

Each distractor

Mixing iron into the milk bottle undoes the treatment. Milk blocks iron absorption, and the bottle at bedtime is part of the problem. An extra bottle of milk adds more of the cause. A transfusion is not needed for a child who is hemodynamically stable, alert, and in no respiratory distress with a hemoglobin of 8.4 g/dL. Oral iron corrects it. Sickle cell anemia causes a normocytic hemolytic anemia with pain crises and is found on newborn screening, not a microcytic anemia explained by diet. Vitamin B12 deficiency causes large red cells, a high mean corpuscular volume, not a low one. Acute lymphocytic leukemia causes anemia with bruising, bone pain, fever, and abnormal white cells, and the anemia is not microcytic. Serum potassium is not affected by iron deficiency or its treatment. Fasting glucose has no link to this condition. Stool color is expected to darken on iron and tells the nurse nothing about whether the anemia is improving.

The teaching point

Toddler + LOTS of milk + pale + LOW MCV = IRON DEFICIENCY ANEMIA. Milk = 16 to 24 oz a DAY, in a CUP, with meals. Iron = BETWEEN meals with VITAMIN C, NEVER in milk. Recheck hemoglobin in about 4 weeks. Expect a rise of 1 g/dL or more.

Answer

The key, and why

Hypermagnesemia is a serum magnesium above about 2.1 mEq/L. The kidneys are the only real exit for magnesium, so a client with advanced kidney disease who takes a magnesium laxative or antacid every day keeps absorbing it with no way to get rid of it. Magnesium blocks nerve signals at the neuromuscular junction and relaxes smooth muscle, so the picture is one of everything slowing down: drowsiness, lost reflexes, slow shallow breathing, a slow heart rate, low blood pressure, and flushed warm skin from dilated vessels. The first action is to stop the source, so every magnesium-containing product is held. Calcium gluconate IV directly opposes magnesium at the nerve and heart muscle and is given for severe symptoms such as these. Because the kidneys cannot clear the excess, dialysis is the definitive treatment in kidney failure. Reflexes disappear before breathing slows, so the patellar reflex is the early warning and the best bedside check that the level is coming down. The respiratory rate and depth matter most for safety, because respiratory depression and then arrest are the deadly end of rising magnesium.

Each distractor

Seizure precautions belong to low magnesium, which makes the nerves irritable. This client's nerves are depressed. Nuts, whole grains, and leafy greens are high in magnesium and would add to the problem. A sodium phosphate enema adds phosphate to a client whose kidneys cannot clear it and can cause dangerous electrolyte shifts in kidney disease. The constipation is treated later with a product that contains no magnesium or phosphate. Hyperkalemia is unlikely with a potassium of 5.1 mEq/L, which is barely above normal and does not explain absent reflexes and flushing. Hypercalcemia also causes lethargy and weak reflexes, but the calcium of 8.8 mg/dL is not high. Hypocalcemia causes tingling, cramps, and twitching, the opposite of this client's depressed nerves. Chvostek sign tests for irritable nerves in low calcium or low magnesium. It tells the nurse nothing about rising magnesium. Fingerstick glucose does not track magnesium. Urine specific gravity says little in a client with stage 4 kidney disease, whose kidneys cannot concentrate urine normally.

The teaching point

HIGH magnesium = everything SLOWS. Lethargy, ABSENT reflexes, slow breathing, bradycardia, hypotension, flushing. Stop the source (magnesium LAXATIVES and ANTACIDS), give IV CALCIUM GLUCONATE, dialysis in kidney failure. Reflexes go FIRST, then breathing. Check the patellar reflex and the respiratory rate.

Answer

The key, and why

A coronary perforation lets blood escape from the torn artery into the pericardial sac, and the filling sac compresses the heart. This is cardiac tamponade. The client has Beck's triad (hypotension, distended neck veins, and distant heart sounds) and pulsus paradoxus, a fall in systolic pressure of more than 10 mm Hg on inspiration, here 16 mm Hg. The pulse pressure has narrowed to 16 mm Hg because the squeezed heart can eject only a small volume. The treatment is to remove the fluid, so the nurse notifies the cardiologist immediately and prepares for pericardiocentesis, a needle drain of the pericardial sac. Until then, a fluid bolus keeps the filling pressure high enough to push some blood into the compressed heart. The blood pressure and pulsus paradoxus show whether the heart is filling better after drainage. The neck veins and central venous pressure fall as the pressure around the heart is relieved.

Each distractor

Furosemide lowers preload, and a compressed heart depends on high filling pressure. It could cause collapse. Nitroglycerin dilates the veins and drops preload and blood pressure, which is dangerous here. Metoprolol slows the heart, but tachycardia is how this client keeps any cardiac output when each beat ejects so little. Left ventricular failure with shock brings crackles and pulmonary congestion, and it does not cause pulsus paradoxus with distant heart sounds. Hypovolemic shock from bleeding at the access site causes flat neck veins, not distended ones. Tension pneumothorax causes absent breath sounds on one side and tracheal deviation, and the heart sounds are not distant. Serum creatinine matters after contrast, but it changes over days and does not track tamponade. Capillary blood glucose does not reflect cardiac filling. Daily weight tracks fluid balance over days, not a compressed heart minute to minute.

The teaching point

TAMPONADE = Beck's triad (LOW BP, JVD, MUFFLED sounds) + PULSUS PARADOXUS over 10 mm Hg + NARROW pulse pressure. Treat = PERICARDIOCENTESIS, FLUIDS to support preload. AVOID = diuretics, nitrates, beta blockers.

Answer

The key, and why

Flank pain and chills, a fever, a fast heart rate and a falling blood pressure 20 minutes into a unit are the signs of an acute hemolytic reaction. The donor red cells are being destroyed inside the client's vessels. The two actions stop the harm and protect the client's circulation. The transfusion is stopped at once so no more incompatible blood goes in. Then the blood tubing is disconnected and 0.9% sodium chloride runs through new tubing at the hub, which keeps the vein open for drugs and supports the falling blood pressure. The two parameters show whether the client is getting better or worse. Free hemoglobin from the destroyed cells is filtered by the kidneys and can block them, so urine output and color, watching for a fall in volume and for red or dark urine, tell the nurse whether the kidneys are being damaged. The blood pressure tells the nurse whether the client is sliding into shock.

Each distractor

Slowing the unit and rechecking keeps incompatible blood flowing into a client who is already reacting. Giving diphenhydramine and continuing treats an allergic reaction, which this is not, and keeps the cause running. Giving furosemide and continuing treats circulatory overload. This client's pressure is falling, not rising, and the blood is still running. A febrile nonhemolytic reaction brings fever and chills but no flank pain and no fall in blood pressure. A mild allergic reaction brings hives and itching with stable vital signs. Circulatory overload raises the blood pressure and brings crackles and distended neck veins. Blood glucose is not affected by hemolysis and does not track this reaction. Pupil size and reaction assess the brain, which is not what is threatened here. Deep tendon reflexes are monitored with magnesium sulfate and in preeclampsia, not in a transfusion reaction.

The teaching point

HEMOLYTIC reaction = STOP the blood, SALINE through NEW tubing. Watch the KIDNEYS (urine output and color) and the BLOOD PRESSURE. Send the bag, tubing, blood and urine samples to the lab.