Review for Nephro GI 2024

1. How to calculate corrections for glucose and sodium along with albumin and calcium (refer to the corrections document already on Brightspace) ○ Corrected calcium = 0.8(normal albumin - pt albumin) + serum calcium Lab value Ca = 6.8, Albumin = 1.1 ○ 2.4 ((serum glucose - 100)/(100)) Lab value glucose = 900, Na = 140 2. Understand the difference between Granulomatosis with polyangiitis and Good Pastures. What s/s should the pt have? What tests should be preformed and what is the treatment? ○ Goodpasture disease: autoimmune disease where proteins called Anti-glomerular membrane antibodies deposit on the alveoli and glomeruli Viral illness been show to predispose pt to GP Lab = AntiGBM Treatment = steroids/cyclophosphamide/plasmapheresis ○ Granulomatosis with polyangiitis Triad: inflammation with vasculitis of the upper and lower airway (hemoptysis) with kidney involvement ● Hematuria/RBC cast ● DX= Bx of granuloma shows necrotizing granulomatous vasculitis ● Lab + ANCA ● Treatment = steroids and cyclophosphamide 3. Treatment for Rhado. What prevents the formation of ferrihemate? ○ IV hydration- improves solubility of byproducts of muscle degeneration and improves UOP ○ Ferrihemate Myoglobin is not toxic itself but it becomes toxic when it gets converted to ferrihemate due to the acidic environment of the urine Alkalization of urine- improves solubility of myoglobin which decreases damage to the renal tubules 4. Know the differences between the casts and what disease states have specific casts ○ Hyaline casts- prerenal (FeNa less than 1%) ○ Muddy brown casts- ATN (FeNa greater than 1%, usually greater than 2%) ○ White casts- seen with AIN (Goodpasture's/granulomatosis with polyangiitis) What is the most common location for a nephrolithiasis which could cause hydronephrosis? ○ MC location of stone is ureteropelvic junction ○ Hydronephrosis Usually caused by obstruction of the outflow of urine that results in a build up of urine within the nephron causing dilation -> destruction Can also be due to neurogenic bladder/BPH What electrolyte can show long standing renal disease? ○ Phosphorus What are the different causes of prerenal disease, what would the serum osmolality be? What would the FeNa be? ○ Etiologies: *decreased renal perfusion without cellular injury* Decreased CO/Emboli Renal Artery Intravascular Volume Depletion (albumin vs nss/sepsis/trauma) Impaired renal autoregulation Abd compartment syndrome (intra-abdominal pressure > 20 mmHg) ○ Labs= +/- hyaline casts, urine and serum osmolality is HIGH and FENa less than 1% What is the most common cause of ATN? What would the FeNa be? ○ FENa > 2% ○ Most common cause of ATN is untreated PreRenal Azotemia. If a pt has ATN the nephron is affected. Kidney is not able to retain water. ● If the kidney is not able to retain water then there will be elevated Na in the urine 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. Rhadyomyolysis is an example of what type of AKI (Prerenal/Post renal / intrinsic), What labs would you suspect to see with a pt with this disease? Why dose giving these pts HCO3 help with their renal function? ○ Elevated CK / hyperkalemia / hyperphosphatemia ○ UA: + blood but not erythrocytes ○ Alkalinization of urine improves solubility of myoglobin which decreases damage to the renal tubules Know the difference between: Hypervolemic hyponatremia vs euvolemic hyponatremia vs hypovolemic hyponatremia ○ Hypervolemic hyponatremia: excess fluid (edema), found in cirrhosis/CHF ○ Euvolemic hyponatremia: volume status normal, SIADH/Adrenal insufficiency Addisons ds (hyper K/ hypoNa/ hypoglycemia) ○ Hypovolemic hyponatremia: decreased volume (dehydrated), diarrhea and diuretics, cerebral salt wasting syndrome How to hide and eliminate K? What EKG changes will you see with high K and low K? ○ Hiding Insulin- causes extracellular K to move intracellularly, ensure you give D50 prior to insulin to prevent hypoglycemia Beta Agonist- continuous inhaled albuterol treatment, indirectly activates sodium potassium ATPase on the cellular membrane causing K to enter the cell HCO3- causes intracellular shift if potassium due to changes in H+ ions ○ Eliminating Lasix- helps with the elimination of K via the kidneys Kayexalate- causes K to be eliminated through the GI tract ● Can cause gut perforation, CI for SBO IHD vs CRRT- emergent hemodialysis ○ EKG: peaked T waves/ decreased amplitude or complete loss of the P waves prolonged/increased PR interval/prolongation of the QRS/ AV conduction delays What medications would you give during a code due to hyperK (there is one correct/best answer) ○ CaCl stabilizes the myocardium if the cardiac arrest is due to hyperK, does nothing to serum levels, just competes for binding spots What are Troussau and Chvostek sign. What do these signs indicate? ○ Troussau sign - arm contracts with BP cuff inflation ○ Chvostek sign- face contraction with tapping of facial nerve ○ Both indicate low calcium levels What are the Indications for urgent HD? ○ Acidosis ○ Electrolytes ○ Ingestions, medications that can be dialyzed out ○ Overload with fluid ○ Uremia- this usually refers to uremic pericarditis One of the most common uremic sx is nausea Uremia can also lead to encephalopathy IHD vs CRRT, what are the benefits and draw back for each ○ IHD treatment only last 6hrs less exposure to heparin/anticoagulation products more likely to cause hypotension due to massive volume shifts ○ CRRT – lasts 24hrs used for pts on pressers. Longer exposure to heparin/anticoagulation so the blood doesn’t clot in the machine What is a nonlab value way to assess the Mg++ levels in a pt? ○ DTR, weakness, tetany, and seizures (inverse relationship between Mg and reflexes) What are the indications for Foleys? ○ Close monitoring of I/O in hemodynamically unstable pt ○ Desaturation of ventilated patient if moved ○ Decubital ulcers > 3 ○ Palliative care/ comfort measures ○ Urethral damage from frequent straight caths What is the most common cause of fulminate hepatic failure, what is the treatment for the most common cause? ○ 19. 20. 21. 22. 23. 24. 25. 26. 27. Acetaminophen toxicity -> empiric NAC after 4-6 hrs of ingestion, activated charcoal within 4-6 hrs of ingestion, gastric lavage How do you treat elevated levels of ammonia? ○ Lactulose and Rifaximin ○ Dialysis is considered if blood ammonia levels are significantly elevated, often above 200-500 or if theres an inadequate clinical response to other treatment What could cause elevated BUN levels on a basic metabolic panel besides intravascular depletion/prerenal azotemia, and why? ○ Upper GI bleed -> blood becomes metabolized within the stomach which can cause a rise in the BUN Despite the pt making adequate urine Hepitits B antigen/antibodies- who has an active infx, who is immune, who has been cured? ○ Active infection: HBsAg is present ○ Immune: Anti-HBc ○ Cured: Anti-HBs and Anti-HBc What type of fluid resuscitation should you give for a pt who became hypotensive after a paracentesis and why? ○ 25% albumin admin to prevent refractory hypotension Oncotic osmotic gradients causing volume to stay in the intravascular space longer and bring some of that 3rd spaced fluid back into the intravascular space Upper GI bleed: What is the most common cause? What is the treatment for the most common cause? What should be given if the pt has a hx of portal htn/cirrhosis? If the pt continues to bleed despite the addition of these 2 medications what other intervention can be given and what is a complication if that device is left in for too long or if it is over inflated? ○ MCC- PUD (50%) Start on PPI If recurrent -> concerned about H pylori infection ○ If the patient has a hx of portal HTN/cirrhosis -> concerns about esophageal varices that may be bleeding start on Octreotide caution with NGT placement with these patients due to possibility of worsening bleed ○ Sangstaken-Blakemore or Minnesota Tube Large tube that is inserted into the mouth and terminates in the body of the stomach Balloons are inflated which can tamponade bleeding varices This is only a temporizing measure and should be followed by EGD due to risk of esophageal necrosis ○ EGD Is able to isolate the source of the bleeding and intervene via clamping of esophageal varices or cauterizing bleeding ulcers or the injection of epinephrine Hematemesis vs coffee ground vs melena vs hematochezia vs BRBPR. Understand the differences and what disease they are associated with ○ Lower GI bleeding Hematochezia- when blood mixes with fecal matter, stool turns dark and smears very easily, can be confused if pt took bismuth (+FOBT) BRBPR- distal GIT/hemorrhoids ● ABCD are associated with upper GI bleeds whil E and F are associated with lower GI bleedings ○ Upper GI bleeding Hematemesis- vomiting of blood usually indicates an UGI bleed (above the ligament of Treitz Coffee ground- digested blood (UGIT) Melena- passage of black tarry stools due to the digestion of blood by acid and bacteria, usually from the UGIT but may be 2/2 bleed in the right colon What anatomic location is used to differentiate between upper and lower GI bleeds? ○ Ligament of Treitz What abx and bacteria is associated with recurrent PUD? ○ ABX- Metronidazole (Flagyl)/ clarithromycin ○ H Pylori MELD vs Child-Pugh score are used to calculate the mortality of what disease state? ○ MELD- model for end stage liver disease ○ Child-Pugh score: another scoring system used to predict the severity of liver disease and the need for liver transplant 28. Understand the differences between UC vs Crohns 29. Understand the differences between TF vs TPN and what types of patients would benefit from this type of nutrition ○ TF= tube feeds Used for intubates patients/dysphagia/AMS requires NGT/OGT with confirmed placement Should be started within 48 hrs of being admitted into the ICU (unless CI or have excessive BMI) ● Preserves gut mucosa/villi/IgA GALT ● GI flora/mucosa compromise can lead to migration of bacteria into the portal system increasing risk of MOSF CI when elevated pressor requirements/discontinuous GIT/obstruction/ischemia ● Start TPN instead if nutrition is needed 30. Besides elevated abdominal pressures (>20mmHg), what must a pt have in order to be dx with abdominal compartment syndrome? ○ Signs of end organs not being adequately perfused Decreased UOP with elevations in the Crt/BUN Lactic acidosis Distended firm abd. Lack of BMs Increased airway pressures/decreased VT ○ Renal disease- evident with elevated Crt/BUN and or decreased UOP (less than 0.5) 31. What are the most common causes of acute pancreatitis? ○ MCC = EtOH and gallstones 32. What disease is associated with Charcot’s triad and Reynolds pentad, and what are in each ○ Both are associated with acute cholangitis: acute inflammation and infection in the bile duct ○ Charcot’s triad Right upper quadrant pain/ jaundice/fever ○ Reynolds Pentad Charcot’s + hypotension and confusion 33. What are the risk factors for refeeding syndrome? If you were to feed these pts with a high caloric diet, what labs would you expect to see? How do you precent refeeding syndrome? ○ Anorexic, elderly, EtOH abuse and long standing hx of vomiting ○ Hypocalcemia, hypophosphatemia, hypokalemia, hypoalbuminemia ○ When carbs are introduced in a malnourished pt, there is a lyte shift that causes PO4, K, Ca to shift intracellularly, this can cause diaphragmatic problems (respiratory failure) ○ Tx: Controlled increase in caloric intake Starting at ½ of caloric needs and increasing steadily over a period of days Replacement of lyte abnormalities 34. What can be given to pts with hypertriglyceridemia to increase the synthesis of hydrolysis of triglycerides? Why should these pts be given anticoagulation? ○ IV insulin therapy add D5 gtt if hypoglycemic Insulin promotes the synthesis of lipoprotein lipase which also helps with the hydrolysis of TG into fatty acids and facilitates the storage of the fatty acids into adipocytes 35. What beta blocker should be given to pts with recurrent upper GI bleeds that are hemodynamically stable? ○ Propranolol 36. Know the different types of TBI SAH,SDH,EDH. If a vein or artery is affected and what they look like on CT head ○ SAH- trauma is the MCC Headache that is usually described as sudden and abrupt, thunderclap headache ○ SDH- bleeding that results from tears in the bridging veins, can cross sutural margins, can be secondary to infection or from traumatic event S/S = LOC, irritability, seizures, pain, numbness, HA, dizziness, nausea and vomiting ● Gets worse as bleeding worsens AMS gradually increases ○ EDH- arterial bleed associated with traumatic event Bleeding between skull and inner meningeal layer of the dura mater Does not cross sutural margins but does cross dural attachments S/S = AMS, HA, vomiting, confusion, hemiparesis some pts with acute EDH have transient LOC have lucid interval with recovery of consciousness followed by deteriorate due to hematoma enlargement 37. How do you decrease ICP ○ Hypertonic Na- takes longer time to get to goal Na 150, isn’t affected by volume status, when compared to mannitol ○ Mannitol- rapid onset but should avoid with pts who are hypotensive, hypovolemic No M&M benefit between Mannitol vs hypertonic Na ○ Hyperventilation- low CO2 levels causes cerebral vasoconstriction which can result in cerebral ischemia after prolonged periods of time and should only be used for the first 6 hrs Goal less than 25 PaCO2 ○ Position- pts should have the HOB at least 30 degrees, which improves venous returns ○ IVD vs Crani