AG-ACNP - Barkley Review Questions and Answers

AG-ACNP - Barkley Review Questions and Answers Hyperkalemia S/S weakness, flaccid paralysis Abdominal distention diarrhea Tall peaked waves on ECG Management of Hyperkalemia Kayexalate if 6.5 or cardiac toxicity or muscle paralysis is present, consider: Insulin 10U with one amp D50 (pushes K into cell) What are normal calcium levels? Normal total calcium: 8.5-10.5; normal ionized calcium: 4.5-5.5 Does albumin effect calcium levels? Albumin affects calcium level by binding to it Does albumin effect ionized calcium levels? Ionized calcium does not vary with the albumin level What maintains calcium levels in the body? Vitamin D, parathyroid hormone and calcitonin What is the relationship of albumin to calcium? Calcium is ~50% to albumin If calcium is normal and albumin is low, then calcium is high. S/S of hypocalcemia increased DTRs, muscle abdominal cramps, carpopedal spasm (trousseau's sign)convulsions, Chvostek's sign (cheek twitch), and prolonged QT interval Management of hypocalcemia Check pH for alkalosis, if acute give IV calcium gluconate, if chronic give oral supplements, vitamin d, and aluminum hydroxide Acidemia _____ Ionized calcium increases Alkalemia _____ ionized calcium decreases Hypercalcemia causes Causes: hyperparathyroidism, hyperthyroidism, Vitamin D intoxication, prolonged immobilization, thiazide diuretics S/S of hypercalcemia Fatiguability, muscle weakness, depression, anorexia, n/v, constipation, severe hypercalcemia can cause coma or death. Serum Ca 12 is considered medical emergency Management of hypercalcemia Calcitonin if impaired cardiovascular or renal fx, dialysis, if 12 begin NS and loop diuretics. Respiratory acidosis pH and pCO2 levels pH 7.35 with pCO2 45 Causes of respiratory acidosis Decreased alveolar ventilation What happens in acute respiratory acidosis? In acute respiratory failure, there is a sharp rise in pCO2 with only a small increase in plasma HCO3 What happens in 6-12 hours after acute respiratory failure in terms of respiratory acidosis? After 6-12 hours, the increase in pCO2 will evoke the renal compensatory mechanism (this takes several days to manifest) S/S of respiratory acidosis Somnolence and confusion Myoclonus with asterixis increased cerebral blood flow causes increased CSF pressure causing increase ICP Lab/diagnostics of respiratory acidosis Low arterial pH PCO2 45 Serum HCO 26 Low serum chloride (93) in chronic patients Management of respiratory acidosis Narcan 0.4-2mg Improve ventilation, intubate if necessary Increase vent rate Respiratory alkalosis causes Hyperventilation decreases arterial PCO2 and increases pH; clinical symptoms are related to decreased cerebral blood flow S/S of respiratory alkalosis Light headedness, anxiety, paraesthesia, stocking/glove tingling, tetany if very severe Labs/diagnostics of respiratory alkalosis Increased pH 7.45 Low PCO2 35 Serum HCO3 low if chronic Management of respiratory alkalosis management Manage underlying cause If acute hyperventilation, have patient breath into paper bag Decrease rate of vent Sedation may be necessary Rapid correction of chronic alkalosis may result in metabolic acidosis Metabolic acidosis hallmark sign Hallmark sign is a low serum HCO3 What is a normal anion gap? What does an increased anion gap indicate?What does an increased anion gap indicate? Normal: 7 to 17 (12 - or +5 either way) If gap is increased the clinical situation is generally more acute Causes of increased anion gap When is it expected to have an anion gap? DKA, alcoholic ketoacidosis, lactic acidosis, drug or chemical anion Diarrhea, ileostomy, renal tubular acidosis, recovery from DKA What is the treatment for an increased anion gap? Treat underlying disorder, fluid resuscitation HCO3 not indicated if acidosis is due to hypoxia or DKA HCO3 is indicated if significant hyperkalemia is present Normal gap treatment for chronic conditions Common with chronic conditions like renal failure Bicitra 10-30 cc with meals and h.s. Metabolic Acidosis with normal gap causes "Hard ASS" Hyperalimentation Addisons Renal tubular necrosis Diarrhea Acetazolamine Spironolactone Metabolic Acidosis with wide gap causes "MUD PILES" Methanol Uremia (kidney failure) DKA Propylene glycol IRON/INH Lactic Acidosis/lack of O2 Ethylene glycol (oxalic acid) Salicylates (late response) How is HCO3 affected in metabolic alkalosis? pCO2? High plasma HCO3 and compensatory pCO2 rarely exceeds 55mmHg (If PCO2 is 55, superimposed resp. acidosis is likely) Causes of metabolic alkalosis post-hypercapnia alkalosis NG suctioning Vomiting Diuretics Saline responsive (volume contraction)-most common Management of saline responsive alkalosis Correct volume deficit with NaCl and KCL D/C diuretics H2 blockers in pts with GI loss Acetazolamide 250-500mg IV q4-6hr if volume Replacement is contraindicated S/S of metabolic alkalosis None normally Weakness and hyporeflexia may be present if K is very low Lab/diagnostics of metabolic alkalosis Arterial pH 7.45 Arterial HCO3 26 Arterial pCO2 45 and 55 Serum K and Cl --decreased May see increased anion gap R-O-M-E Respiratory Opposite, Metabolic Equal Resp: pH and CO2 are opposite Metabolic: pH and CO2 are equal (moving in same direction) First Degree Burns Dry, red, no blisters, involves epidermis only Second degree (partial thickness) Moist, blisters, extends beyond epidermis Third degree (full thickness) Dry leathery, black, pearly, waxy, extends beyond epidermis to dermis to underlying tissues, fat, muscle and/or bone Rule of nines Each Arm=9 Each Leg=18 Thorax= 18 front and 18 back Head=9% Perineum/genitals=1 Fluid resuscitation for Burns: Parkland Formula 4ml/kg X TBSA in the first 24 hours 1/2 of all fluid should be given in the first 8 hours the remaining fluid given over the next 16 hours. ALL NS or LR **Fluid resuscitation begins at time of burn injury Monitor what electrolyte during fluid resuscitation for burns? Monitor for hyperkalemia during the first 24-48 hours then monitor for hypokalemia following fluid resuscitation/diuresis around 3 days post burn Indication for prophylactic intubation post burn Burns to the face Singed nares or eyebrows Dark soot/mucous from nares and/or mouth Emergent management of burns Submerge injured area in clean water as soon as possible Wrap area in clean wet towel and transport Sterile NS in initial treatment Affected areas wrapped with sterile towels Maintain normal temp IV fentanyl and/or morphine Silver Sulfadiazine- used to treat second and third degree burns Tar burn treatment Use petroleum based product to remove the burning tar Which wounds should be left open? wounds of hands or lower extremities or any wound older than 6 hours Abx given for what type of bite Human and animal bites, give 3-7 day course of p.o prophylactic abx for coverage of both staph and anaerobes (Augmentin) Most common causes of cellulitis - inpatient and outpatient Outpatients: Strep pyogenes (Gp A Strep) --Usual cause S aureus--less common Inpatients: Gram negative organisms (E Coli, Klebisiella, Pseudomonas, Enterobacter), S. Aureus (MRSA, CA-MRSA), Strep Meds for CA-MRSA cellulitis Trimethoprim-Sulfamethoxazole (Bactrim) Doxy/minocycline Clindamycin Meds for Group A strep cellulitis Trimethoprim-Sulfamethoxazole+ beta lactam Doxy/minocycline+ beta lactam Clindamycin S/S of acetaminophen intoxication asymptomatic in early phase around 24-48 hours, nausea and vomiting will occur right upper quad pain signs of hepatotoxicity: Jaundice, elevated LFTs, prolonged PT, altered mental status, delirium Management of acetaminophen Emesis for recent ingestions; gastric lavage/activated charcoal N-Acetylcysteine (mucomyst) with loading dose p.o should be ordered as needed S/S of Salicylate intoxication Nausea, vomiting, tinnitis, dizziness, h/a, dehydration, hyperthermia, apnea, cynaosis, metabolic acidosis, elevated LFTs Normal LFT 35-40 Management of salicylate intoxication emesis for recent ingestions; gastric lavage/activated charcoal sodium bicarbonate IV to correct sever acidosis 7.1 Oranophosphate poisoning insecticide poisoning S/S of insecticide poisoning N/V, cramping, diarrhea, excessive salivation, H/A, blurred vision and miosis (constricted pupils), bradycardia, mental confusion, slurred speech, coma Management of insecticide poisoning Wash skin activated charcoal atropine-drug of choice for insecticide poisoning Mydraisis dilated pupils Myosis constricted pupils / notice o in both! S/S of antidepressant toxicity confusion, hallucinations, blurred vision, urinary retention hypotension, tachycardia, dysrhythmias, hypothermia, seizures Management of antidepressant toxicity Admit to ICU if CNS or cardiac toxicity Gastric lavage/activated charcoal Benzodiazepine IV to control seizures Sodium bicarb IV to counter dysrhythmias and maintain pH Management of serotonin syndrome Treated with dantroline (Dantrium); clonazepam used to treat rigor; cooling blankets to control temperature Narcotic Toxicity can be caused by Codeine, Heroin, Morphine, and Opium S/S of narcotic Toxicity Drowsiness, hypothermia, respiratory depression, shallow respirations, mitosis (pinpoint pupils), coma Note: cocaine causes mydriasis Management of narcotic toxicity emetics are contraindicated Gastric lavage/activated charcoal Narcan Stadol Benzodiazepine OD drugs Diazepam, clonazepam, lorazepam S/S of Benzodiazepine OD drowsiness, confusion, slurred speech, respiratory depression, hyporeflexia Management of Benzodiazepine OD Respiratory and blood pressure support, romazicon IV, gastric lavage/activated charcoal Organ transplant considerations Acute rejection flu like s/s suggest immediate failure of the organ immediate biopsy indicated Organ transplant anti-rejection agents what do they do lower circulating lyphoid cells that are critical to rejection response Transplant rejection drug combos calcineurin inhibitor+ antimetabolite+steriod CI=tacrolimus or cyclosporine Antimetabolite=Azathioprine, or Mycophenolate (cellcept) Steroid=deltazone,prednasone,orazone,Metocorten Herpes Zoster (Shingles) define Vesicular eruption due to infection with varicella-zoster wires; maybe life-threatening in immunocompromised adults S/S of Herpes Zoster Pain along a dermatomal distribution, usual on the trunk grouped vesicle eruption of erythema and exudate along the dermatomal pathway Regional lymphadenopathy may be present Management of Herpes Zoster Treatment: Acyclovir, famciclovir, valaciclovir If suspected ocular involvement, immediate referral to ophthalmologist Post herpetic neuralgia: Gabapentin and pregabalin Zostavax @ 50 Actinic Keratoses define, treatment Small patches on sun exposed parts of body Premalignant Asymptomatic Rough, flesh colored, pink or hyper pigmented Treatment: liquid nitrogen Squamous Cell Carcinoma come from what? Treatment? Arise out of actinic keratoses firm, irregular papule or nodule Develop over a few months; 3-7% metastasis Prolonged, sun-exposed areas in fair skin people Keratotic, scaly bleeding Treatment: Biopsy and surgical excision Seborrheic Keratoses define? Treatment? Benign non painful lesions Beige, brown or black plaques "stuck on" appearance 3-20mm in diameter Treatment: None or liquid nitrogen Basal Cell Carcinoma define? Treatment? Most Common Slow Growing Waxy, pearly appearance (may be shiny red) Central depression or rolled edge May have telangiectatic vessels Treatment: Shave/punch biopsy & surgical excision Malignant Melanoma? Define? Treatment? Mortality rate highest of all skin cancers Median age at diagnosis = 40 May metastasize to any organ Treatment: Biopsy and surgical excision ABCDEE of melanoma A: asymmetry B: border irregularity C: Color variation D: diameter 6mm E: elevation E: enlargement 2 or more of ABCDEE = 90% sensitivity End of life considerations brain death criteria Rewarmed, absent crainial reflexes Terminal extubation considerations morphine for tachypnea and resp distress, scopolomine for secretions Diabetes (Type I) Most common in adolescents by may occur in adulthood strongly associated with human leukocyte antigens Islet cell antibodies found in approximately 90% of patients within 1st year of diagnosis Ketone development usually occurs S/S of Type I Diabetes Polyuria, Polydipsia, Polyphagia, nocturnal enuresis, weight loss, weakenss/fatigue Lab/Diagnostics of Type I DM Random plasma glucose 200 Serium fasting blood sugar 126 on 2 separate occasions ketonemia or ketonuria or both HgbA1c (Normal)= 5.5-7 6=good Impaired glucose tolerance FBG 100 & 125 Management of Type I DM If Ketones present: Insulin therapy is warranted. General rule: begin with 0.5 u/kg/day giving 2/3 of the dose in the AM and 1/3 of the does in the evening Diabetes Mellitus (type 2) Most common type; 90% diabetes in the US Circulating insulin exists enough to prevent ketoacidosis Caused by either tissue insensitivity to insulin or an insulin secretory defect resulting in resistance and/or impaired insulin production Metabolic Syndrome Waste Circumference: 40 inches in men and 35 inches in women BP: 130/85--only need one number Triglycerides 150 FBG 100 HDL: 40 in men and 50 in women abnormal lipids ANY 3=Metabolic syndrome S/S of Type 2 DM May be asymptomatic, polyuria, polydipsia, recurrent vaginitis in women, blurred vision, peripheral neuropathies, Statins can cause Type II DM Lab/Diagnostic for type 2 diabetes Same for type I except no ketones in blood or urine Management of type 2 DM Oral Antidiabetics (5 classes) Sulfonylureas what do they do? Examples? Most widely prescribed; stimulate the pancreas to release more insulin -2nd generation: glipizide, glyburide, glimepiride Biguanides what are they? Side effects? Good adjunct to sulfonylureas by can be used alone, especially for obese patients Metformin: Standard of care upon the diagnosis of DM type 2 Lactic acidosis is a potential side effect Alpha-glucosidase inhibitors how do they work? less glucose is absorbed by the gut Acarbose and miglitol Thiazolidinediones "glitazones" MOA Decrease gluconeogenesis Rosiglitazone maleate (Avandia) (Increase MI and HF) Pioglitazone hydrochloride (Actos) (increase bladder CA)