AGACNP Barkely Review 2026 Questions and Answers

AGACNP Barkely Review 2026 Questions and Answers Nutrition Laboratory measurements: 1. Albumin levels of 3.5 indicate protein malnutrition, edema can be expected if the albumin level is 2.7 2. Magnesium 1.7- 2.2 3. Hemoglobin 12 for women and 13.5 for men can indicate lack of iron or protein resulting in inadequate oxygen perfusion 4. Clinical observations should be used to support laboratory data ie: hair not easily plucked, musculature, clear nail beds free of ridges, pink moist mucous membranes Determining the type of nutritional support: 1. Can I use the GI tract: yes + supplements for 6 weeks= enterostomal tube 2. Can I use the GI tract: yes + supplements 6 weeks = nasoenteric tube · At risk for aspiration: yes = duodenal tube · At risk for aspiration: no = NG tube 3. Can I use the GI tract: no = parenteral nutrition need support for 2 weeks: yes = central vein 4. Can I use the GI tract: no = parenteral nutrition need support 2 weeks = peripheral vein Complications of ENTERAL nutrition support: 1. Aspiration 2. Diarrhea 3. Emesis 4. GI bleeding 5. Mechanical obstruction of the tube 6. Hypernatremia 7. Dehydration 8. Refeeding syndrome: hypophosphatemia, hypokalemia, hypomagnesemia, hypocalcemia, thiamine deficiency Complications of PARENTERAL nutritional support (may occur in up to 50% of patients) 1. Pneumothorax/hemothorax 2. Arterial laceration 3. Air emboli 4. Catheter thrombosis 5. Catheter sepsis 6. Hyperglycemia/ HHNK Hyponatremia the most common electrolyte abnormality. There are multiple causes and the 1st step in treating is determining the cause. Eval should include: 1. Urine sodium: normal 10-20 mEq 2. Serum osmolality: usually 2 x Na 3. Clinical status o Measuring urine sodium helps distinguish renal from non-renal causes o For example: urine sodium 20 suggest renal salt wasting (ie a problem w/ the kidneys), urine sodium 10 suggest renal retention of Na to compensate for extrarenal fluid losses (ie problem other than the kidneys) Isotonic hyponatremia/pseudohyponatremia serum osmo 284-295, a laboratory artifact: 1. Occurs w/ extreme hyperlipidemia or hyperproteinemia 2. Body water is normal, and the patients are asymptomatic 3. Treatment: cut down fat (ie no fluid restrictions) Hypotonic hyponatremia serum osmo 280, state of body water excess diluting all body fluids, clnical s/s arise from water excess 1. Need to assess if the patient is hypovolemia or hypervolemic 2. If hypovolemia assess whether hyponatremia is d/t extrarenal salt losses or renal salt wasting § Hypovolemic w/ urine Na 10: d/t dehydration, diarrhea, vomiting § Hypovolemia w/ urine Na 20: low volume and kidneys cannot conserve Na: d/t diuretics, ACE-I, mineralocorticoid deficiency § Hypovolemic hypotonic hyponatremia: NEED TO RESTRICT WATER: d/t edematous states, CHF, liver disease, advanced renal failure Hypertonic hyponatremia serum osmo 290: d/t hyperglycemia (usually HHNK), osmo high and Na is low Management of hyponatremia: 1. Treatment based on cause, treat underlying condition 2. If hypovolemic give NS IV 3. If urine sodium 20, treat the cause 4. If hypervolemic, implement water restriction 5. If the patient is symptomatic, give NS IV with a loop diuretic 6. If CNS s/s present consider 3% NS IV with loop diuretic Hypernatremia usually d/t excess water loss, always indicated hyperosmolality (ie deficiency of water). Excessive Na intake is rare o Management: 1. Severe hypernatremia w/ hypovolemia should be treated w/ NS IV followed by ½ NS 2. Hypernatremia w/ euvolemia should be treat w/ free water (D5W) 3. Hypernatremia w/ hypervolemia should be treated w/ free water and loop diuretics, may need dialysis Hypokalemia causes include chronic use of diuretics, GI loss, excess renal loss and alkalosis. Elevated serum epinephrine in trauma pts may contribute to low K o s/s: 1. muscular weakness, fatigue, and muscle cramps 2. constipation or ileus d/t smooth muscle involvement 3. if severe (ie 2.5) may see flaccid paralysis, tetany, hyporeflexia, and rhabdomyolysis o Laboratory/Diagnostic: 1. Decreased amplitude on EKG 2. Broad T waves 3. Prominent U waves 4. PVCs, v-tach, or v-fib o Management: 1. Oral replacement if 2.5 and no EKG abnormalities 2. If 2.5 or severe s/s are present may give 40 mEq/hr IV- check every 3 hrs and institute continuous EKG monitoring 3. **Mg deficiency frequently impairs K correction Hyperkalemia causes include excess intake, renal failure, drugs (ie NSAIDs), hypoaldosteronism, and cell death. Shifts of intracellular K to the extracellular space occur w/ acidosis. K increases 0.7 with each 0.1 drop in pH. o s/s: 1. weakness, flaccid paralysis 2. abdominal distention 3. diarrhea o Laboratory/Diagnosis: 1. EKG no particularly sensitive- 50% of pt with K 6.5 will not have EKG changes, however Tall peaked T waves are a classic finding o Management: 1. Exchange resins (ie kayexalate) 2. If 6.5 or cardiac toxicity or muscle paralysis is present, consider insulin 10 u with one-amp D50 (pushes K into cell) Hypocalcemia causes include hypoparathyroidism, hypomagnesemia, pancreatitis, renal failure, severe trauma, and multiple blood transfusions, among others o s/s: 1. increased DTRs 2. muscle/abdominal cramps 3. carpopedal spasms (Trousseau's sign) 4. Convulsions 5. Chvostek's sign: contraction of facial muscles provoked by lightly tapping over the facial nerve anterior to the ear as it crosses the zygomatic arch 6. Prolonged QT interval o Management: 1. Check blood pH- look for alkalosis 2. If acute, IV calcium gluconate 3. If chronic, oral supplements, vitamin D, aluminum hydroxide Hypercalcemia causes include hyperparathyroidism, hyperthyroidism, vitamin D intoxication, prolonged immobilization. Rarely thiazide diuretics will promote ^Ca o s/s: 1. fatiguability 2. muscle weakness 3. depression 4. anorexia 5. n/v 6. constipation 7. severe hypercalcemia can cause coma and death o Management: 1. May need calcitonin if impaired cardiovascular or renal function 2. May need NS with loop diuretics 3. Dialysis in severe cases STD treatments Cuties (Chlamydia) All (Azithromycin) Get (Gonorrhea) Cooties (Ceftriaxone) To (Trichomoniasis) F@ck (Flagyl) Suck (Syphilis) & Play (Penicillin) Mean corpuscular volume (MCV) expression of the average volume and size of RBC (erythrocyte) · Microcytic 80: Ddx = iron deficiency anemia and thalassemia · Normocytic 80-100: Ddx= anemia of chronic disease, sickle cell disease, renal failure, blood loss, hemolysis Macrocytic. 100: Ddx=B12 or folate deficiency, alcoholism, liver failure, and drug effects Iron deficiency anemia microcytic, hypochromic anemia d/t an overall deficiency of iron o Incidence/cause: 1. Most common cause of anemia 2. Iron loss exceeds intake so that storage is depleted decrease in iron available for RBC formation 3. Caused by: blood loss, inadequate iron intake, impaired absorption of iron o s/s: 1. usually slow in onset, few s/s with Hct 30 2. as the HCT falls will see: a. pica: unusual food cravings such as ice, clay, etc b. dyspnea and mild fatigue w/ exercise c. headache d. palpitations e. weakness f. tachycardia g. postural hypotension h. pallor o Lab/Diagnostics: 1. low: hgb, hct, MCV (microcytic), MCHC (hypochromic), RBC, serum iron, serum ferritin 2. HIGH: TIBC, RDW (red cell distribution width) o Management: 1. Oral ferrous sulfate 300-325mg 1-2 hrs after meals 2. Iron should not be taken w/ antacids as they interfere with absorption 3. Taking iron w/ vitamin C containing juice increases absorption 4. Foods high in iron: raisons, green leafy vegetables, red meats, citrus products, and iron fortified bread and cereals Thalassemia genetically inherited disorders resulting in abnormal Hgb production and microcytic, hypochromic anemia o Incidence: found mainly in Mediterranean, African, Middle Eastern, Indian and Asian populations o s/s: 1. general physical findings unremarkable unless the form of thalassemia is severe 2. Beta thalassemia: most familiar type of thalassemia · Etiology: decreased production of normal adult Hgb (HbA). The globin part of HbA has 4 protein sections called polypeptide chains. 2 chains are identical alpha chains and 2 chains are identical beta chains. In pts with beta thalassemia, there is reduced or absent production of beta globin chains o Presentation: 2 forms of beta thalassemia: § Thalassemia Minor: · have only 1 copy of the beta thalassemia gene, together w/normal beta chain gene: heterozygous for beta thalassemia · have only mild anemia: may mimic iron-deficiency anemia § Thalassemia Major: Cooley's anemia · Have 2 genes for beta thalassemia and no normal beta-chain gene: homozygous, causes deficiency in production of beta chain and HgA · Normal presentation at birth d/t protective effects of fetal Hgb · Anemia develops within first few months of life and becomes progressively severe · Other findings in early life: failure to thrive, feeding difficulties (d/t easy fatigue, lack of O2), bouts of fever, diarrhea, hepatosplenomegaly and jaundice, maxillary enlargement o Labs/diagnostics: 1. Low hgb, MCV, MCHC, decreased alpha or beta hgb chains 2. Normal TIBC and ferritin o Management: 1. No treatment for mild to moderate forms 2. RBC transfusion/splenectomy for more severe forms 3. Iron is CONTRAINDICATED as iron overload can result 4. Prenatal genetic testing of parents if desired Folic acid deficiency a macrocytic, normochromic anemia d/t folic acid deficiency o Causes: inadequate intake/malabsorption of folic acid (needed for RBC production) o s/s: *No neurological s/s are seen which differentials B12 from folic acid deficiency* 1. fatigue 2. dyspnea on exertion 3. pallor 4. headache 5. tachycardia 6. anorexia 7. glossitis: inflammation, causes the tongue to swell in size, change in color, and develop a different appearance on the surface o Labs/diagnostics: 1. Low hct, RBC, serum folate, RBC folate 100 2. High MCV 3. Normal MCHC (normochromic) o Management: 1. Folate 1mg orally every day 2. Food high in folic acid: bananas, peanut butter, fish, green leafy vegetables, iron-fortified breads and cereals Pernicious anemia a macrocytic, normochromic anemia d/t deficiency of intrinsic factor while results in malabsorption of B12 o s/s: Neuro 1. weakness 2. glossitis 3. palpitations 4. dizziness 5. anorexia 6. paresthesia 7. loss of vibratory sense 8. loss of fine motor control 9. + Romberg, + Babinski o Labs/diagnostics: 1. Low hgb, hct, RBC, serum B12 (200) 2. High MCV 3. Anti-IF (intrinsic factor) and antiparietal cell antibody test o Management: 1. B12 (cyanocobalamin) 100 mcg IM daily x 1 week 2. Maintenance treatment requires continuous lifelong monthly administration Sickle cell anemia chronic hemolytic anemia that is genetically transmitted characterized by sickle shaped RBCs o General concepts: 1. An acute, periodic exacerbation in which RBCs become sickle-shaped and cause vessel obstruction 2. Cellular hypoxia results in acidosis and tissue ischemia 3. Pain occurs from tissue ischemia and blood hyper viscosity 4. Factors which precipitate sickling include hypoxia, infections, high altitudes, dehydration, physical/emotional stress, surgery, blood loss, acidosis o s/s: 1. signs of disease develop in infancy or childhood 2. delayed growth and development, increased susceptibility to infections are common 3. in crisis, patients experience: · sudden onset of severe pain in extremities, back, chest, and abdomen, aching joint pain, weakness, dyspnea o Labs/diagnostics: 1. Low hgb 2. Peripheral smear shows classic distorted sickle-shaped RBC o Management: 1. Treat both acute and chronic complications of the disease 2. Acute: fluids for dehydration, analgesics for pain, and oxygen or hypoxemia Von Willebrand disease genetic disorder reduced ability to create blood clots, d/t mutation/deficiency in von Willebrand factor and clotting factor VIII o s/s: 1. frequent, prolonged, or severe episodes of bleeding 2. easy bruising o Management: 1. Desmopressin, recombinant vWF, vWF/factor VIII concentrate Leukemias neoplasms arising from hematopoietic cells in the bone marrow o Cause/incidence: often no direct cause can be found, more frequent in males o Classifications: 1. Acute myelogenous leukemia (AML): · Constitutes 80% of acute leukemia in adults · Remission rates from 50-85% · Long term survival ~ 40% 2. Acute lymphocytic leukemia (ALL): · More difficult to cure in adults than children, 90% remission rate in children · Pancytopenia (deficiency of all three cellular components of the blood RBC, WBC, platelets) with circulating blasts (hallmark of disease) 3. Chronic lymphocytic leukemia (CLL): · Most common leukemia in adults, occurs in both middle and old age, median survival is 10 years · Lymphocytosis (^WBC) (hallmark of disease) 4. Chronic myelogenous leukemia (CML): · Occurs most often in pt aged 40 and older, survival ~65% of those dx are still alive at 5 years · Philadelphia chromosome seen in leukemic cells - hallmark of disease Leukemias: s/s, labs, management o s/s: 1. may be asymptomatic 2. fatigue 3. weakness 4. anorexia 5. generalized lymphadenopathy 6. weight loss o labs/diagnostics: 1. CBC w/ subnormal RBCs and neutrophils 2. Elevated ESR 3. Peripheral blood smear usually distinguishes acute and chronic leukemia but a bone marrow aspiration is required to confirm the dx o Management: 1. Chemotherapy: initiate allopurinol to reduce tumor lysis syndrome in high risk patients 2. Bone marrow transplantation 3. Control of symptoms Lymphomas lymphoctic malignancy o Diagnosis/staging: 1. Diagnosed by biopsy of enlarged lymph nodes 2. Staging: · Stage 1: disease localized to single lymph node or group · Stage 2: more than 1 lymph node group involved, confined to one side of the diaphragm · Stage 3: lymph nodes or the spleen involved, occurs on both sides of the diaphragm · Stage 4: liver or bone marrow involvement o Types: 1. Non-Hodgkin's lymphoma: · Cause is unknown, may have viral etiology · Often presents with lymphadenopathy · Most common neoplasm between ages 20-40 · Less predictable pattern of spread than Hodgkin's disease · Advanced stage disease is usually apparent 2. Hodgkin's disease: · Cause is unknown · More common in males, average age is 32 · Usually presents with cervical adenopathy and spreads in a predictable fashion along lymph node groups · Characteristic Reed-Sternberg cells differentiate from non-Hodgkin's disease o Labs/diagnostics: 1. CT, xrays, US, MRI used to locate and stage the disease 2. Biopsy and histopathologic exam confirm diagnosis o Management: 1. Radiation 2. Chemotherapy 3. Bone marrow transplantation Idiopathic thrombocytopenia purpura (ITP) thrombocytopenia resulting from autoimmune destruction of platelets w/ or w/o suppression of thrombopoiesis o General concepts/incidence: 1. In adults ITP is usually chronic, causing mild to severe thrombocytopenia that may be asymptomatic for long intervals 2. Only occasionally do patient with ITP develop bleeding that requires hospitalization 3. Women outnumber men in incidence by a ratio of 3:1 o Labs/diagnostics: 1. Bone marrow analysis 2. Low platelet count w/ other causes of thrombocytopenia ruled out, there may be a history of easy bruising or bleeding o Management: 1. May not be necessary until the platelet count is 20,000 2. High dose corticosteroids may help to elevate the platelet count within 2-3 days 3. IV gamma globulin usually produces a response within 2-3 days 4. Gamma globulin is preferred to steroids in HIV- related ITP 5. Platelet transfusion may occasionally benefit o Other considerations: 1. Thrombocytopenic precautions · Avoid constipation: increase fiber, laxatives, etc · No flossing · No shaving · Hold pressure for 5 min or more for cuts, line insertion etc 2. Heparin-induced thrombocytopenia purpura (HIT) · Argatroban · Lepirudin (Refludan) 3. How to differentiate ITP from SLE: these both have thrombocytopenia Disseminated intravascular coagulation (DIC) an acquired coagulation disorder which results from the intravascular activation of both the coagulation and fibrinolytic systems (thrombin and plasmin are activated) causing simultaneous thrombosis and hemorrhage. Mortality rate is 50-85% o Associated conditions: malignant neoplasms, infections/sepsis, liver disease, massive trauma, extensive burns, shock, obstetrical complications, acute leukemia o Pathophysiology: 1. Thrombin causes conversion of fibrinogen to fibrin, producing fibrin clots in the microcirculation 2. Coagulation factors (ie fibrinogen, prothrombin, platelets, factors V and VIII) are thus reduced 3. Circulating plasmin activates the fibrinolytic system which lyses fibrin clots into fibrin degradation products (FDPs) 4. Hemorrhage results from the anticoagulant activity of FDPs and the depletion of coagulation factors o s/s: 1. DIC varies greatly in clinical severity (bleeding vs thrombosis) 2. Patients presenting in acute DIC demonstrate profound disturbances in hemostasis with ecchymosis, oozing from venipuncture sites, and petechiae to mucous. Membranes o Labs/diagnostics: 1. Thrombocytopenia: platelets 150,000 2. Hypofibrinogenemia: fibrinogen 170 3. Decreased RBCs 4. Increased fibrin degradation products (FDPs) 45 or present at 1:100 dilution 5. Prolonged PT 19 seconds 6. Prolonged PTT 42 seconds 7. D-dimer + at 1.8 dilution, reflects simultaneous activation of thrombin and plasmin · With increased FDPs, gives a predictive accuracy of 96% for diagnosing DIC o Management: 1. Goal: treat the underlying condition and control bleeding 2. Platelet transfusion (for thrombocytopenia), FFP (to replace clotting factors) and cryoprecipitate (to maintain fibrinogen levels) are given if bleeding is severe 3. The use of heparin to decrease thrombin generation remains controversial 4. Overall, therapy i Transplant considerations 1. All patients are immunosuppressed pre-transplant (consider risk of infection) 2. Acute rejection of an organ: a. Immediate failure of that organ b. Flu-like symptoms: fever, chills, malaise, etc c. Immediate biopsy of the transplanted organ is usually warranted as soon as possible 3. Most effective anti-rejection regimens involve triple therapy (3 immunosuppressants from different classes) a. Patients take a 1. Corticosteroid + 2. Antimetabolite and 3. either a calcineurin inhibitor or a mammalian target of rapamycin (mTOR) inhibitor b. Agent examples: i. Steroids: methylprednisolone or prednisone ii. Antimetabolites: antiproliferative agents, maintenance immunosuppressants: Imuran or Cellcept or Myfortic or Cytoxan iii. Calcineurin inhibitors: Tacrolimus (Prograf) or Gengraf/Neoral iv. Mammalian target of rapamycin (mTOR) inhibitor: Sirolimus, Torisel, Afinitor Infectious skin disorders § General approach to managing infections: P-S-S-P 1. Establish PRESENCE of infection: s/s: ^WBC, fever, infiltrates on CXR, erythema, pus, secretions 2. Establish SEVERITY of infection: age of patient, immune status, comorbidities 3. Establish SITE of infection: respiratory, skin, blood, IV line, urine 4. Establish likely PATHOGEN: based on anatomical site and/or patient factors Pressure ulcers any lesion caused by unrelieved external pressure resulting in occlusion of blood flow, tissues ischemia, and cell death. Staging pressure injuries: 1. Stage 1 pressure injury: intact skin with erythema that does not blanch; color changes do not include purple or maroon discoloration 2. Stage 2 pressure injury: partial thickness loss of skin with exposed dermis; wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum- filled blister; adipose and deeper tissues are not visible; should not be used to describe moisture associated skin damage (MASD) including incontinence associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive related skin injury (MARSI), or traumatic wounds (skin tears, burns, abrasions) 3. Stage 3 pressure injury: full-thickness skin loss; adipose is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present; slough and/or eschar may be visible, if slough or eschar obscures the extent of tissue loss = unstageable pressure injury 4. Stage 4 pressure injury: full-thickness skin and tissue loss; with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone in the ulcer; slough and/or eschar may be visible; epibole (rolled edges), undermining and/or tunneling often occur, if slough or eschar obscures the extent of tissue loss= unstageable pressure injury § Unstageable pressure injury obscured full-thickness skin and tissue loss: full-thickness skin and tissue loss; the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar (ie dry, adherent, intact w/o erythema or fluctuance) on the heel or ischemic limb should not be softened or removed § Deep tissue pressure injury (DTPI): persistent non-blanchable deep red, maroon or purple discoloration: Dog, Cat, Human bites 1. All bites, can obviously lead to infection, particularly cat bites 2. Timely copious high-pressure irrigation w/ NS may be useful to reduce infection rates 3. For animal bites, ascertain rabies status 4. Consider x-rays as needed (ie skull if bite is to the head) 5. Primary closure of certain wounds remains controversial 6. Wounds of the hands or lower extremities should be left open. Any wound older than 6 hours is generally left open to heal by secondary intention 7. Plastic surgery consult as appropriate 8. Antibiotic necessity for human bites remains controversial. Yet for human and animal bites, employ 3-7 day course of oral prophylactic abx w/ coverage for both staphylococci and anaerobes (Amoxicillin-clavulanate (Augmentin) 875/125 mg twice daily PLUS Metronidazole (Flagyl) 500 mg 3 times daily Actinic keratoses 1. Small patches occurring on sun-exposed parts of the body 2. Premalignant (1:1000 lesions progress to squamous cell carcinoma) 3. Asymptomatic: small patches may be tender 4. Rough, flesh colored, pink, or hyperpigmented Treatment: liquid nitrogen Squamous cell carcinoma 1. Arise out of actinic keratosis 2. Firm, irregular papule or nodule 3. Develop over a few months, 3-7% metastasis 4. Prolonged sun-exposed areas in fair skin people 5. Keratotic, scaly bleeding o Treatment: biopsy and surgical excision (Mohs) Seborrheic Keratosis 1. Benign, not painful lesions 2. Beige, brown, or black plaques 3. "Stuck on" appearance 4. 3-20mm in diameter o Treatment: none or liquid nitrogen Basal cell carcinoma 1. The most common skin caner 2. Slow growing lesion 1-2 cm after years 3. Waxy, "pearly" appearance, may be shiny red 4. Central depression or rolled edge 5. May have telangiectatic vessels Treatment:shave/punch biopsy and surgical excision Malignant melanoma 1. Mortality rate highest of all skin cancers 2. Median age at diagnosis is 40 3. May metastasize to any organ 4. Asymmetry Border irregularity Color variation Diameter 6mm Elevation Enlargement o Treatment: biopsy and surgical excision Acid-base imbalances ROME= RESPIRATORY OPPISITE (pH (up or down) = CO2 (opposite direction) METABOLIC EQUAL (pH (up or down) + HCO3 (same) Respiratory acidosis d/t decreased alveolar ventilation. In acute respiratory failure, there is a sharp rise in pCO2 with only a small increase in plasma HCO3 o s/s: 1. somnolence and confusion, coma 2. myoclonus with asterixis (inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements) o Laboratory/Diagnostics: 1. Low arterial pH 7.35 2. pCO2 45 o Management: 1. Naloxone/Narcan for all patients with no obvious cause: 0.04 to 2mg 2. Improve ventilation, intubate if necessary Increase rate on ventilator Respiratory alkalosis hyperventilation decreases arterial pCO2 and increases pH. Clinical s/s are r/t decreased cerebral blood flow o s/s: 1. light-headedness 2. anxiety 3. paresthesia 4. stocking/glove tingling 5. tetany if very severe o Laboratory/Diagnostics: 1. Increased pH 7.45 2. Low pCO2 35 3. Serum HCO3 low if chronic o Management: 1. Manage underlying cause 2. If an acute hyperventilation syndrome is present, have the pt breathe into a paper bag 3. Decease rate of ventilator as needed 4. Sedation may be necessary 5. Rapid correction of chronic alkalosis may result in metabolic acidosis Metabolic acidosis the hallmark sign is low serum HCO3. Measurement of anion gap lends to some clues toward evaluation the cause and considering treatments o *Anion gap = [Na + K] - [HCO3 + CL] 10 is normal. if the anion gap is increased (+10), the clinical situation is generally more acute metabolic acidosis: increased anion gap Increased anion gap: o DKA o Alcoholic KA o Lactic acidosis o Management for increased gap: o Treat underlying cause Fluid resuscitation metabolic acidosis: normal anion gap Normal anion gap: o Diarrhea o Ileostomy o Renal tubular acidosis Recovery from DKA Metabolic alkalosis characterized by a high plasma HCO3 and compensatory pCO2 rarely exceeds 55. If pCO2 is 55, superimposed respiratory acidosis is likely o Causes: saline responsive (volume contraction) most common: 1. Post-hypercapnia alkalosis 2. NG suction 3. Vomiting 4. Diuretics o Management: saline responsive: 1. Correct volume deficit with NaCL and KCL 2. Discontinue diuretics 3. H2 blockers in patients with GI losses 4. Acetazolamide 250-500 mg IV every 4-6 hrs if volume replacement is contraindicated o Laboratory/Diagnostics: 1. Arterial pH 7.45 2. Arterial HCO3 26 Fever term to describe an increase in body temp above normal 37˚C, monitoring of body temp is commonly used to determine the presence of infection § Causes of fever: 1. Bacterial, viral, rickettsial, fungal, or parasitic infections 2. Autoimmune disease: SLE, arteritis 3. CNS disease: cerebral hemorrhage, brain tumor, MS -interference w/thermoregulatory process rather than fever 4. Malignant neoplastic disease: primary and liver metastasis of cancer 5. Hematologic disease: lymphoma, leukemia 6. CV disease: MI, phlebitis, PE 7. GI disease: IBD, alcoholic hepatitis 8. Endocrine disease: hyperthyroidism, pheochromocytoma 9. Miscellaneous causes: familial Mediterranean fever, hematoma 10. Neuroleptic malignant syndrome § Treatment of fever: 1. Antimicrobials only when a microbe is present 2. Antipyretics 3. Treat underlying condition Post-operative fever § Causes of non-infectious post-op fever: 1. Postoperative atelectasis 2. increased basal metabolic rate 3. dehydration 4. drug reactions: Amphotericin B, trimethoprim-sulfamethoxazole, beta-lactam abx, procainamide, isoniazid, alpha-methyldopa, quinidine, others § Causes of infectious post-op fever: 1. Usually w/ subjective complaints and a WBC^ with L shift/bandemia 2. WBC ^ +30,000 is usually not d/t infection 3. Surgical incisions 4. IV sites 5. point of entry for catheter: culture 6. Urinary tract 7. Lungs 8. Sinusitis: NG tubes associated w/ increased incidence 9. Abscess (ie intra-abdominal) § Initial treatment of post-op fever: 1. in the absence of any indication of infection, the first response should include hydration and measures to expand lung inflation § Treatment infectious post-op fever: 1. Supportive fluid therapy and acetaminophen 2. Treat underlying source 3. Gram stain and C&S all invasive lines or catheters as indicated Herpes Zoster (shingles) acute vesicular eruption d/t infection w/ varicella-zoster virus, may be life-threatening in immunocompromised patients o s/s: 1. pain along a dermatomal distribution, usually on the trunk 2. grouped vesicle eruption of erythema and exudate along the dermatomal pathway 3. regional lymphadenopathy may be present o Management: 1. Treatment options include: acyclovir, famciclovir, valacyclovir 2. If suspected ocular involvement, immediate referral to ophthalmologist 3. Post-herpetic neuralgia: gabapentin (Neurotin), pregabalin (Lyrica) 4. Shingrix: indicated for all adults 50 years of age regardless of previous shingles or Zostavax vaccine, 2 dose regimen w/ 2nd dose given 2-6 months after initial dose Pain descriptor of a subjective perception of distress, 5th VS § Types: 1. Acute: duration is usually short (6 months) caused by tissue damage 2. Chronic: continual or episodic pain of longer duration 6 months, combination therapy usually needed to effectively treat § Locations: 1. Cutaneous: localized on the skin or surface of the body 2. Visceral: poorly localized (internal organs) 3. Somatic: non-localized, originates in muscle, bone, nerves, blood vessels and supporting tissue 4. Neuropathic: frequently caused by a tumor, involves nerve pathway injury or compression § Subjective findings: pt self-report or physical evidence is the most reliable indicator of existence and intensity of acute pain § WHO's ladder of pain management: 1. 3 step progressive ladder starting with aspirin, acetaminophen, or an NSAID, continuing to build through the 3 steps with heavier narcotics added, while maintaining the initial choice of aspirin, acetaminophen, or NSAID · Step 1: ASA, APAP, NSAID, + Adjuvants · Step 2: ASA/APAP + codeine, hydrocodone, oxycodone, dihydrocodeine, tramadol (not available with ASA/APAP), +Adjuvants · Step 3: morphine, hydromorphone, methadone, levorphanol, fentanyl, oxycodone, +nonopioid analgesics, + Adjuvants 2. Next: Break-through cancer pain: use of fentanyl patches for sustained release recommended 3. Metastatic bone pain management: consider bisphosphonates (inhibitors of bone resorption, acting by inducing osteoclast apoptosis and thereby preventing the development of cancer-induced bone lesions) 4. Management: Conservative but LIBERAL Asthma/restrictive airway disease Characterized by an increased responsiveness of the trachea and bronchi to various stimuli, and manifested by wide spread narrowing of the airways, hypertrophy of smooth muscle, mucosal edema, and hyperemia thickening of epithelial basement membrane, hypertrophy of mucus glands, acute inflammation, and plugging of airways by thick, viscid mucus o Causes: Most important allergens are encountered indoors 1. Dust mites 2. Pets: cat/dog 3. Cockroaches 4. Indoor molds 5. Exercise 6. Cigarette smoke o s/s: *ominous s/s include fatigue, absent breath sounds, paradoxical chest/abdominal movement, inability to maintain recumbency, cyanosis, etc 1. respiratory distress at rest 2. difficulty speaking in sentences 3. diaphoresis 4. use of accessory muscles 5. respiratory rate 28 bpm 6. pulse 110 7. pulsus paradoxus 12 8. hyperresonance 9. cough 10. chest tightness o Labs/diagnostics: 1. Slight WBC elevation with eosinophilia 2. PFTs reveal abnormalities typical of obstructive dysfunction § Hospitalization is recommended if the initial FEV1 is 30% predicted or does not improve after vigorous therapy § Hospitalization is recommended if peak flow is 60 l/min initially or does no improve after treatment 3. Initially respiratory alkalosis with mild hypoxemia on ABG 4. CXR is unnecessary unless to r/o other conditions, may show hyperinflation Asthma management o Management: Stepwise approach for managing asthma in adults: 1. Step 1: preferred: short acting beta 2 agonist (SABA) ie albuterol/Proventil, levalbuterol/Xopenex PRN § Work by stimulating enzymes that convert adenosine triphosphate to cyclic cAMP which in turn relaxes bronchial smooth muscles 2. Step 2: preferred: low-dose inhaled corticosteroids (ICS) ie budesonide/Pulmicort, fluticasone/Flovent, triamcinolone/Azmacort etc § Side effects include candida infection of the oropharynx, dry mouth, sore throat § Alternatives: Cromolyn, leukotriene receptor antagonist (LTRA) ie montelukast/Singulair, nedocromil/Alocril, or theophylline 3. Step 3: preferred: Low dose ICS + long-acting beta 2 agonist (LABA) ie salmeterol/Serevent, formoterol/Perforomist § Combo preparation examples: fluticasone + salmeterol= Advair, or formoterol + budesonide = Symbicort § Or medium-dose ICS § Alternatives: low-dose ICS + either LTRA, theophylline, or zileuton/Zyflo 4. Step 4: preferred: medium dose ICS + LABA § Alternatives: low-dose ICS + either LTRA, theophylline, or zileuton/Zyflo 5. Step 5: preferred: high-dose ICS + LABA and consider omalizumab/Zolair for patient who have allergies 6. Step 6: preferred: high-dose ICS + LABA + oral corticosteroid and consider omalizumab/Zolair for patient who have allergies o Notes: 1. Because of limited studies and the need to monitor liver function, zileuton is a less desirable alternative 2. Theophylline requires serum concentration monitoring 3. If an alternative is used and the response is inadequate, used preferred treatment before stepping up Asthma inpatient mangement 1. Supplemental low flow O2 2. Inhaled SABA: albuterol/Ventolin via MDI or nebulizer 3. Inhaled anticholinergics: ie ipratropium/Atrovent 4. Systemic glucocorticoids: IV methylprednisolone for those intolerant of PO 5. Mg sulfate: single dose IV administration 2g infused over 20 min for pt not responding to the above 6. For suspected anaphylaxis, epi 0.3-0.5 mg SQ/ 0.3-0.5 ml of 1mg/ml also labeled 1:1,000 solution 7. At any point, mechanical ventilation as needed Status asthmaticus term used to describe severe, acute asthma presenting in an unremitting pooly response life-threatening manner. Clinical findings are no reliable indicators of the severity of asthma o Management: 1. Oxygen 2. IV D 5 ½ NS 3. Inhalation and parenteral sympathomimetics: catecholamines/ epinephrine 4. Methylprednisolone 60-125 mg or hydrocortisone 300mg IV immediately 5. Consider Atrovent 6. Monitor pulse ox continuously 7. Monitor ABG q 10-20 min 8. Intubate Chronic bronchitis excessive secretion of bronchial mucus and is manifested by productive cough for 3 months or more in at least 2 consecutive years s/s: 1. Intermittent mild to moderate dyspnea 2. Onset of symptoms after age 35 3. Copious sputum production (purulent) 4. Body habitus: stocky, obese 5. Chest A-P diameter normal 6. Percussion normal 7. CXR: hyperinflation 8. Hematocrit increased Emphysema abnormal, permanent enlargement of the alveoli s/s: 1. Progressive, constant dyspnea 2. Onset of symptoms after age 50 3. Mild sputum: clear 4. Body habitus: thin, wasted 5. Chest A-P diameter increased 6. Percussion hyperresonant 7. Hematocrit normal 8. Total lung capacity increased COPD o Labs/diagnostics: 1. Low flattened diaphragm by CXR 2. FEV1 and all other measurements of expiratory airflow reduced 3. TLC, FRC, and RV may be increased o Outpatient management: 1. Discontinuation of smoking 2. Avoidance of irritants or allergens 3. Postural drainage may clear excess secretions 4. Inhaled ipratropium bromide or sympathomimetics: mainstay of therapy 5. Inhaled tiotropium bromide (Spiriva) promotes bronchodilation o Inpatient management: 1. O2 at 1-2 LPM NC or 24-28% venti mask 2. Pharmacologic progression as for in-pt management of asthma Tuberculosis systemic disease cause by M.tuberculosis. pulmonary disease is the most common clinical presentation. Other sites of involvement include: lyphatics, genitourinary, bone, meninges, peritoneum, and heart o Patients at increased risk include those in crowded living conditions, the institutionalized, HIV + and those afflicted with DM, chronic renal insufficiency, malignancy, malnutrition, and other forms of immunosuppression. Tuberculosis management o Management: 1. Local health department should be notified of all cases of TB 2. Hospitalization is not required but sold be considered if pt is non-compliant or is likely to expose susceptible individuals (negative pressure room) o Tuberculosis medication regimen: RIPE 1. (1) Rifampin 600 mg, (2) Isoniazid 300mg, (3) Pyrazinamide 1.5-2.0gm and (4) Ethambutol 15mg/kg daily initially 2. If the isolate proves to be fully susceptible to INH and RIF then the 4th drug may be dropped 3. Continue the first 3 drugs daily for 2 months, then 4 more months of RIF and INH daily § Persons with active HIV should be treated for 9 months § A variety of DOT options are also available at twice/three times weekly dosing o Monitoring therapy: 1. Patient with pulmonary TB should have weekly sputum smears and cultures for the first 6 weeks after initiation of therapy, then monthly until negative cultures documented. Continued symptoms or positive cultures after 3 months should raise the suspicion of drug resistance o Baseline evaluation: 1. Liver function studies, CBC, and serum creatinine should be obtained at baseline. Patients with normal baseline studies do not require monthly labs but should be questioned about symptoms of drug toxicity. Patients taking Ethambutol should be tested for visual acuity and red-green color perception. Tuberculosis s/s o s/s: 1. majority of patients are asymptomatic 2. fatigue, anorexia 3. dry cough progressing to productive and sometimes blood tinged 4. weight loss, low grade fever, night sweats o Labs/diagnostics: 1. Definitive dx by culture of culosis x 3 2. AFB smears are presumptive evidence of active TB 3. Small homogenous infiltrate in upper lobes by CXR 4. PPD shows exposure: NOT diagnostic for active disease Tuberculosis PPD o Chemoprophylaxis: Those with a positive skin test should receive 6 months of INH: 1. A + test is 5mm for HIV infected pts, contacts of a known case, or pts w/ a chest film typical for TB 2. A + test is 10mm for immigrants from high prevalence areas, or those in high-risk groups including health care workers 3. A + test is 15mm for all others not in high-risk groups Community-acquired pneumonia Pneumonia: inflammation of the lower respiratory tract as microorganisms gain access by aspiration, inhalation, r hematogenous dissemination. Pneumonia accounts for 10% of admission to medical services. Strep. Pneumoniae is the most common etiological agent of CAP o s/s: 1. Fever 2. Shaking chills 3. Purulent sputum 4. Lung consolidation on physical exam 5. Malaise increased fremitus o Labs/diagnostics: 1. Elevated WBC: may be low in immunocompromised or elderly 2. Infiltrates on CXR 3. Consider sputum GS and culture if indicated 4. CXR and consider 3 blood cultures 5. ABG if respiratory failure suspected CAP screening tools o Screening tools: for the prediction of morbidity and mortality in patients with CAP 1. Pneumonia severity index (PSI)/Patient outcomes research team (PORT) score § PORT: score for severity of pneumonia is based points for 20 relevant characteristics: age, gender, nursing home, neoplastic disease, chronic liver disease, congestive heart failure, cerebrovascular disease, chronic renal disease, altered mental status, respiratory rate, SBP, temp, heart rate, pH, BUN, sodium level, glucose level, hematocrit, PaO2, and pleural effusion § Class I-II Score 70 low risk mortality 1% treatment outpatient § Class III Score 71-90 low risk mortality 2.8% treatment brief inpatient § Class IV Score 91-130 moderate risk mortality 8.2% treatment inpatient § Class V Score 130 high risk mortality 29.2% treatment ICU 2. CURB-65 criteria: § Confusion w/ abbreviated mental test score 8 § BUN 19 § Respiratory rate 30 § SBP 90 or DBP 60 § age 65 § Score 0-1 low risk consider home treatment § Score 2 moderate risk consider brief hospital admission w/ supervised treatment § Score 3 high risk hospital admission for severe pneumonia, consider ICU CAP outpatient management Previously healthy macrolide: Azithromycin 500mg x1 then 250mg daily x 4 days OR doxycycline 100mg PO BID x 5-7 days ---high-dose amoxicillin (1 g orally three times daily x 5 days) plus either a macrolide (ie, azithromycin, clarithromycin) or doxycycline (Up to date) Comorbidities: DM, heart/lung/liver/renal disease and ETOH, neoplastic disease, asplenia fluroquinolone: Levofloxacin 750mh PO q 24hrs x 5 days OR beta-lactam: Augmentin 875mg/125mg PO BID x 5-7 daysPLUS doxycycline 100mg PO BID x 5-7 days or macrolide (see above) Viral Oseltamivir 75mg BID x 5 days or zanamivir if onset of symptoms 48 hours CAP inpatient management Non-ICU fluroquinolone OR beta-lactam + doxycycline or macrolide ICU Beta-lactam + macrolide or fluoroquinolone ICU: If inosa suspected Piperacillin/tazobactam or meropenem or cefepime PLUS AMG/azithromycin ICU: If MRSA suspected Above + vancomycin or linezolid ICU: Viral Oseltamivir, peramivir, zanamivir +/- abx for secondary infection Hospital-acquired pneumonia pneumonia that occurs 48 hrs or more after admission which was not incubating at the time of admission (includes VAP and HCAP). Staph aureus, strep pneumonaie, and h. influenzae are the most common causative organisms. HAP management Not at high risk of mortality and No factors increasing the likelihood of MRSA: One of the following: - piperacillin/tazobactam - cefepime - levofloxacin - imipenem or meropenem Not at high risk of mortality WITH factors increasing the likelihood of MRSA: One of the following: - piperacillin/tazobactam - cefepime or ceftazidime - levofloxacin or ciprofloxacin - imipenem or meropenem - aztreonam PLUS -vancomycin or linezolid High risk of mortality OR IV antibiotics within the last 90 days: TWO of the following: - piperacillin/tazobactam - cefepime or ceftazidime - levofloxacin or ciprofloxacin - imipenem or meropenem - amikacin or gentamicin or tobramycin -Aztreonam PLUS -vancomycin or linezolid Ventilator acquired pneumonia (VAP) pneumonia that arises + 48-72 hrs after endotracheal intubation. Pseudomonas is the most common causative organism VAP management Abx w/ MRSA activity: -Vancomycin or Linezolid Gram - abx w/ antipseudomonal activity: Beta-lactam based agents: -piperacillin/tazobactam or - cefepime/ceftazidime or - imipenem/meropenem or - aztreonam Gram - absx w/ antipseudomonal activity: non beta-lactam based agents: - levofloxacin/ciprofloxacin or - amikacin/gentamicin/tobramycin or - colistin/polymyxin B Pneumothorax gas in the pleural space that raises pleural pressures and can impair respiration, resulting in collapsed lung § s/s: 1. chest pain, dyspnea, cough 2. hyperresonance on affected side 3. diminished breath sounds and diminished fremitus on affected side 4. mediastinal shift toward the unaffected side (tension) 5. hypotension § Labs/diagnostics: 1. CXR is diagnostic 2. ABG may be indicated § Management: 1. 20% pneumothorax in asymptomatic pt requires no intervention 2. Chest tube is used 1st if available, in emergency needle decompression 2nd ICS MCL § Chest tube placement 4th or 5th ICS MAL Sarcoidosis disease of unknown etiology characterized by interstitial lung disease and non-caseating granulomas o Overview: 1. Various anatomical sties may be involved, but most commonly affect the lungs and lymph nodes within the chest 2. More common among females, North Americans, African Americans, and northern European Causasians 3. Onset of symptoms typically between 20-40 years of age o s/s: 1. progressive dyspnea 2. nonproductive cough 3. rales "Velcro crackles" may be noted o labs/diagnostics: 1. CXR for staging 2. PFT 3. Routine chemistries, ABG if needed 4. Bronchoscopy w/ transbronchial biopsy of the lung parenchyma for diagnosis o Management: 1. Corticosteroids: mainstay of therapy 2. Alternative therapies (controversial): immunosuppressive agents (Cytoxan, Imuran, methotrexate) Acute pulmonary embolus Diagnosed based on clinical suspicion (history extremely important) and the results of specific diagnostic studies. Predisposing risk factors are often in the history, a leading cause of in-hospital death, ultimately as a result of right ventricular failure. o Risk factors: § Prolonged bed rest/immobility § Oral contraceptives § Surgery to long bones § Venous stasis § Hypercoagulable states § Cardiac thrombi o s/s: § usually occur abruptly, unexplained dyspnea and tachycardia are most common, chest pain (retrosternal or lateralized and pleuritic), hemoptysis, low grade fever may occur, hypotension, cyanosis o Labs/diagnostics: § VQ scan should be performed in all clinically stable patients § ABG: hypoxemia SaO290%, PaO2 80 § Hypocapnia: PaCO2 35 d/t reflexive hyperventilation § Spiral CT/d-dimer § Pulmonary angiography when clinical data and VQ scan are contradictory o Management: § Supplemental oxygen § IVF for those with hypotension and reduced cardiac output § Worsening hypercapnia w/ progressive obtundation is indication for intubation § Heparin 80 u/kg bolus followed by continuous infusion of 18 u/kg/hr to maintain a PTT of 1.5-2 x normal, begin Coumadin simultaneously to an INR of 2-3 § Fibrinolytics therapy in those w/ hemodynamic compromise or shock before stating fibrinolytics/thrombolytics, PT, PTT must be 2 x normal Acute respiratory distress syndrome (ARDS) Form of acute lung injury attributable to a wide variety of insults o s/s: § severe dyspnea and respiratory distress, cyanosis, tachycardia, rales, and wheezes o labs/diagnostics: § refractory hypoxemia is hallmark feature § CXR may be "white out" or have diffuse bilateral infiltrates o Management: § Mechanical ventilation w/ PEEP ~10, TV 6-8 ml/kg of ideal body weight (IBW) Treat underlying condition