Medicine Flashcards

Question

Negative Pressure Pulmonary Edema

Answer 1

or postobstructive pulmonary edema is a well-described cause of acute respiratory failure that occurs after intense inspiratory effort against an obstructed airway, usually from upper airway infection, tumor, or laryngospasm.

Answer 2

Complete or partial blockage of pulmonary arterial vasculature leading to ventilation-perfusion mismatch (V/Q) Common sources: lower extremity venous system, mural thrombus from A Fib, fat embolism from long bones Signs: Dyspnea, chest pain, hemoptysis, tachypnea, cyanosis, JVD, diminished breath sounds D-dimer less than 500ng/mL CXR: Westermark-A prominent central pulmonary artery with local oligemia or pleural-based areas of increased opacity that represent intraparenchymal hemorrhage (Hampton hump). Helical CT-PA Wells Criteria: look up. PERC for low risk patients Treatment: Anticoagulation impedes additional thrombus formation, allowing endogenous fibrinolytic mechanisms to lyse existing clot. Streptokinase, recombinant tissue plasminogen activator rt-PA, Thrombolectomy or pulmonary embolectomy. Inferior vena cava filters if contraindications to anticoagulation. Virchows Triad Stasis, Endothelial damage, Hypercoagulability

Answer 3

Pathologic elevation in pulmonary arterial pressure. Can develop into right sided heart failure. 5 groups. Treatment: Nitric oxide pathway: Phosphodiesterase inhibitors (sildenafil), Endothelin pathway: Endothelin receptor antagonist (bosentan, ambrisentan) and Prostacyclin pathway: Prostacylin analogs (Epoprostenol, Treprostinil) Normal is 20mm Hg

Answer 4

Accumulation of air in the pleural space due to trauma, idiopathic, or spontaneous. Tension pneumothorax: Positive-pressure of air in the pleural space exceeding alveolar and venous pressures throughout the respiratory cycle; resulting in compression of lung and decreased venous return. Signs: Chest pain, dyspnea, cough CXR: Lucency without lung markings between the chest wall and lung, and visualization of the visceral pleura. Stable, spontaneous may be observe. Needle decompression. Chest tube.

Answer 5

Is a mycobacterial infection resulting in granulomatous formations mainly in the lungs Symptoms: Fatigue, weight loss, fever, night sweats, and productive cough CXR: pulmonary opacities, including nodular or cavitating Acid-Fast bacilli on smear of sputum, rapid molecular testing positive, 4,6,9 month regimen, new evidence of 4 month treatment regimen as appropriate. 4 month: 8 weeks of daily treatment with rifapentine, moxifloxacin, isoniazid, and pyrazinamide, followed by 9 weeks of daily rifapentine, moxifloxacin, and isoniazid.

Answer 6

Abnormally high amount of adipose tissue compared with lean muscle mass with an excess body weight >20% over the predicated ideal body weight BMI=kg/m2 Class 1 – BMI 30-35; Class 2 – BMI 35-40; Class 3 – BMI >40 Body Mass index: kgs / height (m2) Review effects on all systems in the body Pediatric: BMI (used for 2+ years as best measure for adiposity) Management: Know which drugs are based on ideal body weight vs total What is your plan to establish IV access in a difficult venipuncture? BP cuff appropriate size Decreased FRC --> more preoxygenation BMI 30-40 = ASA 2, >40 = ASA 3 (ASA last amended in 2020, does not take into account other comorbidities)

Answer 7

Is a metabolic disorder characterized by insulin resistance or decreased insulin production leading to hyperglycemia. How to diagnose: >126 fasting BG, HbA1c - 6.5% (pre- is 5.7), 200 random BG Type 1 (10%) or type 2 (90%), Duration of disease, complications of diabetes (eye, kidney, nerve), Recent episodes of DKA, HHS, or severe hypoglycemia, History of coronary disease or stroke Evaluate HBA1C: The HBA1C test looks at how much hemoglobin is glycosylated. HbA1 has two alpha and two beta chains and makes up about 98% of our hemoglobin, the other two percent being HbA2 and a small amount of HbF or fetal hemoglobin. The c added onto the HbA1 means it is glycosylated. Measures last 1-3 months. The more recent time interval, the last 6 weeks before the test, are more weighted than the prior 6 weeks. There is an average chart that correlates the % of HBA1c to blood sugar, for example an HBA1C of 6 corresponds to an average blood sugar of 126, whereas an HBA1c of 9 correlates to an average blood sugar of 212. Normal, 5.7 of below. 5.7-6.4 is prediabetic or high risk of DM, and 6.5 or higher is indicative of DM. DM 1: autoimmune destruction of pancreatic Beta cells DM2: Insulin resistance and relative lack of insulin (fat) The “Polys” Polyuria Polydipsia Polyphagia Blurry vision Fatigue Weight loss Recurrent urinary tract infections Dysuria In the absence of symptoms, must have TWO positive tests on same or different days Separate criteria for pre-diabetes TXTs: Lifestyle modifications, Oral hypoglycemics, Injectable hypoglycemics, Insulin: Injectable or continuous pump Rapid-acting insulins include lispro (Humalog), aspart (Novalog) and glulisine (Aprida) . They have an onset of five to 15 minutes, peaks of one to two hours and durations of four to six hours . Short-acting or regular insulins (Humulin R and Novolin R) have an onset of 30 to 60 minutes, peaks of two to three hours and durations of six to eight hours . Intermediate insulins include NPH or Lente (Humulin N and Novolin N) and have an onset of two hours, peaks of 12 hours and durations of 24 hours . Long-acting insulins include Ultralente (Humulin), glargine (Lantus) and detemir (Levemir) with onsets of six to eight hours, peaks of 16 to 24 hours and durations of 36 hours . Combination insulin preparations also are available with NPH/Regular ratios of 70/30 and 50/50 . Type 2 DM is treated with weight loss and exercise as well as oral or injectable medications . The classes of medications used today are: 1 . Sulfonylureas: glyburide (DiaBeta, Glynase PresTab, Euglucon), gliclazide (Diamicron), glimepiride (Amyryl) 2 . Meglitinides: repaglinide (Prandin), nateglinide (Starlix) 3 . Biguanides: metformin (Glucophage, Glumetza, Fortamet, Riomet) 4 . α-Glucosidase inhibitors: acarbose (Precose, Glucobay), miglitol (Glyset) 5 . Thiazolidinediones: rosiglitazone (Avandia), pioglitazone (Actos), Sodium-glucose co-transporter 2 (SGLT-2) inhibitors: dapagliflozin (Farxiga), canagliflozin (Invokana) 6 . Dipeptidyl peptidase-4 (DPP-4) inhibitors: sitagliptin (Januvia), saxagliptin (Onglyza) 7 . Glucagon-like peptide-1 (GLP-1) receptor agonist: liraglutide (Saxenda, Victoza), exenatide (Byetta Prefilled Pen), dulaglutide (Trulicity Pen, Trulicity) The hypoglycemic agents sulfonylureas and meglitinides increase the release of insulin to decrease blood glucose levels . The biguanides reduce hepatic glucose production in the presence of insulin, increase anaerobic glycolysis, increase glucose uptake and use by muscles, and decrease intestinal glucose absorption . The α-glucosidase inhibitors break down disaccharides and complex carbohydrates by competitive inhibition of the α-glucosidase enzyme in the proximal intestinal wall, delaying carbohydrate absorption . They do not cause hypoglycemia in a fasting patient . Thiazolidinediones reduce insulin resistance and improve the peripheral action of insulin by increasing the uptake and use of glucose by peripheral tissues and reducing hepatic glucose production . SGLT-2 inhibitors reduce renal reabsorption of glucose, thereby increasing urinary glucose excretion . DPP-4 inhibitors increase insulin secretion, decrease gastric emptying and decrease blood glucose . GLP-1 receptor agonists slow gastric emptying, suppress pancreatic glucagon secretion and stimulate insulin secretion in response to hyperglycemia A major surgical and anesthetic concern in the diabetic patient is the difficulty maintaining a balance between insulin and the counterregulatory hormones . Insulin lowers blood glucose levels by glucose uptake in the muscle and fat cells, decreasing gluconeogenesis and glycogenolysis in the liver . Counterregulatory hormones – such as epinephrine, glucagon, cortisol and growth hormone – can increase blood glucose levels by stimulating gluconeogenesis and glycogenolysis in the liver, increase lipolysis and ketogenesis, and inhibit glucose uptake in the muscle and adipose cells of the body . Other concerns include poor wound healing secondary to inflammatory response inhibition, decrease in macrophage infiltration, angiogenesis, fibroplasias, collagen accumulation and collagen maturation . They also have decreased phagocyte capabilities of the polymorphonuclear leukocytes, decreased chemotaxis and decreased migration . Increased plasminogen activator inhibitor concentrations and abnormal platelet function also are seen . Patients with poorly controlled DM have increased postoperative infections due to these effects . Patients with DM also can have a higher risk of aspiration due to delayed gastric emptying Peri-op Consider additional work up with EKG and labs (BMP, HbA1C), pre and post op finger stick to check levels Morning procedures are preferred for insulin-dependent diabetics ↓ bedtime long-acting insulin dose, if morning procedure basal insulin dose can be cut in half. (short and rapid acting held morning of), if basal is taken in the morning, can reduce dose by 25 to 50%. For ultra long-lasting insulin, consult endocrine. Do not administer rapid-acting insulin on morning of procedure Consider IV dextrose if longer procedure or unable to eat afterwards Pumps: consult endocrinology, NEVER STOP THE PUMP In general, may hold all orals EXCEPT for SGLT-2 inhibitors for which the current recommendation is 24 hours, drugs that end in -liflozin like canagliflozin Higher risk for infections due to impaired white blood cells from the glycosylation. Be careful with steroids. GLP-1 agonists (about 8 drugs currently on the market), Glucagon-Like-Peptide 1 receptor agonists Semaglutide aka Ozempic Jan 2023, “For adolescents with refractory obesity who opt for pharmacologic therapy, we suggest subcutaneous semaglutide rather than other agents (Grade 2C), Evidence is developing, ASA and AAOMS among others have appointed task forces to come up with recommendations Problem is it delays gastric emptying increasing risk of aspiration Currently (SEP 23) rec from ASA is for patients on DAILY dosing, hold day of, for WEEKLY dosing, hold a week prior, all irrespective of type of surgery or indication Consider IV dextrose if longer procedure or unable to eat afterwards. D50 is dextrose 50%, and the most appropriate to use for severe hypoglycemia. In a crash cart, this often comes as a 50 cc syringe, or in a hospital setting, a 50 ml bag, with a concentration of 0.5g/ml, which equates to 25 grams of dextrose. It is given over 1-5 minutes IV. Generally, 1 gram of dextrose raises blood sugar by 4-6, so giving 25 grams raises it by about 100-150. This effect is short lived, about 30 minutes or so. Can also do D5W added to fluids like LR or NS

Answer 8

Is a hyperthyroid autoimmune disease stimulating increase secretion of T3/T4 Most common cause of hyperthyroidism. Palpable goiter ocassionally with bruit, ophthalmopathy concerns. Thyroid stimulating immunoglovulins or antibodies bind TSH receptors. Treatment: Propanolol, Thiourea drugs (methimazole or Propulthiouracil )PTU)) methimazole's mechanism of action is its potent inhibition of thyroperoxidase (TPO), an enzyme crucial for thyroid hormone synthesis Iodinated Contrast agents- Iopodate sodium, Iopanoic acid Radioactive Iodine Surgery when Euthyroid

Answer 9

Is a chronic lymphocytic thyroiditis resulting in hypothyroidism Levothyroxine-hyroid hormones exert their physiologic actions through control of DNA transcription and protein synthesis

Answer 10

Is an endocrine disorder of excess cortisol, endogenous, or exogenous steroids Caused by supraphysiologic dose of steriods, benign ACTH pituitary adenoma, neoplasms. Central obesity, muscle wasting, hirsutims, purple striae. Osteoporsis, hypertension, poor wound healing, hyperglycemia, leukocytosis, lymphocytopenia, hypokalemia.

Answer 11

Is an endocrine disorder characterized by insufficient glucocorticoids and mineralocorticoids usually due to destruction of adrenal gland or insufficient ACTH secretion Weakness, vomiting, diarrhea, abdominal pain, amenorrhea Increased skin pigmentation Hypovoemic hypotension, hyponatremia, hyperkalemia, hypoglycemia, eosinophilla

Answer 12

Anemia is a reduction in hemoglobin (Hb) or hematocrit (HCT) or RBC count. It is a presentation of an underlying condition and can be subdivided into macrocytic, microcytic, or normocytic. Patients with anemia typically present with vague symptoms such as lethargy, weakness, and tiredness. Severe anemia may present with syncope, shortness of breath, and reduced exercise tolerance. Erythropoietin (EPO), which is made in the kidney, is the major stimulator of red blood cell (RBC) production The etiology of anemia depends on whether the anemia is hypoproliferative (i.e., corrected reticulocyte count <2%) or hyperproliferative (i.e., corrected reticulocyte count >2%). Hypoproliferative anemias are further divided by the mean corpuscular volume into microcytic anemia (MCV<80 fl), normocytic anemia (MCV 80-100 fl), and macrocytic anemia (MCV>100 fl). 1) Hypoproliferative Microcytic Anemia (MCV<80 fl) Iron deficiency anemia [1] Anemia of chronic disease (AOCD) Sideroblastic anemia [2] (may be associated with an elevated MCV as well, resulting in a dimorphic cell population) Thalassemia Lead poisoning 2) Hypoproliferative Normocytic Anemia (MCV 80-100 fL) Anemia of chronic disease (AOCD) Renal failure Aplastic anemia Pure red cell aplasia Myelofibrosis or myelophthisic processes Multiple myeloma Macrocytic anemia can be caused by either a hypoproliferative disorder, hemolysis, or both. Thus, it is important to calculate the corrected reticulocyte count when evaluating a patient with macrocytic anemia. In hypoproliferative macrocytic anemia, the corrected reticulocyte count is <2%, and the MCV is greater than 100 fl. But, if the reticulocyte count is > 2%, hemolytic anemia should be considered. 3) Hypoproliferative Macrocytic Anemia (MCV>100 fL) -Alcohol -Liver disease -Hypothyroidism -Folate and Vitamin B12 deficiency [3] -Myelodysplastic syndrome (MDS) Refractory anemia (RA) Refractory anemia with ringed sideroblasts (RA-RS) Refractory anemia with excess blasts (RA-EB) Refractory anemia with excess blasts in transformation Chronic myelomonocytic leukemia (CMML) -Drug-induced Diuretics Chemotherapeutic agents Hypoglycemic agents Antiretroviral agents Antimicrobials Anticonvulsants 4) Hemolytic anemia. Hemolytic anemia (HA) is divided into extravascular and intravascular causes. Extravascular hemolysis: red cells are prematurely removed from the circulation by the liver and spleen. This accounts for a majority of cases of HA Hemoglobinopathies (sickle cell, thalassemias) Enzyemopathies (G6PD deficiency, pyruvate kinase deficiency) Membrane defects (hereditary spherocytosis, hereditary elliptocytosis) Drug-induced Intravascular hemolysis: red cells lyse within the circulation, and is less common. PNH AIHA Transfusion reactions MAHA DIC Infections Snake bites/venom

Answer 13

Is a hematologic disorder characterized by an increase in red blood cells, measured by hematocrit over 55%

Answer 14

An autosomal recessive disorder where a point mutation (Valine for Glutamic acid) causes sickling of RBCs and hemolysis Questions similar to asthma WU; hospitalizations, treatments, what causes crises for you, etc TXT: Hydroxyurea increases HbF which prevents sickling, bone marrow transplant Peri-op: keep every as normal as possible and control pain well, deviations can cause a crisis Normothermia, euvolemia, well oxygenated, control pain

Answer 15

Is a term used to describe several acute conditions of sickle cell anemia, most commonly describing a painful, vaso-occlusive crisis. [Can also be splenic sequestration crisis, hemolytic crisis, aplastic crisis]

Answer 16

Is a coagulopathy due to reduced quantity or quality of von Willebrand’s factor, which is responsible for stabilizing platelet adhesion. vWF mediates PLT adhesion, adhesion to endothelium, and prevents degradation of Factor 8 Inherited phenotypic forms of Von Willebrand disease are: Type 1: This is an autosomal dominant disease (AD, incomplete penetrance approximately 60%) and is caused by a partial quantitative deficiency of von Willebrand factor. Type 2: This is an autosomal dominant disease caused by several qualitative defects in von Willebrand factor. It has four subtypes (2A-AD or AR, 2B-AD, 2N-AR, 2M-AD). 2A is the most common variant. Type 3: This is an autosomal recessive disease (AR) and is caused by a complete quantitative defect. The von Willebrand factor levels are not detectable, and the severe bleeding disorder characterizes this variant. Normal PT and PTT, ristocetin cofactor assay and vWF assay Often a DDAVP trial is done by heme team to assess response Type 1: partial quantitative def (MC). DDAVP, 0.3 mcg/kg IV or 150 mcg spray to each nostril, 20 mins before procedure Type 2: Qual def (2A, 2B, 2N, 2M), cannot give DDAVP to 2B, will induce hypercoag state Type 3: total quan def Cryoprecipitate (8, 9, vWF, fibrinogen) can help in all types Humate-P = (vWF, 8) concentrate

Answer 17

Is a coagulopathy due to X-linked genetic deficiency of factor 8

Answer 18

Is a coagulopathy due to X-linked genetic deficiency of factor 9 PTT prolonged (intrinsic pathway), normal PT Classified based on severity Mild: Factor lvls over 5% but below normal Moderate: Factor lvls 1-5%, infrequent spontaneous bleeding, prolonged bleeding from surgery Severe: Less than 1%, multiple spon bleeds per year TXT: Recomb Factor 8 or 9, goal of 80-100% normal lvls pre-op and maintain at 50% for 1-2 weeks to allow for healing. Infuse 20 min before surgery DDAVP helps as well (causes release of Factor 8 a vWF from endothelial cells)

Answer 19

Is a systemic, intravascular activation of the clotting cascade which can lead to microvascular thrombi in various organs Supportive treatments may include: Plasma transfusions to replace blood clotting factors if a large amount of bleeding is occurring. Blood thinner medicine (heparin) to prevent blood clotting if a large amount of clotting is occurring.

Answer 20

Is a complication caused by heparin that causes decreased platelets in the blood Heparin induced thrombocytopenia (HIT) is an immune‐mediated event that can have severe life‐ and limb‐threatening complications. Despite thrombocytopenia, bleeding is rare; rather, HIT is strongly associated with thromboembolic complications. When a diagnosis of HIT is suspected immediate cessation of all forms of heparin, including unfractionated heparin (UFH), low molecular weight heparin (LMWH) and heparin flushes, is imperative. Treatment of HIT should be initiated based on clinical suspicion and must never be delayed pending laboratory confirmation of HIT. A direct thrombin inhibitor, such as lepirudin, danaparoid or argatroban, is considered the agent of choice for treatment of HIT. Warfarin should not be used until the platelet count has recovered

Answer 21

Is a hemoglobinopathy with absent Alpha/Beta globulin leading to microcytic anemia Mild thalassemia (Hb: 6 to 10g/dl): Signs and symptoms are generally mild with thalassemia minor and little if any, treatment is needed. Occasionally, patients may need a blood transfusion, particularly after surgery, following childbirth, or to help manage thalassemia complications. Moderate to severe thalassemia (Hb less than 5 to 6g/dl): Frequent blood transfusions: More severe forms of thalassemia often require regular blood transfusions, possibly every few weeks. The goal is to maintain Hb at around 9 to 10 mg/dl to give the patients a sense of well being and also to keep a check on erythropoiesis and suppress extramedullary hematopoiesis. To limit transfusion-related complications, washed, packed red blood cells (RBCs) at approximately 8 to 15 mL cells per kilogram (kg) of body weight over 1 to 2 hours are recommended. Chelation therapy: Due to chronic transfusions, iron starts to get deposited in various organs of the body. Iron chelators (deferasirox, deferoxamine, deferiprone) are given concomitantly to remove extra iron from the body. Stem cell transplant: Stem cell transplant, (bone marrow transplant), is a potential option in selected cases, such as children born with severe thalassemia. It can eliminate the need for lifelong blood transfusions. Gene therapy Genome editing techniques Splenectomy

Answer 22

Factor 5 Leiden disorder, Protein C deficiency, Antithrombin-3 deficiency, pregnancy.

Answer 23

Is an X-linked recessive disorder characterized by enzymatic deficiency of glucose-6-phosphate dehydrogenase. This deficiency leads to RBC breakdown which ultimately limits the patient’s ability to respond to oxidative stress. Antimalarial medicines such as quinine. Aspirin (high doses) Nonsteroidal anti-inflammatory drugs (NSAIDs) Quinidine. Sulfa drugs. Antibiotics such as quinolones, nitrofurantoin.

Answer 24

Is a non-progressive, motor disorder characterized by spasticity, dyskinesia, and ataxia Therapies Drug Treatments Oral medications such as diazepam, baclofen, dantrolene sodium, and tizanidine are usually used as the first line of treatment to relax stiff, contracted, or overactive muscles. Botulinum toxin (BT-A), injected locally into muscles, has become a standard treatment for overactive muscles in children with spastic CP. Intrathecal baclofen therapy uses an implantable pump to deliver baclofen, a muscle relaxant, into the fluid surrounding the spinal cord. Baclofen decreases the excitability of nerve cells in the spinal cord, which then reduces muscle spasticity throughout the body. Baclofen is an agonist for gamma-aminobutyric acid (GABA)B receptors on pre- and postsynaptic neurons in the central nervous system (CNS) and peripheral nervous system.

Answer 25

Is a neurologic disorder characterized by abnormal electrical activity causing at least 2 unprovoked seizures more than 24hrs apart Seizure-transient disturbance of cerebral function due to an abnormal paryoxysmal neuronal discharge in the brain. Focal Onset, Generalized Onset, Combined general and focal. Focal- Restricted to one cerebral hemisphere. Meds: Brivaracetam-act by binding to the ubiquitous synaptic vesicle glycoprotein 2A (SV2A), like levetiracetam, but with 20-fold greater affinity. Carbamazepine-binds preferentially to voltage-gated sodium channels in their inactive conformation Lamotrgine-acts by inhibiting sodium currents by selective binding to the inactive sodium channel, suppressing the release of the excitatory amino acid, glutamate. Levetiracetam (Keppra)- The exact mechanism through which levetiracetam exerts its anti-epileptic effects is unclear Phenobarbital-increases the amount of time chloride channels are open, consequently depressing the central nervous system. This action occurs by acting on GABA-A receptor subunits. Topiramate- an anticonvulsant medication that blocks sodium channels and enhances the activity of gamma-aminobutyric acid (GABA) Clonazepam (klonopin) long acting benzo Valproic Acid-Proposed mechanisms include affecting GABA levels, blocking voltage-gated sodium channels, inhibiting histone deacetylases, and increasing LEF1 Cannabidiol-CBD has been shown to act as a negative allosteric modulator of the cannabinoid CB1 receptor,

Answer 26

Is an injury of the spine causing sympathetic/parasympathetic dysfunction along with motor and sensory deficits

Answer 27

Is a neurologic disorder characterized by terminal peripheral neurodegeneration leading to a lack of motor function

Answer 28

Transient loss of consciousness and postural tone from vasodepressor or cardiogenic causes with prompt recovery without resuscitative measures Vasovagal- Most frequent normally initiated by pain, stress, or claustrophobia that is characterized by a excessive vagal tone or impaired reflex control of the peripheral circulation Orthostatic- Nausea, diaphoresis, tachycardia, pallor ECG recommended for all patients requiring a syncope work up. May require EP testing. Midodrine- alpha-agonist that can increase peripheral vasoconstriction

Answer 29

Is a neurologic disorder characterized by progressive loss of cognitive ability due to accumulation of plaques The cholinesterase inhibitors most commonly prescribed are: Donepezil (Aricept®): Rivastigmine (Exelon®): Galantamine (Razadyne®): Glutamate regulators Memantine (Namenda®):

Answer 30

Is a neurologic disorder characterized by progressive loss of dopaminergic neurons manifesting with tremors and rigidity Amantadine- is poorly understood.[19] Amantadine is a weak antagonist of the NMDA-type glutamate receptor, increases dopamine release, and blocks dopamine reuptake Levodopa- Levodopa converts to dopamine in both the CNS and periphery Dopamine Agonists (Pramiexole, ropinirole) act directly on dopamine receptors Selective MAO inhibitors (rasagiline). MAOs=Monoamine oxidase inhibitors (MAOIs) are a class of drugs that work by inhibiting the activity of the enzyme monoamine oxidase (MAO), which is responsible for breaking down neurotransmitters such as serotonin, dopamine, and norepinephrine COMT-Catecholamine O methyltransferase inhibitors reduce the metabolism of levodopa to 3-O-methyldopa leading to more sustained plasma levels.

Answer 31

Is a neurologic disorder characterized by inflammation and demyelination of the central nervous system [with recurrent relapse]

Answer 32

Vascular ischemia or hemorrhage of the brain leading to neurological deficits

Answer 33

a transient episode of neurologic dysfunction due to the focal brain, spinal cord, or retinal ischemia, without acute infarction or tissue injury

Answer 34

Is a neurologic disorder characterized by headaches with or without aura [with photophobia, sonophobia] Triptans such as almotriptan, eletriptan (Relpax), frovatriptan (Frova), naratriptan (Amerge), rizatriptan (Maxalt, Maxalt-MLT), sumatriptan (Imitrex), zolmitriptan (Zomig)- serotonin 5-HT1B and 5-HT1D receptors in blood vessels (causing their constriction) and nerve endings in the brain, and subsequent inhibition of pro-inflammatory neuropeptide release, including CGRP and substance P. Ergots such as dihydroergotamine nasal (Migranal, Trudhesa), or ergotamine tartrate (Ergomar)-activating 5-HT 1D receptors located on intracranial blood vessels, leading to vasoconstriction, which correlates with the relief of migraine headache1 Calcitonin gene-related peptide antagonists (gepants) such as oral ubrogepant (Ubrelvy), rimegepant (Nurtec ODT) or intranasal zavegepant (Zavzpret)- small-molecule calcitonin gene-related peptide receptor antagonist Ditans such as lasmiditan (Reyvow) TCAntidepressants: amitriptyline (Elavil), or nortriptyline (Aventyl, Pamelor)-function by inhibiting serotonin and norepinephrine reuptake within the presynaptic terminals, resulting in elevated concentrations of these neurotransmitters within the synaptic cleft CGRP inhibitors used to block the calcitonin gene-related peptide: atogepant (Qulipta), eptinezumab (Vyepti), erenumab (Aimovig), fremanezumab (Ajovy), galcanezumab (Emgality), and rimegepant (Nurtec ODT -- helps treat and prevent migraines)

Answer 35

systemic autoimmune disease characterized by inflammatory arthritis and extra-articular involvement Cotricosteroids-Blocking the action of inflammatory mediators (transrepression) and inducing anti-inflammatory mediators (transactivation) to mediate anti-inflammatory effects. Suppressing delayed hypersensitivity reactions by direct action on T-lymphocytes to mediate immunosuppressive effects. Inhibiting genes responsible for expression of cyclooxygenase-2, inducible nitric oxide synthase, and pro-inflammatory cytokines, including tumor necrosis factor alpha and various interleukins. Disease-modifying antirheumatic drug- Methotrexate- antimetabolite of the antifolate type. inhibition of enzymes involved in purine metabolism, leading to accumulation of adenosine; inhibition of T cell activation and suppression of intercellular adhesion molecule expression by T cells; NSAIDs, which can affect the kidney function and increase the risk of toxicity2 Certain antibiotics, which can interfere with the metabolism or clearance of methotrexate

Answer 36

Is a disorder characterized by joint inflammation and stiffness for greater than six weeks in children under the age of 16

Answer 37

Is a disorder characterized by chronic inflammation due to autoantibody production responsible for multisystem tissue damage Antinuclear antibody Lab Hydroxychloroquine- rashes or joint treatment. alkalinizing lysosomatropic drug that accumulates in lysosomes where it inhibits some important functions by increasing the pH. Mycophenolate mofetil-The active metabolite of mycophenolate, mycophenolic acid, prevents T-cell and B-cell proliferation and the production of cytotoxic T-cells and antibodies Cyclophosphamide-Cyclophosphamide is an alkylating agent that is used as chemotherapy and to suppress the immune system Azathioprine- metabolism are thiouric acid (38%) and various methylated and hydroxylated purines, which are excreted via the urine. Mechanism of action. Azathioprine inhibits purine synthesis. Purines are needed to produce DNA and RNA

Answer 38

is an autoimmune disorder affecting the postsynaptic “motor end plate” nicotinic acetylcholine receptor causing weakness and rapid fatigue of skeletal muscles Anticholinesterase- Neostigmine or pyridostigmine

Answer 39

Is a multisystem granulomatous disorder of unknown etiology characterized by non-caseating granulomas May involve skin, eyes, peripheral nerves, liver, kidney, heart. Malaise, fever, dyspnea, iritis, lupus pernio. CXR: Typically bilateral hilar lymphadenopathy. Biopsy needed Treatment: Corticosteroids, Immunosuppressive therapy to include methotrexate, azathiprine, infliximab.

Answer 40

Is an infection with the HIV retrovirus leading to immunocompromise via CD4 T-helper cells If a patient is taking ART and has an HIV viral load <200 copies/mL and a CD4 count >200 cells/mm3, the clinician should proceed with the surgical plan as with a patient who does not have HIV CYP3A4 There is increased potential for drug-drug interactions in patients taking ART due to cytochrome P450 interactions with PIs, NNRTIs, and regimens boosted with ritonavir or cobicistat. Increased levels of fe

Answer 41

Is an HIV infection with a CD4 count below 200 or the occurrence of HIV-associated diseases

Answer 42

Is an autoimmune disorder characterized by the formation of granulomas and inflammation of vessels [most commonly affecting URT, lungs, and kidneys]

Answer 43

Is an IgE mediated anaphylactic response to an antigen due to release of histamine from mast cells and basophils Anaphylaxis, hay fever, eczema, asthma, food allergies,

Answer 44

Hypersensitivity reaction characterized by IgG or IgM directed complement attack against cell surface antigens Acute transfusion reaction, good pasteur syndrome, hemalytic disease of newborn

Answer 45

Hypersensitivity reaction characterized by IgG or IgM antigen/antibody complex deposition Rheumatoid, SLE

Answer 46

Hypersensitivity reaction characterized by a delayed, cell-mediated T-cell attack on allergens Contact dermatitis, graft rejection, tubercillin reaction

Answer 47

Is a gastrointestinal disease characterized by reflux of acidic gastric contents to the esophagus GERD is caused by multiple different mechanisms that can be intrinsic, structural, or both, Medical therapy is comprised of antacids antisecretory agents like histamine (H2) receptor antagonists (H2RAs) or PPI therapy and prokinetic agents. Currently, there are two US Food and Drug Administration (FDA) approved H2RAs (famotidine and cimetidine) available in the US and are available over-the-counter. The other commonly used H2RA known as ranitidine has been recalled as a potential health hazard or safety risk due to an unexpected impurity in the active ingredient. The less commonly known prescription-only H2RA nizatidine has also been recalled as well due to similar concerns. In the US, there are six PPIs that are currently available, of which three (omeprazole, lansoprazole, and esomeprazole) are available over-the-counter, and the remaining three (pantoprazole, dexlansoprazole, and rabeprazole) are prescription-only medications.

Answer 48

A gastrointestinal disease characterized by inflammation of the liver caused by alcoholism or infection A Fecal-oral; B - DNA Virus; C - RNA Virus; D - Dependent on B, MASH – Metabolic dysfunction-associated steatohepatitis (non-EtOH) Other causes include acetaminophen toxicty either intentional or not. Antiepileptics, antibiotics, or anti TB meds. Patients with serious liver dieases are at increased risk for perioperative morbidity, and decompensated liver disease is associated with an extremely high perioperative mortality. Patients with suspected or known liver diease should have measurement of liver enzyme levels as well as tests of hepatic synthetic function performed prior to surgery. Elective surgery in patients with acute viral or alcoholic hepatitis should be delayed until resolution. In patients with cirrhosis, postoperative complications correlate with the severity of liver dysfunction. Severity assessed with Child-Pugh score. The Model for End-stage Liver Disease (MELD) score-based on serum bilirubin and creatinine levels, and the prothrombin time expressed as the INR. Less than 10 predicts low risk, greater than 16 indicates high risk. The VOCAL Penn score can also be used. When surgery is elective, controlling ascites, encephalopathy, and coagulopathy preoperatively is prudent.

Answer 49

A component of end stage liver disease characterized by fibrosis of the liver

Answer 50

A chronic autoimmune disease with patchy transmural inflammation of the entire GI tract

Answer 51

A chronic autoimmune disease with diffuse and continuous mucosal inflammation of the colon

Answer 52

A superinfection of clostridium difficile due to recent antibiotic usage The recent IDSA/SHEA update suggests fidaxomicin preferentially over vancomycin for initial CDI,3 and new ESCMID guidelines concur with this recommendation, with vancomycin being acceptable for a first episode and metronidazole only if other agents are unavailable.4 The older ASID guidelines still recommend metronidazole for a first episode of non-severe CD

Answer 53

An intestinal disease characterized by inflammatory outpouchings of the colon

Answer 54

Is an autosomal dominant connective tissue disorder of fibrillin [which can result in cardiac issues such as aortic dilation and mitral regurgitation]

Answer 55

A connective tissue disorder characterized by elastic skin, hypermobility, bleeding tendency, possible aortic fragility, POTS

Answer 56

An X-linked recessive disorder characterized by a mutation in dystrophin leading to progressive loss of skeletal muscle function

Answer 57

An autosomal recessive disorder characterized by a deficiency in cathepsin C, leading to precocious periodontitis and loss of teeth

Answer 58

An autoimmune disorder characterized by rapid-onset muscle weakness caused by an immune mediated attack on the peripheral nervous system.

Answer 59

Is a heritable condition characterized by abnormalities in two or more ectodermal structures such as hair and teeth.

Answer 60

Is a bacterial infection of Clostridium tetani characterized by muscle spasms

Answer 61

A psychiatric disorder characterized by loss of interest, guilt, sleep disturbances, energy loss lasting for longer than 2 weeks Major depression, Persistent depressive disorder (also called dysthymia or dysthymic disorder), Perinatal depression, Seasonal affective disorder, Depression with symptoms of psychosis Selective serotonin reuptake inhibitors/SSRIs (Citalopram (Celexa), Escitalopram (Lexapro), Fluoxetine (Prozac), Sertraline (Zoloft), Paroxetine (Paxil)- inhibition of serotonin reuptake increases serotonin concentration, which causes a downregulation of 5HT1A receptors Serotonin–norepinephrine reuptake inhibitor/SNRIs-Venlafaxine (Effexor), Duloxetine (Cymbalta), Milnacipran (Savella)- SNRIs (serotonin and norepinephrine reuptake inhibitors. Inhibition of presynaptic neuronal uptake of 5-HT (serotonin) and norepinephrine following release from the synaptic cleft Tricyclic Antidepressants/TCAs- Amiltriptyline (Elavil), Nortriptyline (Aventyl) Amoxapine, Desipramine, Doxepin,exert their effects by modulating around 5 distinct neurotransmitter pathways. These medications function by inhibiting serotonin and norepinephrine reuptake within the presynaptic terminals, resulting in elevated concentrations of these neurotransmitters within the synaptic cleft. The increased levels of norepinephrine and serotonin in the synapse can contribute to the antidepressant effect. In addition, the neurotransmitters act as competitive antagonists on postsynaptic cholinergic (alpha-1 and alpha-2), muscarinic, and histamine receptors (H1) Monoamine oxidase inhibitor/MAO inhibitors- Phenelzine (Nardil), Selegiline (Emsam), Tranlcypromine-Monoamine oxidase inhibitors (MAOIs) work by inhibiting the activity of monoamine oxidase, an enzyme involved in removing the neurotransmitters norepinephrine, serotonin and dopamine from the brain Trazodone (Desyrel)-s a serotonin and histamine antagonist that inhibits reuptake and subsensitizes adrenoreceptors Bupropion (Wellbutrin)-The mechanism of action of bupropion in the treatment of depression and for other indications is unclear. However, it is thought to be related to the fact that bupropion is a norepinephrine–dopamine reuptake inhibitor (NDRI) and antagonist of several nicotinic acetylcholine receptors. Mirtazapine (remeron)-is in a group of tetracyclic antidepressants (TeCA). Mirtazapine inhibits the central presynaptic alpha-2-adrenergic receptors, which causes an increased release of serotonin and norepinephrine. Of particular importance is the potential for local anaesthetic solutions containing epinephrine to cause hypertensive crises in patients receiving TCAs and MAOIs. Meperidine can precipitate a serotonergic crisis in patients taking MAOI as it too interrupts presynaptic uptake of serotonin. It should therefore be avoided in patients known to be on an MAOI. The most important anaesthetic consideration for patients taking MAOIs relate to the profound pressor effect that may be seen after administration of both indirectly and directly acting sympathomimetics. There are a number of interactions with implications for the anaesthetist. Probably, the most important is the risk of precipitating a serotonin syndrome when tramadol or meperidine is given in conjunction with an SSRI. The serotonin syndrome features hyper-reflexia, agitation, and hyperthermia. SSRIs (particularly fluoxetine) may interfere with the metabolism of codeine to morphine by inhibiting CYP2D6. This means that patients given codeine may not receive adequate analgesia.1 There is an increased risk of bleeding in patients taking non-steroidal anti-inflammatory drugs (NSAIDs) or warfarin with an SSRI due to their interference with platelet function. n addition to the desired therapeutic effects, TCAs may cause sedation and reduce the seizure threshold. Anti-cholinergic side-effects may be problematic for the patient and may also be potentiated by the administration of other anti-cholinergic agents. The cardiovascular side-effects may be significant, particularly in overdose. These include widening of the QRS complexes and QT prolongation. Concerns regarding arrhythmias precipitated by halothane in patients on TCAs are probably less of a problem now that other inhalation agents are used more commonly. Postural hypotension may be significant in the elderly population and is due to α-receptor block. The combination of TCAs and tramadol can result in seizures and precipitate a serotonergic crisis. One of the most significant interactions for the anaesthetist to be aware of is the potentiation of the effect of indirectly acting sympathomimetics (e.g. ephedrine and metaraminol) by TCAs. These should be avoided if possible and directly acting sympathomimetics used cautiously to prevent hypertensive crises. Abrupt withdrawal of TCAs should be avoided because of the risk of mainly cholinergic symptoms

Answer 62

A psychiatric spectrum disorder characterized by alternating episodes of mania and depression Valproic Acid (for manic events)-inhibition of glycogen synthase kinase and activation of extracellular signal-regulated kinase Lithium- unknown mechanism First-generation antipsychotics are dopamine receptor antagonists (DRA) and are known as typical antipsychotics. They include phenothiazines (trifluoperazine, perphenazine, prochlorperazine, acetophenazine, triflupromazine, mesoridazine), butyrophenones (haloperidol), thioxanthenes (thiothixene, chlorprothixene), dibenzoxazepines (loxapine), dihydroindoles (molindone), and diphenylbutylpiperidines (pimozide).[1][2][3] Second-generation antipsychotics are serotonin-dopamine antagonists and are also known as atypical antipsychotics. The Food and Drug Administration (FDA) has approved 12 atypical antipsychotics as of the year 2016. They are risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole, paliperidone, asenapine, lurasidone, iloperidone, cariprazine, brexpiprazole, and clozapine.[4] Neuroleptic malignant syndrome (NMS) is a life-threatening emergency associated with the use of antipsychotic agents. Both typical and atypical APDs have been implicated, though it is more commonly seen with formerly called neuroleptic agents such as haloperidol and fluphenazine. The most important risk factor is a prior history of NMS. NMS is characterized by the presence of mental status changes, rigidity, fever, and dysautonomia. Non-steroidal anti-inflammatory drugs can increase lithium levels on average by 10–25% [44]. Further, stimulation of urine production with thiazide diuretics should be avoided as it can reduce renal clearance of lithium [44]. Perioperatively, an electrocardiogram should be closely monitored as sinus node dysfunction, atrioventricular block, T-wave changes, hypotension, and ventricular irritability can occur with toxicity. In addition, train-of-four neuromonitoring is important, as lithium can prolong neuromuscular blockade [43]. Due to lithium-blocking brainstem release of norepinephrine, epinephrine, and dopamine, there is a reduction of MAC requirements

Answer 63

A psychiatric disorder characterized by psychosis and hallucinations Antipsychotics

Answer 64

A psychiatric disorder characterized by repeated unwanted, uncontrollable thoughts or actions

Answer 65

A psychiatric disorder characterized by inappropriate reaction to innocuous stimulus impeding daily function Antidepressants, SSRIs and SNRIs in particular, are considered first-line therapies for GAD and PD Benzodiazepines are not more effective than antidepressants for treating anxiety disorders and should not be used as first-line therapy.13,37 Generalized Anxiety Disorder. SSRIs and SNRIs are the mainstay of pharmacotherapy for GAD.12 A recent meta-analysis found that escitalopram (Lexapro), duloxetine (Cymbalta), venlafaxine, and pregabalin (Lyrica) appear to be most effective and well tolerated Pregabalin (Lyrica) -Pregabalin is structurally similar to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). However, pregabalin does not directly bind to GABA-A or GABA-B receptors

Answer 66

A psychiatric disorder characterized by body dysmorphia leading to abstaining from adequate caloric intake

Answer 67

A psychiatric disorder characterized by bingeing, purging that affects nutritional status

Answer 68

A behavioral disorder characterized by inattention, impulsivity, and hyperactivity Amphetamine, the active ingredient of Adderall, works primarily by increasing the activity of the neurotransmitters dopamine and norepinephrine methylphenidate- act as a norepinephrine and dopamine reuptake inhibitor (NDRI) lisdexamfetamine dexamfetamine - Once administered, lisdexamfetamine is converted to its active metabolite, dextroamphetamine, which is taken up by the brain. Dextroamphetamine blocks the reuptake of norepinephrine and dopamine into the presynaptic neuron and increases the release of these monoamines into the extraneuronal space. atomoxetine-selective inhibition of presynaptic norepinephrine reuptake in the prefrontal cortex

Answer 69

A behavioral disorder characterized by spectrum of symptoms affecting social interaction Kanner's Syndrome. ... Asperger's Syndrome. ... Rett Syndrome. ... Childhood Disintegrative Disorder (CDD) ... Pervasive Development Disorder Not Otherwise Specified (PDD-NOS)

Answer 70

Are late-manifesting, severe alcohol withdrawal symptoms such as shaking, confusion, and hallucinations patients with chronic heavy alcohol use, because of neuro-adaptation, there is a down regulation of Gamma-Amino Butyric Acid (GABA) and up-regulation of the glutamate (NMDA receptor) neurotransmission Clinical Institute Withdrawal Assessment for Alcohol (CIWA-A) scale, particularly the 10 item revised version, known as CIWA-Ar First line- Benzodiazapam Alternatives: Haloperidol, a first-generation typical antipsychotic, is commonly used worldwide to block dopamine D2 receptors in the brain and exert its antipsychotic action. Phenobarbital-acts on GABAA receptors, increasing synaptic inhibition.

Answer 71

a condition in which a woman develops high blood sugar levels during pregnancy ACOG and ADA recommend the following target levels to reduce risk of macrosomia Fasting or preprandial blood glucose values < 95 mg/dL Postprandial blood glucose values < 140 mg/dL at 1 hour and < 120 mg/dL at 2 hours Treatment: Insulin

Answer 72

a condition in which a woman develops high blood pressure levels during pregnancy Threshold 140/90 for treatment Methyldopa first line. Labetalol or nifedipine. No ACE or ARBS in any trimester

Answer 73

A condition that affects pregnant women characterized by new onset hypertension and proteinuria Blood pressure of greater than 140 sys or 90 dia after 20 weeks gestation. Proteinuria of greater than 0.3g in 24hrs Can have variation of severe features with bp 160/110, kidney injury, vision changes.

Answer 74

A condition that affects pregnant women characterized by new onset hypertension, proteinuria, as well as seizures IV magnesium sulfate for seizures Labetalol, Nifedipine, Hydralazine for HTN Delivery

Answer 75

Is a complication of pregnancy associated with preeclampsia characterized by hemolysis, elevated liver enzymes, low platelets high morbidity, immediate delivery if unstable

Answer 76

condition defined by the presence of chronic widespread pain, fatigue, waking unrefreshed, cognitive symptoms, lower abdominal pain or cramps, and depression

Answer 77

Is a cancer of white blood cell lineage in bone marrow

Answer 78

Is a cancer of white blood cell lineage in the lymphatic system or elsewhere outside bone marrow

Answer 79

A plasma cell malignancy characterized by production of monoclonal immunoglobulin In bone marrow, leads to bony destruction (lesions, fractures), hypercalcemia Protein electrophoresis detects monoclonal protein Serum and urine M protein Bence Jones proteins, urine test, detects light chains, Kappa and lambda)

Answer 80

Permanent renal insufficiency that develops over month to years resulting in damage to the renal system and decreased function CKD Pt management Consult nephrologist to optimize, control co-morbities and normalize as best as possible Dialysis: undergo day before surgery, if they have shunt, stay away from that arm Increased bleeding risk to due uremic bleeding and PLT dysfunction Local hemostatic measures in surg Renal dosing adjustments Propofol unaffected, benzo metabolites prolonged, small to moderate doses of fentanyl are safe, lidocaine is safe, careful with fluids Theoretically compound A with Sevo If needed, Atracurium and Cis-atracurium are better (Hoffman degradation) 1. GFR> 90 Slight damage with normal or increased filtration 2. Mild decrease in FNC 60-89 3. Moderate decrease in FNC 30-59 4. Sever decrease in FNC 15-29 5. Kidney failure/ESRD <15

Answer 81

Chronic kidney disease that has progressed to a GFR less than 15 Desflurane and isoflurane are metabolised to a minimal extent and there are no concerns regarding their use in CKD. Neuromuscular blocking agents Atracurium is the neuromuscular blocking agent (NMBA) of choice in patients with CKD. Its metabolism is unique. Atracurium undergoes ester hydrolysis and Hofmann degradation, both of which are independent of renal function. Cisatracurium can also be used in patients with CKD. It is predominantly eliminated by Hofmann degradation. Its clearance is reduced by 13% in CKD, and its terminal elimination half-life is increased by 4.2 min. Up to a third of rocuronium is excreted renally in a 24-h period. Its clearance is reduced by 39% in CKD therefore prolonging time to recovery. The effects of rocuronium become less predictable in renal failure. Pancuronium has reduced clearance and a prolonged half-life in those with CKD and so is best avoided. Suxamethonium should be avoided because of the risk of exacerbating pre-existing hyperkalaemia. Sugammadex has been used successfully in clinical research to reverse blockade from aminosteroid NMBAs in patients with severe renal impairment. The sugammadex–rocuronium complex can persist in vivo for up to 7 days. The rocuronium–sugammadex complex is very stable and can be cleared by high-flow dialysis.25 Opioid analgesics Opioids have no direct nephrotoxic effects. They do have an antidiuretic effect, which may manifest clinically as urinary retention. The metabolite responsible for the potent analgesic, sedative and respiratory depressant effects of morphine is morphine-6-glucuronide. Its elimination is dependent on renal function, and its half-life is prolonged from 2 to 27 h in patients with CKD. Therefore, an appropriate dose reduction should be considered. Remifentanil is not dependent on renal function for its elimination. Both oxycodone and its metabolites accumulate in patients with CKD with a related prolongation in elimination half-life of 2.3–3.9 h. This may necessitate a dose reduction and an increase in dose interval. Tramadol is 30% excreted unchanged in the urine. It may be epileptogenic in the context of uraemia because of the lowered seizure threshold. The elimination half-lives of codeine and dihydrocodeine are significantly prolonged, and these drugs should therefore be used with caution. Coagulation abnormalities must be borne in mind and might pose a contraindication to spinal or epidural anaesthesia. Irrespective of the technique and drugs used, it is essential to maintain normovolaemia and renal perfusion pressure. Blood pressure targets should be individualised for the patient using preoperative baseline readings as an estimate. Careful fluid balance extends to the postoperative period. Patients may require dialysis. Patients with CKD are vulnerable to the sedative effects of opioids amongst other drugs and can take longer to emerge from anaesthesia with more prolonged residual drowsiness. They may therefore require an extended period of supplemental oxygen therapy and continuous oxygen saturation monitoring.

Answer 82

Hyperparathyroidism caused by disease outside parathyroid gland, most often CKD and failure to convert Vitamin D to its active form Management of SHPT targets abnormal phosphocalcic metabolism. Maintaining the serum calcium and phosphorus levels within the normal range along with control of PTH and vitamin D levels is the key in management of secondary hyperparathyroidism. Primary hyperparathyroidism is the most frequent cause of hypercalcemia in ambulatory patients. The condition is most common in postmenopausal women, although it can occur in persons of all ages, including pregnant women. If symptoms are present, they are attributable to hypercalcemia and may include weakness, easy fatigability, anorexia, or anxiety. However, most persons have no symptoms, and primary hyperparathyroidism usually is diagnosed after an elevated serum calcium level is found incidentally on multiphasic chemistry panel testing. Persistent hypercalcemia and an elevated serum parathyroid hormone level are the diagnostic criteria for primary hyperparathyroidism. Other causes of hypercalcemia are rare, and usually are associated with low (or sometimes normal) parathyroid hormone levels. Malignancy is the most frequent cause of hypercalcemia in hospitalized patients. Parathyroidectomy is the definitive treatment for primary hyperparathyroidism.

Answer 83

Goldenhar syndrome (GS), also known as oculoauriculovertebral dysplasia or hemifacial microsomia has a wide range of clinical manifestations, including craniofacial, vertebral , cardiac, renal, and central nervous system anomalies1. The typical presentation of GS includes epibulbar dermoids, microtia, mandibular hypoplasia, and vertebral anomalies8,10-11. The classic facial aspect of GS patients, described as hemifacial microsomia, and the other anomalies of this syndrome are probably caused by development defects of the first and second brachial archs12. The causes for these developmental defects seem to be heterogeneous2. GS is a condition with a prevalence ranging from 1:3,500 to 1:7,000 live births, and a male-female ratio of 3:24. Although most cases are sporadic, familial occurrences have been observed8. Oral manifestations of GS are clearly heterogeneous, and range from malocclusion to a more complex phenotype with complete absence of the mandibular ramus and temporomandibular joint (TMJ)3,13. Different forms of cleft lip and palate and decreased palatal width are frequently found in GS patients4.

Answer 84

Hemifacial microsomia (HFM), also known as unilateral otomandibular dysostosis or lateral facial dysplasia, is an asymmetrical, congenital malformation of the 1st and 2nd branchial arches and the second most common craniofacial anomaly after cleft lip and palate.[1] Patients present with unilateral hypoplasia of the ear, facial skeleton (maxilla, mandibular, zygoma, and temporal bones), and surrounding soft tissue.[2][3] HFM and Goldenhar syndrome are considered variants under the same clinical continuum of disorders termed the oculoauriculovertebral spectrum (OAVS), with Goldenhar syndrome encompassing HFM phenotypes along with epibulbar dermoid and vertebral anomalies.[1][4]

Answer 85

Treacher Collins syndrome is a severe congenital disorder of craniofacial development characterized by numerous developmental anomalies that are restricted to the head and neck (Figure 2). Hypoplasia of the facial bones, particularly the mandible (78% of cases) and zygomatic complex (81%), is an extremely common feature of TCS. Hypoplasia of the facial bones may result in dental malocclusion, with anterior open bite a common finding. The teeth may be widely spaced, malpositioned or reduced in number. In a large proportion of cases, the palate is high, arched and occasionally cleft (28%) and in severe cases, the zygomatic arches may be completely absent (Poswillo, 1975). Ophthalmic abnormalities include downward slanting of the palpebral fissures (89%) with notching of the lower eyelids (69%) and a paucity of lid lashes medial to the defect (69%) (Figure 2). Other clinical features of TCS include alterations in the shape, size and position of the external ears, which are frequently associated with atresia of the external auditory canals and anomalies of the middle ear ossicles. Radiographic analysis of the middle ears of TCS patients has revealed irregular or absent auditory ossicles with fusion between rudiments of the malleus and incus, partial absence of the stapes and oval window, or even complete absence of the middle ear and epitympanic space.10 Consequently, bilateral conductive hearing loss is common in TCS patients, whereas mixed or sensorineural hearing loss is rare.

Answer 86

Cleidocranial dysplasia (CCD) spectrum disorder is a skeletal dysplasia that represents a clinical continuum ranging from classic CCD (triad of delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and dental abnormalities), to mild CCD, to isolated dental anomalies without other skeletal features. Individuals with classic CCD spectrum disorder typically have abnormally large, wide-open fontanelles at birth that may remain open throughout life. Clavicular hypoplasia can result in narrow, sloping shoulders that can be opposed at the midline. Moderate short stature may be observed, with most affected individuals being shorter than their unaffected sibs. Dental anomalies may include delayed eruption of secondary dentition, failure to shed the primary teeth, and supernumerary teeth. Individuals with CCD spectrum disorder are at increased risk of developing recurrent sinus infections, recurrent ear infections leading to conductive hearing loss, and upper airway obstruction. Intelligence is typically normal.

Answer 87

is an autosomal dominant disease characterized by the presence of familial adenomatous polyposis (FAP) as well as extraintestinal manifestations such as osteomas, dental anomalies, epidermoid cysts and ocular abnormalities.

Answer 88

is an infrequent multisystemic disease that is inherited in a autosomal dominant way, which shows the high level of penetrance and variable expressiveness.[1–3] NBCCS characterized mainly by the presence of multiple odontogenic keratocysts (75%), basal cell carcinoma (50-97%), bifid ribs (40%), palmar and planter pits (60-90%) and ectopic calcification of the falx cerebri (37-79%)

Answer 89

classically described as a triad of micrognathia, glossoptosis, and airway obstruction. Infants frequently present at birth with a hypoplastic mandible and difficulty breathing. The smaller mandible displaces the tongue posteriorly, resulting in obstruction of the airway. Typically, a wide U-shaped cleft palate is also associated with this phenomenon.

Answer 90

is a genetically inherited syndrome characterized by craniosynostosis (premature fusion of coronal sutures) resulting in the skull and facial deformities. The syndrome was first described in 1912 by French physician Octave Crouzon when he identified both a mother and daughter with what was originally called “craniofacial dysostosis.” He described a triad of skull deformities, facial anomalies, and proptosis.

Answer 91

disorder characterized by postnatally reduced growth, distinctive facial dysmorphic features, congenital heart defects (CHD), hypertrophic cardiomyopathy (HCM), skeletal anomalies, and webbing of the neck. Other relatively common features are bleeding diathesis, ectodermal anomalies, lymphatic dysplasias, cryptorchidism, and cognitive deficits Noonan syndrome is associated with increased ERK-activity induced by RAS activation and, therefore, RANKL up-regulation may lead to development of multiple central giant cell lesions

Answer 92

Stickler syndrome is a connective tissue disorder that can include ocular findings of myopia, cataract, and retinal detachment; hearing loss that is both conductive and sensorineural; midfacial underdevelopment and cleft palate (either alone or as part of the Pierre Robin sequence); and early-onset degenerative joint disease. Medialization of the internal carotid artery

Answer 93

a developmental disorder characterized by distinct physical characteristics manifesting in facial, cardiac, and skeletal features. Physical traits – include upslanting palpebral fissures, flat nasal bridge and midface, decreased muscle tone (hypotonia), wider space between first and second toe (“sandal gap”), nystagmus, brachycephaly, incurving of the fifth finger (clinodactyly), narrow palate, overfolded helix of the ear (especially with a small ear), short-appearing neck with redundant skin on the back of the neck, broad and short hands and feet, and single transverse crease in the palm of the hand. Airway management can be difficult as a result of macroglossia, macrognathia, and a narrow hypopharynx. Macroglossia and pharyngeal muscle hypotonia tend to cause upper airway obstruction. The nares and the trachea may be smaller than in normal children. There is also an increased incidence of subglottic stenosis. Disordered breathing during sleep, including upper airway obstruction and obstructive sleep apnea, is seen in 30%-60% of children with Down syndrome. These patients are at risk for congenital cardiac disease (mostly endocardial cushion defects, but also mitral valve abnormalities recognized at a later age). Pulmonary hypertension can result from cardiac disease or chronic obstructive sleep apnea. Patients with Down syndrome have an increased incidence of duodenal atresia, Hirschsprung’s disease, hypothyroidism, and leukemia. They are also at increased risk for atlantoaxial instability. The American Academy of Pediatrics recommends getting an anteroposterior/lateral x-ray of the neck once between the ages of 3 and 5 years old. One should inquire about it, but it is not required prior to the patient’s receiving general anesthesia. It is not a perfect screening tool, and we should always consider these patients at risk and use precautions when manipulating their cervical spines. To screen for pain or abnormal movement in an uncooperative patient, you can use keys, a light, a toy, or something else interesting that they will want to follow with their eyes and move it around them. Also, parents may describe regression in certain milestones, even regression in toilet training, or less tolerance for walking. These kinds of symptoms should prompt a neurologic evaluation. Ensure that you have a recent cardiovascular evaluation, and evaluate for any residual defects or pulmonary hypertension. Remember that the degree of intellectual impairment varies widely in patients with trisomy 21. ANESTHETIC MANAGEMENT Expect obstruction or difficult mask ventilation because of a small mouth, large tongue, and large tonsils, but intubation is generally easy. Consider moderate continuous positive airway pressure with jaw thrust during mask induction to prevent pharyngeal airway collapse. Avoid manipulating the cervical spine during direct laryngoscopy. These patients can present with profound bradycardia upon induction with sevoflurane, presumably because of a predominant parasympathetic response or abnormal sympathetic response.

Answer 94

Is a group of symptoms that may occur with use of serotonergic medications, usually presenting with high blood pressure and tachycardia without fever Serotonin syndrome Precipitated by serotonergic drugs - Classic triad: AMS, autonomic hyperactivity, and neuromuscular abnormalities. -Mild: hypertension, ↑HR, diaphoresis, tremor, myoclonus, mydriasis, hyperreflexia. -Moderate: mild features plus hyperthermia, hyperactive bowel sounds, agitation, and hypervigilance. -Severe cases: above features plus worsening hyperthermia, muscle rigidity, and delirium -Discontinuation of serotonergic drugs. -Mild: benzodiazepines, IV fluids -Moderate: telemetry, serotonin antagonist (cyproheptadine). -Severe cases: ICU admission with sedation, paralysis, and intubation.

Answer 95

Is a late-presenting, life-threatening reaction that can occur in response to antipsychotic (neuroleptic) medications characterized by high fever, confusion, “lead pipe” muscle rigidity Neuroleptic Malignant Syndrome Anti-dopaminergic drugs (e.g., antipsychotics, metoclopramide) Abrupt cessation of dopaminergic drugs (Levodopa) -Muscle rigidity, hyperthermia, ↑CK, myoglobinuria, ↑HR, diaphoresis, ↑secretions, tremor, AMS, urinary incontinence. -chorea, akinesia, opisthotonos, trismus, blepharospasm, and oculogyric crisis - Tx: Discontinue offending agent (or restarting drug if dopaminergic drug withdrawal) -Aggressive hydration if ↑CK -If severe, bromocriptine or dantrolene. -Cool patient

Answer 96

Is a decompensated form of hypothyroidism, usually first manifesting as altered mental status and low body temperature Patients most commonly present for emergency services with altered mental status and hypothermia, below 35.5°C (95.9° F). The lower the body temperature, the worst is the prognosis.[45] The absence of mild diastolic hypertension in severely hypothyroid patients is a warning sign of impending myxedema coma Prompt initiation of thyroid hormone therapy is of paramount importance when myxedema coma is highly suspected, even before having thyroid hormone results back (even though results usually come back quickly in most clinical institutions).[59] A delay could increase the mortality and morbidity of the patient.[60] Hydrocortisone is recommended to be administered prior to thyroid hormone therapy, especially if the patient is hypotensive to avoid adrenal crises; suggestions are that levothyroxine will increase cortisol metabolism, and hypothyroidism may mask an underlying adrenal insufficiency. Treat hypothermia and respiratory failure with ventilation

Answer 97

Is a condition of elevated methemoglobin in the blood that can precipitate seizures and heart arrhythmias The main findings are cyanosis, pallor, fatigue, weakness, headache, central nervous system depression, metabolic acidosis, seizures, dysrhythmias, coma, and death. When treatment with methylene blue is ineffective or not recommended, additional options may include ascorbic acid, exchange transfusion, hyperbaric oxygen therapy.[18][19] High-dose ascorbic acid (vitamin C), up to 10 g/dose intravenously, can be considered to treat methemoglobin

Answer 98

Is a life-threatening complication of adrenal insufficiency most commonly manifesting hypovolemic shock The most prevalent clinical manifestations of adrenal crises include weakness, severe fatigue, unintentional weight loss, nausea, vomiting, abdominal pain, reduced appetite, back or limb pain, dizziness, somnolence, confusion, and loss of consciousness ACTH: High ACTH levels with low cortisol and aldosterone indicate primary adrenal insufficiency, whereas low ACTH levels with low cortisol suggest secondary or tertiary adrenal insufficiency. The recommended treatment regimen includes administering an initial dose of 100 mg of hydrocortisone through intravenous or intramuscular (IV/IM) bolus injection. This is followed by administering an additional 200 mg of hydrocortisone as IM or IV over the next 24 hours, with a dosage of 50 mg every 6 hours or as a continuous infusion.[5] The suggested treatment approach for hypoglycemia is administering either 1 L of normal saline or 5% dextrose in 1 L of normal saline, followed by maintenance fluids.

Answer 99

Is a neurologic condition characterized by a single seizure lasting more than five minutes, or two or more seizures within the same five-minute period without a return to normal. Initial management is airway maintenance and 50% dextrose if hypoglycemia is responsible. 10mg midazolam IM. Fosphenytoin and phenobarbital administraction

Answer 100

extreme form of asthma exacerbation that is poorly responsive to standard therapeutic measures characterized by hypoxemia, hypercarbia, and secondary respiratory failure.

Answer 101

Is a complication of myasthenia gravis that can lead to respiratory failure Myasthenic crisis is a life-threatening exacerbation of myasthenia gravis that is defined as worsening of myasthenic weakness requiring intubation or noninvasive ventilation [1]. While the respiratory failure is due to weakness of respiratory muscles, severe bulbar (oropharyngeal) muscle weakness often accompanies the respiratory muscle weakness, or may be the predominant feature in some patients. When this results in upper airway obstruction or severe dysphagia with aspiration, intubation and mechanical ventilation are necessary. Symptomatic acute treatment: ◦ pyridostigmine (Mestinon®) p.o. 3-6x60mg, max. 540 mg/d or ◦ pyridostigmine iv. (equivalent: orally:parenterally ~ 30:1) ▪ 360 mg/d p.o. equals to 12 mg/d i.v., max. 24 mg/d ▪ bolus 1–3 mg followed by 0.5–1 mg/h ◦ alternatively: ▪ neostigmine iv. (equivalent:: orally:parenterally = ~ 80:1) ▪ 360 mg/d Pyridostigmine p.o. = 4.5 mg/d neostigmine i.v. ▪ starting dose 6–12 mg/24 h, adjust 0.2–0.8 mg/h, bolus of 0.5 mg possible ◦ atropine 0.5–1 mg s. c. oder iv. against side effects (bronchial secretion) ◦ consider “drug-holiday” when intubated and not breathing spontaneously Effects of causal acute therapy can be observed after a few days usually (see Table 4). Indication for each regime depends on whether there is a crisis or an exacerbation and on complications. ◦ plasma exchange (PLEX) or immunoadsorption (IA) ▪ first-line therapy of crisis

Answer 102

Is an overstimulation at the level of the neuromuscular junction due to an excess of acetylcholine, which can lead to flaccid paralysis Cholinergic crisis Excessive use of AChEI (pyridostigmine, neostigmine), organophosphate poisoning -Muscarinic receptor stimulation: salivation, ↓HR, lacrimation, urinary frequency/urgency, diarrhea, GI cramping, emesis, and miosis. -Cholinergic receptor stimulation: muscle fasciculations, weakness, respiratory muscle weakness, ↑HR, ↑BP. -CNS stimulation: seizures, coma, ataxia, slurred speech, agitation. -Discontinue offending agent. -Secure airway if GCS < 8, excess secretions, respiratory muscle weakness -Atropine to reverse muscarinic effects. -Pralidoxime if organophosphate poisoning

Answer 103

Is a set of symptoms that follow cessation or reduction in alcohol use after a period of excessive use The revised Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) scale is a validated 10-item assessment tool that can be used to quantify the severity of alcohol withdrawal syndrome, Chlordiazepoxide (Librium), 50 to 100 mg Diazepam (Valium), 10 to 20 mg Lorazepam (Ativan), 2 to 4 mg

Answer 104

Is a condition characterized by an inappropriate release of antidiuretic hormone from the pituitary gland or nonpituitary sources or its continued action on vasopressin receptors The choice of treatment depends essentially upon the severity of symptoms at presentation. A mild but rapid fall in sodium levels can cause severe symptoms like delirium, confusion, and seizures, while chronic but significant hyponatremia (less than 125 mEq/L) may produce mild or no symptoms. So, in patients with mild to moderate symptoms, the mainstay of the treatment is the restriction of oral water intake with the goal of less than 800 mL/day. If hyponatremia is persistent, sodium chloride in the form of oral salt tablets or intravenous saline can be given. Loop diuretics such as furosemide (20 mg twice daily) can also be added to salt tablets as it helps decrease the urine concentration and thereby increase water excretion, particularly among the patients whose urine osmolality is much higher than serum osmolality (greater than 500 mOsm/kg)

Answer 105

Is a condition related to vasopressin characterized by polydipsia and polyuria that can be either central, nephrogenic, dipsogenic, or gestational Diabetes insipidus is a rare but treatable chronic condition caused by the lack of the posterior pituitary hormone vasopressin (AVP, also known as anti-diuretic hormone) resulting in uncontrolled diuresis. It is treated with desmopressin (DDAVP, a synthetic AVP analogue) which reduces diuresis. Treating patients with diabetes insipidus Diabetes insipidus is treated with demopressin/DDAVP in the following doses: oral or sublingual - 100-200µg (0.1-0.2mg) intranasal spray - 10=20µg IM or IV injection - 1-2µg Please note, in patients with decompensated diabetes insipidus fluid replacement should be the primary treatment with the aim of reducing hypernatraemia and 1-2ug IV or IM DDAVP administered with close attention paid to the clinical and biochemical response to prevent over-rapid overcorrection of hypernatraemia

Answer 106

Is a condition of orthostatic intolerance that causes increased heart rate and other symptoms

Answer 107

The 2016 recommendations define sepsis as life-threatening organ dysfunction due to a dysregulated host response to infection. Septic shock is defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities substantially increase mortality. To facilitate sepsis diagnosis, the task force identified clinical criteria that physicians can use in their offices, emergency departments, and hospital wards to quickly evaluate patients for sepsis. The quick SOFA (qSOFA) consists of these three simple tests that clinicians can conduct at the bedside to identify patients at risk for sepsis: Alteration in mental status, Decrease in systolic blood pressure to less than 100 mm Hg,Respiratory rate greater than 22 breaths/min. If a patient has at least two positive components of the qSOFA, the patient should be examined for organ failure. Septic shock differs from sepsis in that the complications are more severe and the risk of patient death is greater. The task force identified two new clinical criteria that clinicians should use in diagnosing patients with septic shock: 1 Persisting hypotension requiring vasopressors to maintain mean arterial pressure at or above 65 mm Hg and 2. Blood lactate level greater than 2 mmol/L despite adequate volume resuscitation

Answer 108

Unexpected nontraumatic death in clinically well or stable patients who die within 1 hour after onset of symptoms Most common causative rhythm is ventricular fibrillation. 70% attributable to underlying CHD. In young patients causes (long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, Brugada syndrome, HCM, arrhythmogenic RV cardiomyopathy, dilated cardiomyopathy)

Answer 109

Hypertensive emergencies are defined as severe elevations in BP (>180/120 mm Hg) associated with evidence of new or worsening target organ damage For adults without a compelling condition, SBP should be reduced by no more than 25% within the first hour; then, if stable, to 160/100 mm Hg within the next 2 to 6 hours; and then cautiously to normal during the following 24 to 48 hours.

Answer 110

Obesity-hypoventilation syndrome, awake alveolar hypoventilation appears to result from a combination of blunted ventilatory drive and increased mechanical load.

Answer 111

is a highly contagious infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)

Answer 112

encompasses various genetic and acquired disorders that describe elevated lipid levels within the body Lipids typically include cholesterol levels, lipoproteins, chylomicrons, VLDL, LDL, apolipoproteins, and HDL. Patients with a high risk of ASCVD (>7.5% 10-year risk) should receive statin therapy for primary prevention: Statin therapy should be initiated for secondary prevention in patients with known ASCVD, absent any contraindication: Tx: Statins (Hydroxymethylglutaryl-Coenzyme A Reductase Inhibitor- inhibit the rate-limiting enzyme in the formation of cholesterol. High intensity: Atorvastatin, rouvastatin. Moderate: Simvastatin, pravastation.

Answer 113

increased levels of cholesterol in the blood

Answer 114

ls known as 22q11.2 deletion syndrome, is a syndrome caused by a microdeletion on the long arm of chromosome 22.[7] While the symptoms can vary, they often include congenital heart problems, specific facial features, frequent infections, developmental delay, intellectual disability and cleft palate.[7] Associated conditions include kidney problems, schizophrenia, hearing loss and autoimmune disorders such as rheumatoid arthritis or Graves' disease.[7][8]

Answer 115

Hypothyroidism: weakness, cold intolerance, weight gain. MCC Hashimoto’s (low T3, T4, high TSH), txt replacement (levothyroxine)

Answer 116

is a set of disorders that involve excess synthesis and secretion of thyroid hormones by the thyroid gland. Symptoms include unexpected weight loss, rapid or irregular heartbeat, sweating, and irritability, although the elderly often experience no symptoms. Toxic Multinodular Goiter-autonomous hyperfunctioning thyroid nodules (Plummers Disease) Iodine deficient regions Thyroiditis-thyroid inflammation with release of stored hormone. Medication induced- Amiodarone, Iodine induced, Tyrokinase inhibitors.

Answer 117

VSD, Concentric RVH, RV outflow obstruction due to infundibular stenosis, dilated aorta (half of patients overrides the septum). If ASD its pentalogy of Fallot.

Answer 118

MC indication: non-ischemic cardiomyopathy Heavily immunosuppressed Resting HR of 90-100 Transplanted heart is denervated, no symp/parasymp inputs, DOES NOT respond to indirect-acting meds (neostigmine, glycol, atropine) Ephedrine is decreased Norepi, Epi, B Blockers work Residual atrial tissue from the original heart, uncommon but does happen, can cause a double P wave on EKG Full medical W/U with their team

Answer 119

Chest radiograph assessment using ABCDEFGHI Last revised by Daniel J Bell on 16 Jun 2021 Citation, DOI, disclosures and article data ABCDEFGHI can be used to guide a systematic interpretation of chest x-rays. Assessment of quality / Airway The quality of the image can be assessed using the mnemonic PIER: position: is this a supine AP file? PA? Lateral? inspiration: count the posterior ribs. You should see 10 to 11 ribs with a good inspiratory effect exposure: well-exposed films have good lung detail and an outline of the spinal column rotation: the space between the medial clavicle and the margin of the adjacent vertebrae should be roughly equal to each other; look for indwelling lines or objects Bones and soft tissues Scan the bones for symmetry, fractures, osteoporosis, and lesions. Evaluate the soft tissues for foreign bodies, swelling, and subcutaneous air. Cardiac Evaluate the heart size: the heart should be <50% of the chest diameter on PA films and <60% on AP films. Check for the heart shape, calcifications, and prosthetic valves. Diaphragm Check the hemidiaphragms for position (the right is commonly slightly higher than the left due to the liver) and shape (may be flattened bilaterally in chronic asthma or emphysema, or unilaterally in case of tension pneumothorax or foreign body aspiration). Look below the diaphragm for free gas. Effusions / Extrathoracic soft tissue Pleural effusions may be large and obvious or small and subtle. Always check the costophrenic angles for sharpness (blunted angles may indicate small effusions). Check the lateral film for small posterior effusions (more sensitive for small effusions). Fields, fissures and foreign bodies Check lungs for infiltrates (interstitial vs. alveolar), masses, consolidation (+/- air bronchograms), pneumothoraces, and vascular markings. Vessels should taper and should be almost invisible at the lung periphery. Evaluate the major and minor fissures for thickening, fluid or change in position. Check the position of foreign bodies e.g. ETT, NGT, pacemaker leads, central venous lines etc. Comment on previous surgery e.g. cholecystectomy clips, sternotomy wires. Great vessels / gastric bubble Check aortic size and shape and the outlines of pulmonary vessels. The aortic knob should be clearly seen. The gastric bubble should be seen clearly and not displaced. Hila and mediastinum Evaluate the hila for lymphadenopathy, calcifications, and masses. The left hilum is normally higher than the right. Check for widening of the mediastinum (which may indicate aortic dissection in the appropriate clinical setting) and tracheal deviation (which may indicate a mass effect, e.g. from large goiter, or tension pneumothorax). In children, be careful not to mistake the thymus for a mass! Impression In most cases, an impression is worthwhile as it not only forces you to synthesize all the findings together but acts as a double check.

Answer 120

A sudden and reversible reduction in kidney function There is no clear definition of AKI: KDIGO (Kidney Disease: Improving Global Outcomes) criteria is MC used Increase in serum creatinine by 0.3 mg/dL or more (26.5 micromoles/L or more) within 48 hours Increase in serum creatinine to 1.5 times or more baseline within the prior seven days Urine volume less than 0.5 mL/kg/h for at least 6 hours Causes: Pre-renal, Renal, Post renal BUN/Cr ratio can aid in loose correlation to identify where problem is Greater than 20:1 (BUN/Cr) = pre-renal 10-20:1 = renal (and sometimes post-renal) Less than 10:1 = post-renal Long list of causes for each, gets deep into work up mixed with electrolytes, FeNA, recommend making a note and looking into more on your own Hydrate and monitor, older rec include NAC

Answer 121

Usually Type 1 Diabetic Ketoacidosis (DKA) Glucose >250 mg/dL All the extra sugar causes Polyuria/Polydipsia/Polyphagia, weight loss, blurry vision, nausea/vomiting, Kussmaul breathing Dehydration (6-8 L often) Often an inciting event - Illness/infection, alcohol Ketosis/Acidosis: break down fatty acids for energy (results in acetone fruity breath) + Urine Ketones and B Hydroxybutyrate Normal or Pseudo hyperkalemia, but its actually low Note: can have DKA in type 2, TXT: rehydrate with LR, start insulin and K+ replenishment, correct other electrolyte abnormalities

Answer 122

Hyperglycemic hyperosmolar state (HHS) Glucose >600 mg/dL Polyuria/Polydipsia Dehydration – greater water deficit (8-10 L often) Blurry vision Polyphagia Nausea/Vomiting Inciting event - Illness/infection, alcohol TX: Fluid replacement and insulin

Answer 123

bone disease that develops when bone mineral density and bone mass decreases, or when the structure and strength of bone changes

Answer 124

disease in which defective metabolism of uric acid causes arthritis allopurinol-xanthine oxidase inhibitor

Answer 125

Malignant Hyperthermia Autosomal dominant inheritance. Triggered by succinylcholine and volatile anesthetics. Hyperthermia, muscle rigidity, ↑CK, myoglobinuria, ↑HR, ↑CO2 production, tachypnea, sympathetic nervous system overactivation (tachyarrhythmias and ↑BP). -Discontinue offending agents. -Hyperventilation with 100% O2 -Immediate administration of dantrolene. -Cool patient if fever -Treat acidosis and electrolyte abnormalities.

Answer 126

Perform procedures if needed in second trimester (1st risks problems with organogesis, 3rd risks inducing a preterm deliver, -use safe drugs Classes A: adequate and well-controlled studies demonstrate no risk in 1st trimester and other trimesters B: animal studies show no risks or animal have but human have shown to be safe, and there are benefits to use C: animal studies show adverse effects and no human studies, or no studies at all D: Routine evidence of fetal risk, in certain situation drug may still be used X: Fetal Abnormalities Class B: penicillin (amoxicillin and augmentin), erythromycin, clindamycin, cephalosporins, metronidazole, acetaminophen, oxycodone, morphine, fentanyl, hydrocodone, lido, prilocaine Class C: codeine, aspirin, articaine, Marcaine, Class D: benzos, do not use Nitrous is not-rated, do not use NSAIDs as of early 2021 are NEVER use, besides ductal issues have been shown now to cause hydramnios. Goal for preg pts is to reduce pain and anxiety. OR: consult OB, consider intraop fetal monitoring

Answer 127

1st trimester is weeks 0-14, 2nd is 14-27, 3rd is 28-40 Organogenesis is weeks 3-14, extremely sensitive to exogenous insults CO increases about 30-50%, 20-30% increase in HR, and 20-50% increase in stroke volume, blood volume increase 20-50%, increase in RBCs, decreased SVR, lowered oxygen reserve with increased consumption, displacement of the diaphragm, 20% decrease in FRC Increased coag factors except 11 and 13, increased fibrin and hematocrit, reduction in protein S activity and resistance to protein C, gravid uterus causes endothelial damage, (makes them all Virchow Triad positive) In chair, position pts in left lateral decubitus to prevent compression of IVC Data shows that in the first 16 weeks acute exposure of 0.6 Gy had risks of growth restriction, mental retardation, etc. Diagnostic tests that deliver less than 0.05 Gy are not believed to be teratogenic. 100 Sieverts = 1 Gray, Pano = (approx.) 20 microsieverts = 0.0002 gray During preg, when intubating, increased friability of upper airway which can lead to lots of bleeding, rate of failed intubations is about 10 fold higher

Answer 128

Sodium: Normal 135* mEq/L to 145* mEq/L Hyponatremia: often asymp, acute and chronic types, s/s lethargy, confusion, AMS, seizures, deep work up including figuring out if hypotonic, isotonic, hypertonic, looking as FeNA and Uosm (probably too deep for this exam) Problems that happen slowly should be corrected slowly (respect corrected rates or you may kill them) Beware central pontine myelinolysis (also called osmotic demyelination syndrome). Correct hyponat. too fast, brain cannot adjust the lytes to keep up, cells swell and explode. 1-14 days after correction, acute encephalopathy develops, seizures, coma, death Severe symptomatic hypoNa (seizures, AMS): 3% NaCl bolus (100mL up to 3x over 10min until symp resolve or Na+ 4-6 mEq/L) Severe asymptomatic hypoNa (Na<120): Goal Na+ 6 mEq/L in first 24h. 3% NaCl with rate based on Sodium Correction Rate, usually 15-30mL/hr. Stop 3% NaCl when Na>125 or if correcting too fast

Answer 129

Etiologies: impaired access to free water or impaired thirst, decreased urinary concentrating ability, or diabetes insipidus ( decreased production or efficacy of ADH) S/S: thirst, weakness, nausea, loss of appetite, with severe (generally over 160) seizures, coma, death Deeper (Calculate free water deficit, WU, hypervolemic, euvolemic and hypovolemic types) If you correct it too fast, (theoretically) can cause uncal herniation of the brain and death

Answer 130

Normal Values: 3.5-5.5* mEq/L, main intracellular cation, 98% intracellular K+ excretion is regulated at the distal nephron, Na+ absorption leads to K+ secretion in the kidney (mechanism of aldosterone) Transcellular shifts most common cause of changes in K+ This means things like acid/base shifts, insulin issues like DKA, etc., affect the measured K levels. However, these are not always true, the K might just be hiding intracellularly, so the cause of it does matter in the treatment Obviously, this is predicated on having functional kidneys…without those and for folks on hemodialysis this all goes out the window

Answer 131

<3.5 Signs and symptoms: usually with K+ < 2.5: cramps, ileus, weakness (LEs > trunk/UEs > respiratory muscle paralysis) ECG: flat T waves, ST dep, U waves (small deflection after the T wave), increased QT, atrial or ventricular ectopy, VT, VF (esp if K+ <3, susceptible pts, or on digoxin Can be lab artifact (pseudo-hypokalemia): WBC >100  WBC absorb K if sample sits out (check K on ABG+) Lack of intake, redistribution, renal loss, extra renal loss…many many things can cause

Answer 132

Hyperkalemia= K> 5.1 mEq/L Paresthesias, paralysis, confusion, respiratory failure, dysrhythmias, muscle cramps Note: Any electrolyte abnormality can cause cardiac arrhythmias, which can be benign or fatal. Some are more predisposed to this than others, and K+ is one of these Evaluate your patient NOW Repeat Potassium, stat-hemolysis rule out, check a CBC, whole blood more reliable than serum K EKG* Review PMH, Medications, renal function, examine patient, and evaluate volume status Treat is K+ is over 6.5, EKG changes present, or pt is symptomatic Stabilize, Redistribute, Eliminate STEP 1: PROTECT THE CORE (aka heart) Want to give calcium to stabilize the cardiac membrane Step 2: Give meds to move K around Step 3: Give more meds to eliminate it from the body Note: Sux intube dose raises K by 0.5

Answer 133

Chloride The major extracellular anion in our body (kind of the opposite of sodium) 101-111 mEq/L normal range Significance: Evaluation of fluid, electrolyte, and acid-base status, osmotic pressure, body water distribution Bicarb (HCO3) Normal 20-34 mEq/L Extracellular buffer Both of these are integral part of acid/base

Answer 134

Renal function is measured by the glomerular filtration rate Estimated using Cockcroft-Gault formula (do not need to memorize), newer formulas include CKD-EPI formula eCCr = (140 – Age) x Mass (kg) x [0.85 if female] / 72 x [Serum Creatinine (mg/dL)] MC measured using creatinine clearance; by product of muscle metabolism, almost exclusively filtered and not resorbed , hence good indicator of FNC Serum Cr is .5-1.3. NOT linear interp. Cr of 2 is 50% decrease in GFR, very much depends on pt baseline to interpret

Answer 135

Angiotensin II receptor blockers (ARBS) competitively antagonize angiotensin receptor type 1 (AT1), block vasoconstriction, sodium retention, reduces production/secretion of aldosterone and reduces secretion of vasopressin Vasopressin and aldosterone both hit the distal convoluted tubule and collecting ducts Related topics, SIADH (too much vasopressin), Diabetes Insipidus (opposite of SIADH; lack of ADH, damage to hypothalamic tract, kidneys do not respond to it, and pregnancy) Conn’s Syndrome

Answer 136

Verify that iodinated contrast material is necessary. If an alternative test is likely to provide an accurate and reliable diagnosis, we proceed without administering contrast material. (See 'Verify that contrast material is necessary' below.) ●Among euvolemic and hypovolemic inpatients, and emergency department patients whose clinical course permits it, we administer intravenous isotonic saline. Hypervolemic patients and patients receiving dialysis in general are not given volume expansion. There are no established dosing, duration, or injection rate recommendations for how the saline should be administered. Commonly used regimens are presented below. (See 'Inpatients and those in the emergency department' below.) In high-risk outpatients, we prefer volume expansion with intravenous isotonic saline, if feasible, similar to our approach among inpatients. However, outpatients are sometimes given oral hydration [41]. There are no established dosing or timing recommendations for how the oral hydration should be administered. Some encourage patient-directed oral hydration before and after the scan (eg, total one to two liters). (See 'Outpatients' below.) ●Use low- or iso-osmolar contrast agents. Use of these agents is standard for all diagnostic imaging examinations. (See "Prevention of contrast-associated acute kidney injury related to angiography", section on 'Dose and type of contrast agent'.) ●If a patient at high risk for contrast-induced AKI (CI-AKI) is taking a metformin-containing medication, it should be discontinued for a minimum of 48 hours after the procedure and, if AKI develops, not reinstated until the kidney function has improved. In addition, metformin should generally be avoided in patients with estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2. (See 'Withdrawal of metformin and nephrotoxic drugs in high-risk patients' below.) If a patient is taking noncritical nephrotoxic medications, these should generally be withheld for 48 hours after administration of contrast material at the discretion of the ordering clinician and, if AKI develops, not resumed until the kidney function has improved. For patients who are not at high risk for AKI after contrast-enhanced CT, we verify the need for contrast material; however, we do not prescribe prophylactic measures, do not withdraw nephrotoxic medications, and do not suspend metformin.

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