ER ROTATION Flashcards

Question

AORTIC ANEURYSM

Answer 1

- aneurysma = greek for "dilation" ANEURYSM = abnormal dilations or bulge in vessel officially termed aneurysm when the bulge or dilation is 1.5x larger than the normal diameter of the vessel Aneurysms can occur to any artery in the body: Aorta, Femoral, Iliac, Popliteal, Cerebral, etc. Aneurysms can occur in veins too, but the likelihood is much lower due to decreased pressure in veins TRUE ANEURYSMS vs PSEUDOANEURYSMS o True Aneurysm - all layers of the blood vessel bulge out together ⦁ Fusiform = the dilation is symmetrical on all sides ⦁ Saccular or Berry = dilation is on one side - because for some reason that side had to put up with higher pressures, or is weaker than other side o Pseudoaneurysm ⦁ not actually an aneurysm, but really a hole in the vessel wall that allows blood to leak out and look like an aneurysm - looks like a perfect bulge due to surrounding structures / tissues that hold blood in that one spot - allowing it to look like a fusiform or berry aneurysm MC Arterial Aneurysms = Aorta ⦁ 60% of aortic aneurysms = Abdominal aortic aneurysm *** (AAA or triple A) ⦁ other 40% of aortic aneurysms = thoracic section * ** Majority of AAA = located just below where the renal arteries branch off, but above the aortic bifurcation into common iliac arteries - this is because there is less elastin in this part of the aorta than others = weaker PATHOPHYSIOLOGY OF ANEURYSMS - weakness in vessel wall, so anything that causes the vessel walls to weaken can cause an aneurysm - when a wall is weakened, it struggles to contain the pressure of blood pushing against it - as the diameter of the weakened section dilates, the pressure on that part increases (Laplace's Law), making the diameter of the aneurysm even bigger --> cycle of continuous bulging until rupture! (this is why blowing up a balloon is tough at first, but gets easier as it stretches = due to positive feedback loop of increased diameter and increased pressure) CAUSES OF ANEURYSMS / WEAKENED VESSEL WALL ⦁ Hypertension ⦁ Hyperlipidemia / plaques ⦁ Mycotic aneurysms = caused by bacterial infections ⦁ smoking ⦁ genetic conditions - affect collagen / fibrillin (Marfans or Ehlers-Danlos) o Hypertension - vessels get blood supply as blood runs through them, but for thicker vessels, like descending aorta (thicker in order to handle high pressure from heart) = have own blood vessels in tunica media + tunica externa (tunica intima still gets supply from lumen blood) called VASA VASORUM - Hypertension causes hyaline arteriosclerosis of vasa vasorum --> narrows lumen of vasa vasorum --> ischemia + atrophy of tunica media/externa smooth muscle --> weakens aorta wall --> aneurysm o Plaques - plaque buildup in tunica intima (atherosclerosis) --> that section of tunica intima doesn't get oxygen --> ischemia (common in abdominal aorta - pressure is high, and vessel wall is nourished by flowing blood) ``` RISK FACTORS FOR ANEURYSMS (same as atherosclerosis) ⦁ male ⦁ > 60 ⦁ hypertension ⦁ family history ⦁ smoking ⦁ tertiary syphilis ``` Risk factors of abdominal aortic aneurysm include history of tobacco use, older age, male gender, and family history. ENDARTERITIS OBLITERANS = inflammation of vasa vasorum (occurs with tertiary syphilis) -> fibrosis -> constricts the lumen of the vessels supplying oxygen to vessel wall - particularly of thoracic aorta (thicker vessels, so have vasa vasorum) --> atrophy Thoracic aortic aneurysms are a common finding in tertiary syphilis. MYCOTIC ANEURYSMS - bacteria (or fungi) from an infection somewhere else in body can break off and travel elsewhere in the blood (embolic bacteria) - usually gets stuck in intercranial arteries, visceral arteries or arteries feeding arms / legs - bacteria weakens the vessels --> aneurysm - commonly caused by ⦁ bacteroides fragilis ⦁ pseudomonas aeruginosa ⦁ salmonella - Mycotic aneurysms = also a complication of infective endocarditis - fungal causes ⦁ aspergillus ⦁ candida ⦁ mucor MARFAN SYNDROME - impaired elastic properties of fibrillin --> weak blood vessel walls EHLERS - DANLOS SYNDROME - disrupted ability to form collagen proteins Thoracic aortic aneurysms are associated with connective tissue disease such as Marfans + ED SIGNS / SYMPTOMS OF ANEURYSMS - intact aneurysms = okay - usually don't cause any symptoms - but bulging vessel can compress nearby organs or vessels - ex: bulge in aortic arch can compress SVC --> decrease amount of blood going to the heart MOST CONCERNING COMPLICATION * ** RUPTURE of aneurysm *** - blood spills out of vessel, and less blood is getting to tissues / cells downstream that need it --> ischemia * ** AORTIC INSUFFICIENCY *** - particularly occurs when there is an aneurysm in thoracic aorta, right above aortic valve - the dilation causes the aortic valve itself to expand and not close properly together, allowing blood to flow back into LV during diastole (Aortic regurgitation) - Aortic insufficiency can also cause a high-pitched BRASSY COUGH due to aneurysm compressing on left recurrent laryngeal nerve that wraps around aorta A bicuspid aortic valve is a known risk factor for thoracic aortic aneurysms. BRAIN ANEURYSM - if cerebral artery aneurysm ruptures = will bleed into SUBARACHNOID space --> puts pressure on brain tissue / irritates the meninges ⦁ sudden / intense HEADACHE ⦁ inability to flex neck forward ANOTHER COMPLICATION OF ANEURYSMS ⦁ *** formation of BLOOD CLOTS *** - as blood is pooling into aneurysm prior to rupture, stasis of blood can form clots - clot can become so big it blocks off entire artery --> ischemia...or - part of clot can break off (thromboembolism) and travel elsewhere --> ischemia ABDOMINAL AORTIC ANEURYSM SIGNS /SYMPTOMS - sometimes asymptomatic, even if it has ruptured ⦁ severe flank pain / abdomen / chest / lower back / groin ⦁ pulsating mass that is in time with heartbeat ⦁ hypotension (in about 50%) - more indicative of rupture Ruptured abdominal aortic aneurysm should be suspected in patients with abdominal pain radiating to the back and associated with hypotension (from retroperitoneal bleeding) and a pulsatile abdominal mass. A presentation of hypotension, abdominal pain, and a pulsatile abdominal mass is characteristic of an abdominal aortic aneurysm which is in the process of rupturing. AAA can be asymptomatic until further progression. AAA rupture is life-threatening and can present with abdominal pain, back pain, syncope, hypotension, tachycardia, pulsating abdominal mass, abdominal bruits, and severe pain. THORACIC AORTIC ANEURYSM SIGNS / SYMPTOMS - usually asymptomatic ⦁ severe chest / back / abdominal pain ⦁ respiratory difficulties ⦁ trouble swallowing ⦁ brassy cough / hoarseness (compression of left recurrent laryngeal nerve) ⦁ cardiac disease ⦁ rupture ⦁ may hear abdominal bruit as blood moves past aneurysm Thoracic aortic aneurysm can lead to coughing and hoarseness due to compression of the left recurrent laryngeal nerve. DIAGNOSIS OF ANEURYSMS - because many are asymptomatic, they are often diagnosed incidentally ⦁ Ultrasound = initial study of choice ⦁ CT with contrast*** = test of choice ⦁ Angiography - Gadolinium = GOLD STANDARD Acutely, AAA can be visualized and sized with an abdominal ultrasound. CT and MRI are used to more accurately localize and determine size. In the emergent setting, (actively rupturing) an abdominal ultrasound should be done because it is quick, noninvasive, sensitive, and has the ability to show free peritoneal fluid. MC IV contrast = Iodine Barium sulfate used for digestive system, Iodine = 2nd line if barium cannot be used Possible adverse effects of iodinated contrast include warmth, contrast-induced neuropathy, and thyroid dysfunction ``` LABS / VITALS IF RUPTURED ⦁ hypotensive ⦁ tachycardic ⦁ leukocytosis (elevated WBC) - infection, malignancy, inflammation ⦁ anemia (decreased hematocrit) ``` Hematocrit = the ratio of the volume of red cells to the volume of whole blood. Normal range for hematocrit is different between the sexes and is approximately 45% to 52% for men and 37% to 48% for women. TREATMENT ⦁ surgery Treatment of non-rupturing AAA's depends on aneurysm size: ⦁ < 5 cm diameter and asymptomatic - monitor with periodic ultrasound - annual ultrasound if 3.0-4.0 cm - q6m ultrasound if 4.0 - 4.5 cm - q3m ultrasound if 4.5 - 5.4 cm + vascular surgeon referral ⦁ > 5.5 cm diameter or symptomatic or grew by 0.5 cm in 6 months - surgical repair using open or endovascular stenting. ⦁ BETA BLOCKER** = reduces shearing forces, decreases expansion and rupture risk. Abdominal aortic aneurysm does not indicate surgery in asymptomatic patients until the aneurysm reaches a diameter of ≥5 cm. In aneurysm cases of larger than 5 cm, EVAR (Endovascular aneurysm repair) is more commonly used because it is less invasive than open aneurysm repair (catheter-based therapy). ⦁ Thoracic aortic aneurysms = surgery if 6cm+ Emergent surgery needed if aneurysm has ruptured or if symptomatic the USPSTF recommends screening in any male 65-75 with a hx of smoking - 1 time screening via ultrasound - screening also recommended in those with Marfans + Ehlers Danlos

Answer 2

hyperkalemia = higher than normal potassium levels in the blood normal K+ range = 3.5 - 5.0 Hyperkalemia = > 5.0 or 5.5 mEq/L Levels > 7.0 can be life-threatening due to its effect on heart muscle Total body potassium can be split into intracellular and extracellular o Extracellular = Intravascular space + Interstitial space ⦁ Intravascular = in blood vessels + lymphatic vessels ⦁ Interstitial = space between cells where other proteins and carbohydrate chains are found o Intracellular = within the cell MAJORITY OF K+ = INTRACELLULAR (98%) = 150mEq/L - about 2% = extracellular = 4.5 mEq/L o INTERNAL POTASSIUM BALANCE ⦁ K+ has a charge, so having much more K+ in the cells creates an electrochemical gradient, called the Internal Potassium Balance, which is maintained by the Na / K pump - pumps 3 Na+ out for every 2 K+ in ⦁ There are also potassium leak channels and inward rectifying channels that are scattered throughout the membrane ⦁ This electrochemical gradient is VERY IMPORTANT for setting the resting membrane potential of excitable cell membranes = needed for normal contraction of SMOOTH, CARDIAC + SKELETAL MUSCLES o EXTERNAL POTASSIUM BALANCE = potassium that you get externally through diet daily - daily basis = typically get 50-150mEq/L = WAYY more than the extracellular K+ level of 4.5 mEq/L ⦁ so body has to excrete most of what it takes in = KIDNEYS - excreted via urine. Small amount of K+ is excreted via GI (poop) and sweat too HOW DO YOU GET HYPERKALEMIA IN THE BLOOD? 1) decreased potassium excretion via kidneys = external balance shift ⦁ kidney failure / acute kidney injury ⦁ hypoaldosteronism (adrenal insufficiency) ⦁ drugs: ACEI / ARBs / Potassium-sparing diuretics KIDNEY FAILURE - potassium is normally freely filtered out of blood and into urine via glomerulus - about 67% of K+ is reabsorbed in proximal convoluted tubule - additional 20% reabsorbed in thick ascending limb - distal tubule + CT can then either secrete or reabsorb remaining 13% depending on what the body needs - ALDOSTERONE increases Na channels for Na to be reabsorbed and increases K channels for K to be excreted, as well as Na/K pumps - Hypoaldosteronism (ADDISON'S)--> hyperkalemia or increased potassium intake = external balance shift ⦁ IV fluids - rapid, excessive intake = iatrogenic cause 2) too much potassium moving out of cells and into interstitium + blood = internal balance shift ⦁ insulin deficiency (type I DM) ⦁ acidosis ⦁ beta adrenergic antagonists (beta blockers) ⦁ alpha agonists ⦁ succinylcholine - causes K efflux from muscles ⦁ hyperosmolarity ⦁ cell lysis ⦁ exercise TYPE I DM - after eating, glucose increases in the blood, so insulin is released. Insulin binds to cells and stimulates the uptake of glucose into cells - insulin increases the activity of the Na / K pump - pulls potassium into cells / pulls sodium out of cells - people with Type I DM don't make insulin, so if they eat a meal, especially high in potassium, and don't take insulin --> don't have increased potassium intake into cells, so potassium sits in blood --> hyperkalemia ACIDOSIS - higher concentration of hydrogen ions in blood = low blood pH - body can lower blood pH by moving H+ ions out of blood and into cells = use H+/K+ pump to move H+ into cell and move K+ out of cell and into extracellular space (blood / interstitium) - so in order to help compensate for acidosis, end up with hyperkalemia - only the case in certain acidosis, NOT respiratory acidosis, as CO2 is lipid soluble and is able to freely move from blood into cell without affecting potassium, and NOT metabolic acidosis of organics such as lactic acid or ketoacids BETA-2 ADRENERGIC RECEPTORS - stimulate Na+ / K+ pump - increase intracellular K+ - so Beta-Blockers do the opposite --> hyperkalemia ALPHA-ADRENERGIC RECEPTORS - cause potassium to shift out of cells and into blood via calcium dependent K+ channels - so Alpha-agonists cause more hyperkalemia HYPEROSMOLARITY - hyperosmolarity in extracellular space causes water to shift out of cells --> excess potassium in cells --> potassium to shift out of cells --> hyperkalemia ``` CELL LYSIS - so much potassium is kept in the cell that with cell lysis --> potassium released from cells --> hyperkalemia ⦁ severe burns ⦁ rhabdomyolysis ⦁ tumor lysis (chemo) ``` EXERCISE - during exercise, excess ATP is used for energy - the depletion of ATP triggers potassium channels to open = allows potassium to move down its gradient and out of the cell --> hyperkalemia - usually the exercise shift is small, but if combined with beta blockers and/or kidney issues --> can lead to hyperkalemia SYMPTOMS - need normal K+ levels inside and outside the cell to maintain resting membrane potential to allow muscle cells to depolarize and contract - if too much extracellular K+ levels = increases resting membrane potential and can cause contraction --> abdominal / intestinal cramping - eventually the resting membrane potential gets so high that it's above the threshold potential, once the muscle depolarizes and contracts, it can't repolarize to allow for another muscle contraction -> weakness ⦁ abdominal / intestinal cramps - increased activity of smooth muscles in peritoneal cavity ⦁ muscle weakness - decreased intracellular K+ for skeletal muscle - ascending muscle paralysis / flaccid paralysis ⦁ diarrhea - increased activity of smooth muscle - peristalsis ⦁ heart arrhythmias / arrest - decreased cardiac myocyte conduction (tends to occur at K+ of 7-8) DIAGNOSIS ⦁ labs: K > 5.5 mEq / L - also check glucose, creatinine, cortisol ⦁ EKG - peaked T waves - best seen in precordial leads (V1 - V6) - shortened QT interval - ST segment depression - in severe cases = can also cause prolonged PR interval, absent P wave, and widened QRS complex could be PSEUDOHYPERKALEMIA - lab error or ** MC due to Venipuncture ** TREATMENT ⦁ potassium-wasting diuretics (Loop + thiazide - Lasix) ⦁ calcium gluconate- to stabilize myocardial cell membrane = 1st line if severe symptoms, EKG changes or > 6.5/7 mEq/L ⦁ insulin + glucose - insulin shifts K+ into the cell. Glucose given to prevent hypoglycemia from insulin ⦁ sodium bicarb - not given unless metabolic acidosis also present ⦁ beta-2 adrenergic agonists ⦁ resins -binds K in GI tract for excretion (kayexalate = sodium polystyrene sulfonate) ⦁ severe cases = dialysis Rapid acting therapies (calcium gluconate, insulin and glucose, β2-adrenergic agonists) are indicated in patients with ECG changes, or those with serum potassium greater than 7 meq/L. Calcium gluconate is used in cases of hyperkalemia because it antagonizes the effect of potassium on the myocyte cell membrane Calcium gluconate or chloride, followed by measures to reduce serum K+ levels, is the immediate treatment to stabilize cardiomyocytes and reduce the risk of arrythmias when hyperkalemia is present ex: if patient on lisinopril and have hyperkalemia = likely developed hyperkalemia due to lisinopril, due to reduction in aldosterone

Answer 3

⦁ A cervical spine MRI scan is the definitive way to diagnose and clear a cervical spine injury on patients of all ages MRI allows for clear visualization of the ligaments, intervertebral disc spaces, spinal cord, and bones. o When a patient presents with a cervical injury, protecting the area with a cervical collar is important in order to maintain spinal alignment and prevent further injury o it is difficult to clinically clear the cervical spine if patient is ⦁ young ⦁ unable to communicate ⦁ unconscious o Obtaining a cervical spine X-ray should be the initial course of action to determine whether or not there is movement between the bones o An X-ray, however, is unable to visualize the spinal cord and ligaments o A CT scan of the cervical spine would be the next ideal imaging technique, but this is best to further investigate the bones and not the ligaments or spinal cord o To determine injury to the spinal cord or ligaments, determine the presence of hemorrhage or edema, and to evaluate the intervertebral disc spaces, an MRI of the cervical spine provides the most amount of information and therefore is the best tool to definitively clear the cervical spine before cervical collar removal. Clinical clearance is a useful technique to clear the cervical collar, but should be reserved for patients who are conscious, able to appropriately provide information, and respond appropriately. Young children should not be expected to adequately answer questions or perform instructed movements and therefore clinically clearing a cervical spine is not appropriate in a young and unconscious patient A cervical spine CT scan is a good technique to evaluate bony injury of the cervical spine, but because it is not an adequate test to evaluate the ligaments and spinal canal, it cannot be used as the definitive test to clear the cervical spine - If plain X-rays are inconclusive or if there is a high suspicion for fracture despite negative X-rays, a CT scan of the cervical spine should then be performed for further evaluation. Cervical spine radiographs are the INITIAL test to determine the presence of a bony injury in a patient suspected of a cervical spine injury, but cannot be the definitive test to clear the cervical spine in a patient with a poor neurologic examination. Even if xray is negative for a bony process, the cervical collar should not be removed until further investigation of the spinal ligaments and spinal cord have occurred

Answer 4

Bilateral facet dislocation is an unstable injury that occurs from ** FORCEFUL HYPERFLEXION OF THE NECK *** Mechanism = Forced Hyperflexion - It occurs when the articular masses of one vertebra dislocate anteriorly and superiorly from the articular surface of the vertebra below it causing anterior displacement of the spine - This injury involves forceful disruption of multiple structures at the level of the injury, including all ligamentous structures, the articular facet joints, and the intervertebral disc This is commonly associated with a COMPLETE SPINAL CORD INJURY due to TRANSECTION of the cord at the level of the injury. DIAGNOSIS ⦁ XRAY - displacement of superior vertebral body anteriorly more than 1/2 of its width - Lateral view = best SYMPTOMS ⦁ severe neurological sequelae ⦁ Loss of all motor and sensory function**

Answer 5

Prognosis = poor Most commonly results from interruption of the anterior spinal artery, resulting in damage to the anterior two-thirds of the cord with sparing of the dorsal columns syndrome caused by ischemia of the anterior spinal artery, resulting in loss of function of the anterior two-thirds of the spinal cord. PATHOPHYSIOLOGY ⦁ The posterior columns carry tracts responsible for ipsilateral position and vibratory sensation ⦁ The lateral spinothalamic tract carries fibers for contralateral pain and temperature ⦁ The lateral corticospinal tract is responsible for ipsilateral motor function Syndromes may be incomplete depending on how much of the cord is affected by the injury In the anterior spinal cord syndrome, just the posterior columns are preserved and so patients lose all pain and temperature sensation as well as motor function ⦁ loss of all motor function ⦁ loss of pain sensation ⦁ loss of temperature sensation ⦁ still have position + vibratory sensation CAUSES ⦁ Most cases of anterior cord syndrome follow ** AORTIC SURGERY ** but it has also been reported in the setting of ⦁ hypotension ⦁ infection ⦁ vasospasm ⦁ anterior spinal artery ischemia or infarct ⦁ In trauma, typically hyperflexion of the cervical spine causes the injury to the spinal cord. SUMMARY Anterior Cord Syndrome o PE will show loss of motor, pain, and temperature below injury o Most commonly caused by flexion injury o Comments: proprioception and vibration intact

Answer 6

Prognosis = average Mechanism = Forced Hyperextension SYMPTOMS ⦁ ** Upper greater than lower motor weakness **

Answer 7

Prognosis = good Mechanism = penetrating trauma SIGNS / SYMPTOMS ⦁ results in weakness or paralysis (hemiparaplegia) on one side of the body and a loss of sensation (hemianesthesia) on the opposite side Ipsilateral loss of Proprioception and Vibration + Paralysis (hIP ViP and walk with a Limp) loss of all sensation at level of lesion Below level of lesion = spastic paralysis and positive ipsilateral Babinski Contralateral loss of Temperature and Pain (ConTemplate the Pain I make) Brown-Séquard Syndrome Patient with a history of penetrating trauma PE will show ipsilateral loss of motor, position and vibration and contralateral loss of pain and temperature Most commonly caused by spinal cord hemisection

Answer 8

Beta adrenergic antagonists, more commonly referred to as beta-blockers, inhibit beta-adrenoceptors They are used in the treatment of a number of disorders including hypertension, heart failure, arrhythmias, ischemic heart disease, migraine headaches, tremor, aortic dissection and portal hypertension Beta-blockers competitively inhibit epinephrine and norepinephrine, which results in the blunting of multiple metabolic and cardiovascular effects normally regulated by these circulating catecholamines. Both the beta-blockade and the differing properties of toxicity among beta-blocking agents have influence on the adverse cardiovascular effects. Beta-blocker poisoning should be considered when patients present with overdose of an unknown medication. The most commonly seen clinical manifestations of beta-blocker overdose include ⦁ hypotension ⦁ bradycardia DIAGNOSIS - history + PE - Labs = hypoglycemia** - EKG = Bradycardia, PR and QRS prolongation. After stabilization in the emergency department, patients with a beta-blocker overdose who have altered mental status or hemodynamic instability should be admitted to the critical care unit for cardiac monitoring and management TREATMENT ⦁ glucagon + insulin

Answer 9

dry socket, also known as acute alveolar osteitis Patients undergo dental extraction and after the procedure a hemostatic blood clot forms in the socket Pain is common for 24 hours post-procedure and then improves When the healing blood clot is lost from the socket, the patient develops acute severe pain Most commonly, EXCRUTIATING PAIN occurs 3-5 days after the extraction and is associated with a foul odor Pain is related to inflammation and a localized infection of the bone EXAM = Exposed bone and no clot in extraction site Treatment includes packing the open socket with iodoform gauze. The gauze is saturated with either a medicated dental paste or eugenol (oil of cloves) Patients will require analgesia and may benefit from a nerve block. Alveolar Osteitis (Dry Socket) Patient will be 3 - 5 days post extraction PE will show inflammation and local osteomyelitis with a clean extraction site Most commonly caused by loss of healing clot Treatment is pack socket with iodoform gauze and eugenol oil

Answer 10

TRUE EMERGENCY!!!! - Inflammation of the epiglottis => can interfere with breathing * **MC CAUSE = HIB (haemophilus influenza B)*** - gram negative rod - has been a decrease in incidence due to vaccination ``` - other causes ⦁ strep pneumo* ⦁ staph aureus ⦁ GABHS ⦁ strep agelectiae ⦁ strep pyogenes ⦁ M. cat ``` Non-HIB seen more commonly in adults (esp crack, cocaine use) MC in children 3 months - 6 years* Males = 2X more common DM = risk factor generally sudden in onset (acute) SYMPTOMS ⦁ ****DROOLING**** ⦁ ****MUFFLED, HOT POTATO VOICE***** 3 D's = DYSPHAGIA, DROOLING, DISTRESS ⦁ fever ⦁ odynophagia (difficulty / painful swallowing) ⦁ inspiratory stridor (also with croup) ⦁ dyspnea ⦁ hoarseness ****often in TRIPOD POSITION - leaning forward**** Patients sit with neck hyperextended and chin protruding (sniffing dog position) DO NOT EXAMINE THE PATIENT - could cause spasm BE PREPARED TO INTUBATE - do not give IV ABX prior to intubation, as this could also cause spasm DIAGNOSIS ⦁ *** LARYNGOSCOPY *** = definitive diagnosis - provides direct visualization, however, could induce bronchospasm! ⦁ ***LATERAL NECK XRAY - STAT - THUMBPRINT SIGN*** TREATMENT Secure airway - call anesthesiology and prepare to establish airway, transfer to OR to perform exam - tracheostomy if necessary to maintain airway ⦁ maintain airway + supportive management = place child in comfortable position and keep them calm. Admit for observation ==> humidified O2, IV antibiotics (ceftriaxone + clindamycin), and IV corticosteroids ⦁ Dexamethasone to decrease airway edema, and be prepared to intubate ⦁ IV ABX = Ceftriaxone (most likely HIB) or Vanco for anti-staph - call ID specialist for regional coverage/most likely etiology EX: Your patient is a 45 year old male that is not immunized. He presents with a fever of 102, dysphagia, drooling, and shortness of breath. Lungs are clear. O2 Sat 100%. Pulse 102. RR-24. Soft tissue neck reveals a thumb sign. All of the following are acceptable management plans except: A Give a Racemic Epinephrine aerosol treatment and discharge the patient home on steroids = NO B Begin Vancomycin and Ceftriaxone C Intubate the patient in the operation room D Consult anesthesia or ENT Question 36 Explanation: In the treatment of epiglottitis racemic epinephrine can help momentarily, but ultimately the patient needs to be intubated and admitted to the hospital. Airway protection is the mainstay of treatment. The patient usually needs to be intubated for 2-3 days prior to weaning attempts. The role of steroids is controversial. Vancomycin helps with anti-staph coverage and Ceftriaxone covers the most common organism haemophilus influenza type B. Anesthesia and/ or ENT should be consulted for airway management. Patient will present as → a 3-year-old who is brought into the emergency room by her parents. The child has had a high fever, sore throat, and stridor. She has a muffled voice and is sitting up on the stretcher drooling while leaning forward with her neck extended. The patients parents are adamantly against vaccinations, claiming that they are a "government conspiracy." You order a lateral neck x-ray, which shows a swollen epiglottis.

Answer 11

``` Anterior fat pad = “sail sign” and Posterior fat pad = Radial head fracture in adults (even if not seen on xray) ``` and Supracondylar fracture in children

Answer 12

``` Anterior fat pad = “sail sign” and Posterior fat pad = Radial head fracture in adults (even if not seen on xray) ``` Patient will be an adult with a history of fall on an outstretched hand (FOOSH) PE will show localized swelling, tenderness, and decreased motion X-ray will show fat pad ‘sail sign’ fat pads = Supracondylar fracture in children

Answer 13

⦁ respiratory depression / hypoventilation ⦁ sedation ⦁ miosis normal pupil size = between 2-5mm Signs of more severe toxicity can include ⦁ bradycardia ⦁ hypotension ⦁ hypothermia Methadone has been associated with a ⦁ prolonged QT interval ⦁ risk of torsades de pointes TREATMENT = NALOXONE (NARCAN)

Answer 14

Acetaminophen is commonly present in the home, which can be unintentionally ingested by young children. The initial signs of acetaminophen toxicity are nonspecific such as nausea and vomiting, which is usually followed by an asymptomatic period. Any child with a history of acute ingestion of greater than 200 mg/kg should be referred to a healthcare facility. If a toxic ingestion is suspected, a serum acetaminophen level should be calculated 4 hours after the reported time of ingestion. ⦁ Toxicity = 150 mcg/mL. For patients who present to medical care more than four hours after ingestion, a stat acetaminophen level should be obtained. Acetaminophen levels obtained < 4 hours after ingestion are difficult to interpret and cannot be used to estimate the potential for toxicity. The serum acetaminophen level is then plotted on the Rumack-Matthew nomogram and any level that is in the possible or probable hepatotoxicity range should then be treated with N-acetylcysteine. gastric lavage + ipecac = no longer used due to risk of aspiration SYMPTOMS ⦁ < 24 hours = N / V / D + anorexia = phase I ⦁ 1-3 days = RUQ pain, elevated AST / ALT, elevated INR, elevated bilirubin (phase II) ⦁ 3-4 days = multiorgan failure / jaundice, coma, death (phase III) ⦁ 4 days - 2 weeks = complete resolution of hepatic dysfunction (phase IV)

Answer 15

- occurs when an embolus (type of blockage - either blood, fat, air, amniotic fluid, bacteria, tumors) suddenly gets lodged inside a pulmonary artery FAT BAT = fat, air, thrombus, bacteria, amniotic fluid, tumors - also can occur from changing central venous lines - to prevent infection, but can cause clot to dislodge - depending on which pulmonary artery or arteries are affected by the embolus, this can decrease the amount of oxygenated blood that gets to the body Most people who die from PE die from subsequent PEs, not their first one PATHOPHYSIOLOGY 1) network of veins bring blood from the body back to the heart via SVC and IVC 2) superficial veins drain into deep veins, which rely on the skeletal muscle pump compress veins and propel blood in legs to move blood forward, one-way valves prevent backflow 3) SVC / IVC --> RA --> RV --> Pulmonary arteries --> lungs - the pulmonary arteries split at the * ** PULMONARY SADDLE *** --> R + L lungs - R + L pulmonary arteries branch further into smaller and smaller arteries --> arterioles --> capillaries 4) The capillaries form networks around alveoli = where gas exchange occurs in lungs 5) an embolus at any of these arteries blocks blood from flowing to lung tissue downstream, and also blocks blood from picking up enough oxygen 6) If no blood flowing past an alveoli ==> alveoli are being ventilated with fresh air, but are not getting perfused with blood - getting oxygen to the alveoli, but no blood to pick up that oxygen = **** VENTILATION PERFUSION MISMATCH **** = V / Q MISMATCH - the body needs oxygen to function, and can therefore only tolerate a small amount of V/Q mismatch before the lungs are no longer able to meet the needs of the body V/Q mismatch depends on the NUMBER, SIZE, + LOCATION of the PE V/Q mismatch essentially tells us the amount of lung tissue that is being denied blood flow ``` ⦁ *** MC CAUSE OF PE = DVT *** o Virchow's Triad ⦁ venous stasis ⦁ hypercoagulability ⦁ damage to vessel endothelium ``` MC location for DVT = left iliofemoral vein Air emboli are associated with scuba divers who ascend quickly from deep depths. Also trauma, surgery, being on a ventilator, and scuba diving Patients who are pregnant can present with an amniotic fluid embolism which is a type of pulmonary embolism that can lead to disseminated intravascular coagulation. Fat emboli are associated with long bone fractures and liposuction; they usually present with the classic triad of hypoxemia, neurologic abnormalities, and petechial rash. ``` RISK FACTORS FOR PE ⦁ smoking ⦁ cancer ⦁ pregnancy ⦁ OCP ⦁ surgery ⦁ infection ⦁ immobilization - long plane / car rides / bed-ridden ⦁ obesity ``` patients who undergo c-section are 3-5x more likely to develop a DVT than a patient with a vaginal delivery. SIGNS / SYMPTOMS OF PE - small PE may not cause any symptoms - large PE can cause sudden / severe symptoms like ⦁ SOB / dyspnea = MC symptom ⦁ chest pain ⦁ fatigue ⦁ hemoptysis ⦁ tachycardia ⦁ tachypnea = * MC sign */ hyperventilation ⦁ hypoxia ⦁ pleuritic chest pain - pain worsens when breathing ⦁ sudden death if PE at pulmonary saddle (blocking blood flow access to both lungs = no oxygen supply whatsoever) - may hear crackles (rales) - JVD - Homan's sign = indicative of DVT = pain with dorsiflexion Classic presentation = post-op patient with sudden tachypnea, tachycardia, with cough or hemoptysis ⦁ hyperventilation (attempt to get more oxygen, despite that fact that problem is blood flow) ==> rapid release of CO2 ==> RESPIRATORY ALKALOSIS (elevated blood pH) If someone has a PE = important to check for ASD (atrial septal defect) - as clot can travel to brain If multiple PEs occur over time = can lead to *** PULMONARY HYPERTENSION *** and *** RIGHT VENTRICULAR FAILURE *** as more pressure is required to move blood past obstructed arteries If massive PE: syncope, hypotension, PEA ** Factor V Leiden = MC predisposing condition ** DIAGNOSIS ⦁ best initial test = Helical CT scan ⦁ ** CT pulmonary Angiography ** = gold standard test = dye injected into vessels to identify blockages ⦁ V/Q scan = reveals areas of the lungs that are ventilated but are not being perfused with blood - use if patient in renal failure, contrast allergy, or pregnant ⦁ EKG = tachycardia + S1Q3T3 (rare) - shows ST segment changes ⦁ CXR = *** Westermark sign *** = avascular markings or *** Hampton's Hump *** = triangular or rounded pleural-based infiltrate usually located adjacent to the hilum - normal CXR = MC finding in PE LABS ⦁ D-dimer = helps to rule out PE = plasmin breaks down fibrin into d-dimer - only get this test if likelihood of PE is LOW ⦁ ABG will show respiratory alkalosis secondary to hyperventilation TREATMENT - some small clots resolve on their own - larger clots typically need intervention ⦁ 1) LMWH (SQ) or IV heparin anticoagulant LMWH - Lovenox / Enoxaparin potentiates antithrombin III - SQ injection. Compliant, low-risk patients can be discharged home during bridging therapy - duration of action = about 12 hours - don't need to monitor PTT - antidote = protamine sulfate, but not as effective as with UFH - lower risk of HIT - CI = renal failure (Cr > 2.0) - because LMWH is excreted by kidneys... and thrombocytopenia IV UFH potentiates antithrombin III + inhibits thrombin / other coagulation factors - continuous IV drip - requires hospitalization for bridging therapy - duration of action = 1 hour after IV drip discontinued - must monitor PTT to 1.5 - 2.5x normal value - antidote = protamine sulfate - risk of HIT - INR between 2.0 - 3.0 = considered therapeutic; when reached INR of 2-3 = add LMWH or Coumadin - discharged on PO Coumadin (Warfarin) x 3-6 months after - warfarin = inhibits vitamin K dependent coagulation factors (2, 7, 9, 10 = extrinsic pathway) - should be overlapped with heparin for at least 5 days - Adjust the warfarin dose to maintain a target INR of 2-3 for at least 24 hours ⦁ thrombolytics (Altepase) = only if hemodynamically unstable = give if acute PE + Hypotension definite CI = CVA or internal bleed within 2 months relative CI = uncontrolled HTN, surgery / trauma within 6 weeks ⦁ pulmonary thrombectomy - surgically remove clot = reserved for patients with CI to thrombolytics or ineffective thrombolytics PREVENTION ⦁ anticoagulant therapy (warfarin / heparin) - inhibit clotting cascade ⦁ IVC filter = helpful in patients at high risk of recurrence who are unable to tolerate anticoagulants ⦁ compression stockings ⦁ frequent calf exercises ⦁ early ambulation

Answer 16

⦁ clinical signs/symptoms of DVT = 3 points ⦁ PE = most likely diagnosis = 3 points ⦁ tachycardia = 1.5 points ⦁ immobility > 3 days = 1.5 points ⦁ previous hx of DVT or PE = 1.5 points ⦁ hemoptysis = 1 point ⦁ malignancy = 1 point ``` CLINICAL SIGNS / SYMPTOMS OF DVT o swelling of leg o redness / discoloration o pain / tenderness of leg o increased warmth ``` > 6 = high probability of PE 2-6 = moderate probability < 2 = low probability

Answer 17

``` ⦁ Age < 50 ⦁ Pulse < 100 ⦁ O2 > 95% ⦁ No prior PE ⦁ no recent trauma or surgery ⦁ no hemoptysis ⦁ no use of exogenous estrogen ⦁ no unilateral leg swelling ```

Answer 18

⦁ intracranial hemorrhage ⦁ stroke or head trauma within the past 3 months ⦁ blood pressures >185 mm Hg systolic or >110 mm Hg diastolic ⦁ active bleeding ⦁ known arteriovenous malformation

Answer 19

- occurs more with uncontrolled type I DM, but can occur with type II DM as well ``` - DKA is a result of INSULIN DEFICIENCY and counterregulatory hormonal excess in diabetics as a direct response to stressful triggers: o ** INFECTION = MC ** o Infarction o Noncompliance with insulin / dosage o undiagnosed diabetes ``` Cortisol = hormone released with stress --> increases glucose levels - these patients are unable to meet the demand of increased insulin requirements in response to hyperglycemia, especially during stress DKA vs HHS - DKA = presence of ketoacidosis - HHS = severity of hyperglycemia - DKA tends to occur in younger patients with type I - HHS tends to occur in older patients with type II DM PATHOPHYSIOLOGY - insulin deficiency --> 1) hyperglycemia 2) dehydration 3) ketonemia (high anion gap metabolic acidosis) 4) potassium deficit (false hyperkalemia) DKA usually occurs in type I DM but can occur in type II 1) If cells are starved for energy due to lack of glucose, Adipose tissue starts to break down fat to convert into glucose (lipolysis) --> weight loss 2) Fat is broken down into free FATTY ACIDS 3) Liver converts fatty acids into KETONE BODIES ⦁ Acetoacetic acid (keto-acid) ⦁ Beta-hydroxybutyric acid (technically not an acid, but a reduced ketone) - These ketone bodies can be used by cells for energy, but they also increase the acidity of the blood* which can have major effects throughout the body SYMPTOMS ⦁ Kussmaul respirations - deep / labored breathing as body tries to move CO2 out of the body to decrease acidity of blood (increase pH) ⦁ False hyperkalemia (due to H/K pump that brings more H+ ions into cells to reduce acidity of blood in exchange for K+ ions being moved out of cells into blood) - Insulin stimulates Na / K pumps so that more K+ enters cells and more Na+ leaves cells. Without insulin, more K+ stays outside of cells ==> also leads to hyperkalemia***** - so while there is excess K+ in the blood, the OVERALL STORES of K+ are low ⦁ High Anion Gap - a large difference in the positive and negative ions in the serum - largely due to buildup of ketoacids (as well as K+) - formula = Na - (Cl + HCO3) (K not included) - normal anion gap = 8-16 - A high anion gap value means that your blood is more acidic than normal. It may indicate that you have acidosis DKA can occur in people who have already been diagnosed with DM and are currently on insulin In states of stress, such as infection, body releases epinephrine --> stimulates release of glucagon --> elevates blood sugars --> hyperglycemia --> polyuria / polydipsia / glycosuria / polyphagia --> need for alternate source of energy --> fat breakdown --> ketoacidosis ⦁ Acetone - fruity smelling breath - both ketone bodies break down into acetone - acetone is excreted via exhalation out the lungs - causes fruity breath ⦁ Nausea / Vomiting ⦁ Mental status changes ⦁ can cause acute cerebral edema ``` SIGNS / SYMPTOMS OF DKA ⦁ hyperglycemia ⦁ polyuria ⦁ polydipsia ⦁ nocturia ⦁ weakness / fatigue ⦁ confusion ⦁ N / V ⦁ may have chest pain ⦁ may have abdominal pain - more in children ⦁ mental status changes / delirium ⦁ weight loss in hx if never been diagnosed with DM I ``` PHYSICAL EXAM OF HHS ⦁ tachycardia ⦁ tachypnea ⦁ hypotension - if dehydrated ⦁ fever if infection was cause ⦁ decreased skin turgor (dehydration) ⦁ *** KUSSMAUL RESPIRATIONS *** - deep continuous respirations as lungs attempt to blow off excess CO2 to reduce acidosis) ⦁ *** KETOTIC BREATH *** - fruity breath with acetone ``` DIAGNOSIS ⦁ blood glucose level > 250 - (then start testing ketones) ⦁ ABGs or VBGs (arterial or venous blood gases) - acidic pH (low): < 7.30 = DKA o 7.25 - 7.29 = mild DKA o 7.0 - 7.24 = moderate DKA o < 7.0 = severe DKA - low bicarb levels (normal = 22-30): < 18 = DKA o 15-18 = mild DKA o 10-14 = moderate DKA o < 10 = severe DKA - shows metabolic acidosis ⦁ Ketones = positive (what distinguishes between DKA and HHS) ⦁ UA ⦁ CMP - anion gap - shows metabolic acidosis (excess H+, decreased bicarb) ``` *** Ketone levels are what distinguishes between DKA and HHS *** TREATMENT 1) *** FLUIDS *** - for dehydration = IV NS (then see hypokalemia) - once hypotension resolves = can be switched to 1/2 NS - when glucose levels reach 250 = then reduce to D5 1/2 NS to prevent hypoglycemia from insulin 2) Insulin to lower blood glucose - do not over-administer insulin and cause hypoglycemia 3) Electrolytes (K+) 4) Glucose - monitor glucose level with insulin drip, make sure patient doesn't become hypoglycemic Lowering of the blood glucose level too fast is thought to predispose to cerebral edema - To minimize risk of cerebral edema, lowering of the blood glucose level should be done no faster than 80mg/dl/hour - treat any infection / stress that may have caused DKA - monitor venous pH to make sure acidosis resolves - monitor bicarb levels (not typically replaced, as will usually gradually improve with stabilizing) Diabetic ketoacidosis (DKA) should always be handled in a hospitalized setting, usually an ICU, and often with an endocrinologist’s consultation, if appropriate.

Answer 20

``` - HHS is a result of INSULIN DEFICIENCY and counterregulatory hormonal excess in diabetics as a direct response to stressful triggers: o ** INFECTION = MC ** o Infarction o Noncompliance with insulin / dosage o undiagnosed diabetes ``` Cortisol = hormone released with stress --> increases glucose levels - these patients are unable to meet the demand of increased insulin requirements in response to hyperglycemia, especially during stress DKA vs HHS - DKA = presence of ketoacidosis - HHS = severity of hyperglycemia - DKA tends to occur in younger patients with type I - HHS tends to occur in older patients with type II DM PATHOPHYSIOLOGY OF HHS - usually occurs in type II DM with some illness that leads to REDUCED FLUID INTAKE - *** MC = INFECTION *** 1) hyperglycemia + dehydration + increased osmolarity 2) potassium deficit (false hyperkalemia) 3) absence of severe ketosis (as type II DM make enough insulin to prevent ketogenesis usually) ``` SIGNS / SYMPTOMS OF HHS ⦁ hyperglycemia ⦁ polyuria ⦁ polydipsia ⦁ nocturia ⦁ weakness / fatigue ⦁ confusion ⦁ N / V ⦁ may have chest pain ⦁ mental status changes / delirium ``` ``` PHYSICAL EXAM OF HHS ⦁ tachycardia ⦁ tachypnea ⦁ hypotension ⦁ fever if infection was cause ⦁ decreased skin turgor (dehydration) ``` DIAGNOSIS ⦁ blood glucose level > 600 ⦁ ABGs or VBGs (arterial or venous blood gases) - pH > 7.30 (whereas DKA = pH < 7.30) - low bicarb levels (normal = 22-30): > 15 = HHS o 15-18 = mild DKA o 10-14 = moderate DKA o < 10 = severe DKA (so if serum bicarb is 16+ = could be HHS or mild DKA) - shows metabolic acidosis ⦁ Ketones = small (what distinguishes between DKA and HHS) ⦁ Serum Osmolarity** = > 320 ⦁ UA ⦁ CMP - anion gap - shows metabolic acidosis (excess H+, decreased bicarb) TREATMENT 1) *** FLUIDS *** - for dehydration = IV NS (then see hypokalemia) - once hypotension resolves = can be switched to 1/2 NS - when glucose levels reach 250 = then reduce to D5 1/2 NS to prevent hypoglycemia from insulin 2) Insulin to lower blood glucose - do not over-administer insulin and cause hypoglycemia 3) Potassium - despite hyperkalemia, patient is total body potassium deficient, so correction of DKA will cause hypokalemia - first verify renal output ⦁ 20-40 mEq/L if potassium is low / normal (K < 5.5) ⦁ if K > 5.5, hold repletion until serum K+ falls into normal range and then start repletion 4) Glucose - monitor glucose level with insulin drip, make sure patient doesn't become hypoglycemic 5) Bicarbonate = only given in severe acidosis (pH < 7, Bicarb < 10) - acidosis usually resolves with IV fluids + insulin - Bicarb is associated with many complications (increased rate of cerebral edema) Lowering of the blood glucose level too fast is thought to predispose to cerebral edema - To minimize risk of cerebral edema, lowering of the blood glucose level should be done no faster than 80mg/dl/hour - treat any infection / stress that may have caused HHS - monitor venous pH to make sure acidosis resolves - monitor bicarb levels (not typically replaced, as will usually gradually improve with stabilizing) HHS should always be handled in a hospitalized setting, usually an ICU, and often with an endocrinologist’s consultation, if appropriate.

Answer 21

⦁ oligomenorrhea = cycle > 35 days ⦁ polymenorrhea = cycle < 21 days ⦁ hypomenorrhea = scanty menstruation ⦁ amenorrhea = absence of menses x 6 months ⦁ menorrhagia = regular cycles, but excessive flow + excessive duration ⦁ metrorrhagia = irregular cycles - light uterine bleeding at irregular times ⦁ menometrorrhagia = irregular cycles + excessive flow

Answer 22

Aortic dissection = where part of the tunica intima (innermost layer of blood vessel) of the aorta, is RIPPED OFF - a TEAR in the tunica intima forms, and the high pressure blood flowing through the aorta begins to tunnel between the tunica intima and tunica media, separating the two layers - high pressure blood continues to tear through between the layers - blood continues to pool, enlarging the vessel diameter "FALSE LUMEN" = the area where blood collects CAUSES OF AORTIC DISSECTION In order for aortic dissection to occur, an underlying condition must be present that has weakened the aorta's wall ⦁ chronic HTN = MC - which is why it most often occurs in aorta - from stress - from increased blood volume (ex: pregnancy) - from coarctation of artery (narrowing) ⦁ weakened aortic wall - Ehler's Danlos (CT disorder) - Marfan's (CT disorder) - fibrillin - Loeys-Dietz syndrome (CT disorder - bifid uvula) - decreased blood flow to vasa vasorum ⦁ aortic aneurysms ---> can cause dissections - dissections can also cause aneurysms MC location for aortic dissection = first 10cm of aorta - closest to the heart o Stanford Type A dissection = involves proximal aorta - Aortic dissection commonly occurs in the proximal aorta, because this is the area of the aorta that is under the most stress. o Stanford Type B dissection = involves distal aorta = is often less fatal compared to other types COMPLICATIONS OF AORTIC DISSECTION - depends on where the blood in the false lumen flows ⦁ blood could flow back up the aorta to the heart into pericardial space and cause * **PERICARDIAL TAMPONADE*** = potentially fatal - causes Equalization of the pressures within the heart - When the pericardial fluid pressure exceeds that within ventricles, the ventricles are no longer able to fill appropriately, and the pressures within the four chambers of the heart equilibrate. This leads to decreased cardiac output and, ultimately, death if a prompt pericardiocentesis is not performed - Signs of cardiac tamponade include a raised jugular venous pressure, hypotension, and pulsus paradoxus. ⦁ blood flowing through false lumen could burst through tunica media + externa - RUPTURE and could bleed into mediastinum - potentially fatal - rapid blood loss ⦁ blood flowing through false lumen could puncture back through tunica intima further down = not great, but could be worse ⦁ ** blood could continue to rip through tunica intima until it reaches another large artery that branches off the aorta, such as subclavian arteries or renal arteries - false lumen could compress these arteries --> decreased blood flow to kidneys / arms / wherever SYMPTOMS ⦁ sharp TEARING chest pain -> often radiates to back ⦁ weak / decreased peripheral pulses (such as radial, carotid, brachial or femoral arteries) ⦁ *** may have differences in blood pressure between right and left arm *** ⦁ hypertension (MC) or hypotension ⦁ tachycardia ⦁ lightheaded / dizzy ⦁ N / V ⦁ diaphoresis ⦁ can lead to shock if significant blood loss from rupture - may have aortic regurgitation (diastolic crescendo-decrescendo), acute MI, or cardiac tamponade o anterior chest pain = more ascending aorta (A) o aortic arch --> neck / jaw pain o interscapular pain = more descending aorta (B) Measuring blood pressure in both arms is a quick clinical method to detect thoracic aortic dissection. AORTIC DISSECTION IS AN EMERGENCY An aortic dissection is considered a medical emergency due to the high risk of life-threatening complications such as cardiac tamponade, aortic regurgitation, and myocardial infarction. A hypertensive emergency may be characterized by organ damage, such as an aortic dissection. DIAGNOSIS ⦁ CT with contrast = rapidly becoming test of choice, especially in the ER ⦁ Angiography = gold standard / definitive *** CT Angiography *** = looks closely at blood vessels ⦁ TEE (transesophageal echo) - ultrasound probe goes through esophagus to get clear view of aorta = best initial test if hemodynamically unstable ⦁ CXR - widened aorta or widened mediastinum CT or MRI with angiography = gold standard for diagnosing an aortic dissection If patient cannot be injected with dye due to impaired renal function or allergy = MRI* = would be done after patient has been stabilized MRI has very high specificity and sensitivity for the detection of aortic dissection and is commonly used as a gold standard for diagnosing the condition in the patient who cannot tolerate IV contrast because of renal insufficiency TREATMENT ⦁ Stanford Type A dissection (Debakey I + II) = SURGERY - removal of as much of dissected aorta as possible, then block re--entry of blood into aorta wall - wall is reconstructed with synthetic graft - sometimes a stent is placed to prop open graft ALL ascending aortic dissections should be managed with surgery; however, surgery is only indicated for descending dissections when there is evidence of end-organ damage. ⦁ BP medication - Beta blockers*** - Esmolol, Labetalol, Propranolol - Stanford type B dissection (Debakey III) = FIRST TREATED WITH BETA BLOCKERS, then vasodilators - then give nitro if needed - can use CCB (Nicardipine) if can't take BB If the hypertension is refractory to the β-blocker, nitroprusside may be used to further lower systolic blood pressure. CCB like verapamil are used if the patient cannot tolerate β-blocker

Answer 23

a condition in which damaged skeletal striated muscle breaks down rapidly - acute breakdown + necrosis of skeletal muscle Breakdown products of damaged muscle cells are released into the bloodstream some of these breakdown products, such as the protein MYOGLOBIN, are harmful to the kidneys and may lead to kidney failure - myoglobin can also block conduits for urine release The damaged muscle then becomes a reservoir for fluid, causing dehydration and further insult to the kidneys Myoglobin can become lodged in the renal tubules --> obstruction --> can cause acute tubular necrosis, leading to acute kidney injury (which can lead to hyperkalemia) and increasing creatinine and BUN. - Myoglobin, CK, LDH, K+, PO4, urate, etc all released with muscle breakdown - hyperkalemia can lead to cardiac arrhythmias / arrest ``` CAUSES OF RHABDOMYOLYSIS ⦁ crush / blunt injury or trauma = MC ⦁ immobility ⦁ medications = statins (MC), fibrates, salicylates ⦁ strenuous exercise / weight-lifting ⦁ drug / alcohol abuse ⦁ infections ⦁ ischemia ⦁ electrocution ⦁ hyperthermia ⦁ seizures ⦁ burns ``` * * Rhabdomyolysis is an adverse effect of STATINS when administered with FIBRATES + NIACIN - statin alone, or fibrate alone may cause it too, but the combination is most likely Statins can inhibit the electron transport chain, causing destruction of myocytes and leading to rhabdomyolysis When there is no history of extreme exertion, alcohol consumption, or trauma, HYPERTHERMIA is a cause of muscle weakness. Geriatric population is more susceptible to heat stroke and is related to reduced mobility, capacity for independent living, compromised end organ function (e.g. renal, hepatic), or abuse by neglect (leading to inadequate hydration, among others). Hereditary muscle condition increases risk of rhabdomyolysis. ``` SYMPTOMS ⦁ severe muscle pains - usually proximal muscles ⦁ muscle weakness ⦁ vomiting ⦁ confusion ⦁ red / brown colored urine ⦁ muscle tenderness to palpation ``` CLASSIC TRIAD o Myalgia + generalized weakness + dark urine Moderate to severe rhabdomyolysis may present with red -brown colored urine due to myoglobin in the urine severity depends on the extent of muscle damage and renal impairment DIAGNOSIS ⦁ elevated creatine kinase (CPK or CK) = best marker for rhabdomyolysis - (normal = 10-120 mcg/L), rhabdo = CPK in thousands - normal = < 200; CK > 1000 = indicative of rhabdo - CK > 5000 = should check for other complications, such as AKI, hyperkalemia, and DIC ⦁ may have elevated LDH (tissue damage) ⦁ elevated AST / LFTs (nothing actually wrong with liver; proteins / enzymes found in the liver are also found in skeletal muscle) ⦁ renal dysfunction = increased creatinine, BUN ⦁ hyperkalemia (intracellular K+ released from damaged muscle) ⦁ hypocalcemia (calcium binds to damaged muscle, also binds to phosphate that is released from muscle) ⦁ UA - myoglobin shows up positive for blood (+ for heme, but - for blood) - blood + - protein + ⦁ may do EKG - signs of hyperkalemia / arrhythmias TREATMENT ⦁ IV fluids - start quickly after a diagnosis of rhabdomyolysis to prevent further kidney injury (4-6L/day) ⦁ Mannitol = induce osmotic diuresis ⦁ Bicarbonate = alkalinize the urine ⦁ calcium gluconate if hyperkalemia with significant EKG changes ⦁ dialysis or hemofiltration if severe / already have renal dysfunction ``` COMPLICATION ⦁ Acute Kidney Injury ⦁ multi-organ failure ⦁ Hyperkalemia ⦁ DIC ```

Answer 24

In order for an ectopic pregnancy to take place: 1) egg is fertilized and is implanted somewhere other than the endometrium of the uterine cavity 2) must implant on a surface with enough rich blood supply to support a developing embryo ``` ECTOPIC PREGNANCIES CAN OCCUR ⦁ Fallopian Tube (MC) - the ampulla of fallopian tube = MC location in tube ⦁ Ovaries ⦁ Intestine ``` After implantation, the embryo starts developing the way it normally would in the uterine cavity OVER TIME, THE FOLLOWING CAN HAPPEN 1) tissue can no longer supply a sufficient blood supply for the embryo ==> eventually dies 2) if tissue can provide adequate blood supply, then hormones from the corpus luteum + placenta ==> missed menstrual period, nausea, breast enlargement (all symptoms seen in early pregnancy) If implantation was in ampulla of fallopian tube, the embryo eventually runs out of space ==> stretches the nerve fibers within the wall of fallopian tube ==> LOWER ABDOMINAL PAIN - can eventually rupture the fallopian tube A ruptured ectopic pregnancy can lead to: ⦁ massive hemorrhaging into abdominal cavity ⦁ blood can irritate the peritoneum, which can cause *** REFERRED PAIN TO SHOULDER *** ⦁ light vaginal bleeding Internal bleeding + severe pain + damage to fallopian tube ==> MEDICAL EMERGENCY CAUSE OF ECTOPIC PREGNANCY ⦁ unknown ``` RISK FACTORS ⦁ smoking ⦁ hx of PID ⦁ in-vitro fertilization ⦁ gynecologic surgery ⦁ current IUD ⦁ tubal ligation ⦁ previous hx of ectopic pregnancy ⦁ hx of infertility ⦁ gestational diabetes ⦁ DES exposure ``` Kartagener (primary ciliary dyskinesia) syndrome is a syndrome with immotile cilia due to a dynein arm defect that results in infertility and an increased risk of ectopic pregnancy. ``` SYMPTOMS ⦁ Amenorrhea ⦁ Abdominal / Pelvic pain ⦁ Vaginal bleeding ⦁ may have nausea / breast enlargement ⦁ may have fever ``` CLASSIC TRIAD of ectopic pregnancy = 1) abdominal pain 2) amenorrhea 3) vaginal bleeding Other symptoms of ectopic pregnancy may be related to early pregnancy (nausea, breast fullness, constipation) or symptoms of ectopic rupture (hemodynamic instability, dizziness or weakness, fever, vomiting, tachycardia, hypotension) which warrants urgent surgical treatment!! The major risk of ectopic pregnancy is severe hemorrhage, which can lead to hypovolemic shock, and eventually death. Typically develop pelvic pain around 6-8 weeks into pregnancy if implantation is in fallopian tube If implantation occurs where there is much more space available ==> pain and bleeding may not occur until several weeks later Ectopic pregnancy is often clinically mistaken for appendicitis as presenting symptoms of pain, nausea, and fever are shared between the two. A PSEUDOSAC is a collection of fluid within the endometrial cavity created by bleeding from the decidualized endometrium = is often associated with an ectopic pregnancy. PHYSICAL EXAM ⦁ may have palpable mass near uterus ⦁ abdominal tenderness - but these symptoms mimic a normal pregnancy - which can contribute to a delay in diagnosis DIAGNOSIS ⦁ first - patient needs to be hemodynamically stable = vital signs in normal range, no hypotension or tachycardia If hemodynamically unstable = IMMEDIATE SURGERY for both diagnosis + treatment If hemodynamically stable ⦁ first = urine pregnancy test ⦁ serial hcg testing = check to see that levels are doubling every 2 days = typical in an early pregnancy - Compared to a normal pregnancy, hcg is DECREASED in ectopic pregnancy ⦁ Transvaginal ULTRASOUND- to check for intrauterine pregnancy = visible by week 5-6 *** may see FREE FLUID in abdomen *** = blood = ruptured ectopic pregnancy Transvaginal ultrasound is safe and commonly performed during all stages of pregnancy, including the first trimester - The transabdominal ultrasound is not as sensitive for the detection of a gestation sac or fetal heartbeat compared with transvaginal ultrasound *** gestational sac should be visualized on transvaginal US when serum ßhCG levels reach 1,500-2,000 IU/L or when transabdominal US reaches 3600 mIU/ mL with abdominal ultrasonography.*** (4.5-5weeks) Ectopic = Beta HCG is > 1,500, but no fetus in utero A TUBAL RING is an echogenic, ringlike structure found outside of the uterus on ultrasonography, that represents an early ectopic pregnancy. "ring of fire" = doppler ultrasound If transvaginal ultrasonography does not show an intrauterine pregnancy when the β-hcg levels are reached, the pregnancy can be considered ectopic. TREATMENT o if patient is hemodynamically stable, diagnosed early, and hcg levels are already declining ⦁ may not need any additional treatments / procedures - can continue to monitor via serial hcg - if diagnosed later (≤ 8 weeks) + hemodynamically stable ⦁ Methotrexate IM - can be used to terminate the pregnancy MTX requires careful patient selection and is most successful in patients with a b-hCG is <5000 IU/L, and a gestational sac <3.5cm, and no pulmonary, renal or hepatic disease - monitor on days 0, 4, 7 (b-hcg should drop by 15%+ by day 4-7) Methotrexate is the standard medication used in the treatment of an unruptured ectopic pregnancy. Methotrexate is a folic acid analog that competitively inhibits dihydrofolate reductase and is used to treat ectopic pregnancy and medical abortion - if hemodynamically unstable = EMERGENT SURGERY! ⦁ salpingostomy = open fallopian tube, remove pregnancy, close ⦁ salpingectomy = removal of fallopian tube (laparoscopic or open) Surgical management is indicated for any patient who is medically unstable, is hemorrhaging, has a gestational sac >3.5cm, or a higher b-hCG level (making medical management is more likely to fail) - if MTX doesn't work = surgery GIVE RHOGAM IF MOTHER IS Rh- Use contraception x at least 2 months Patient will present as → a 22-year-old female complaining of severe left lower quadrant abdominal pain associated with some spotting. She is sexually active, does not use contraception, and has a history of PID. She denies being pregnant. Her last period was 9 weeks ago. On physical exam, the patient is hypotensive and tachycardic. A vaginal ultrasound is performed demonstrating free fluid and a mass in the right adnexa. TRIAD = LOWER ABDOMINAL PAIN + AMENORRHEA + VAGINAL BLEEDING (also seen with threatened abortion, but will have open os)

Answer 25

Tubo-ovarian abscesses are inflammatory masses found in the ovary or fallopian tube and may extend to adjacent structures TOA = an inflammatory mass involving the fallopian tube, ovary, and, occasionally, other adjacent pelvic organs (eg, bowel, bladder) TOA typically occurs as a complication of PID. These abscesses are found most commonly in reproductive-age women and typically result from upper genital tract infection TOA may occur without preceding PID Tubo-ovarian abscess (TOA) is an inflammatory mass found in the fallopian tube, ovary and adjacent pelvic organs. TOAs occur in about 15% of women with pelvic inflammatory disease (PID) TOA is a serious and potentially life-threatening condition. Aggressive medical and/or surgical therapy is required, and rupture of an abscess may result in sepsis CAUSES A tubo-ovarian abscess usually presents in young women with an upper genital tract infection as a severe complication of PID or from local spread of an inflammatory disease of the bowel or adnexal surgery. They tend to be polymicrobial infections with both aerobic and anaerobic bacteria. ``` The most common organisms include ⦁ Escherichia coli ⦁ Streptococci ⦁ Bacteroides fragilis ⦁ Prevotella. ⦁ Intrauterine devices are associated with Actinomyces israelli ``` ** Interestingly, both N. gonorrhea and C. trachomatis are rarely isolated from a TOA ** (even though they are the MC organisms in PID) The major risk factors for TOA are: 1) Multiple sexual partners 2) Prior history of PID 3) Age 15-40 years old (reproductive age women) 4) abdominal/pelvic surgery (ex: hysterectomy) ``` SYMPTOMS They are characterized by ⦁ acute lower abdominal pain ⦁ fever ⦁ chills ⦁ dyspareunia ⦁ vaginal discharge ⦁ N / V ⦁ +/- abnormal vaginal bleeding ``` PID can present in a similar manner Mucopurulent (green or yellow) discharge on speculum examination and acute cervical motion tenderness, uterine or adnexal tenderness are indicative for PID and TOA - Pain that is severe, intermittent and unilateral with associated nausea and vomiting is more consistent with a TOA - Women with a ruptured TOA can present with signs and symptoms of an acute abdomen and sepsis. DIAGNOSIS ⦁ Ultrasound = best initial test - would show complex multilocular masses that disrupt the normal architecture of the ovary/ fallopian tube, + internal echoes consistent with inflammatory debris ⦁ UA ⦁ blood work - elevated WBC count + left shift ⦁ vaginal + blood cultures ⦁ CT - An abdominal/pelvic CT scan is preferred if a GI tract process is strongly considered in the differential. When a patient presents with classic signs and symptoms of a TOA and is hemodynamically stable, then a TVUS or pelvic CT should be ordered. However, if the study is non-diagnostic or if the patient is unstable (indicative of a potential ruptured TOA), then a diagnostic laparoscopy or laparotomy should be performed, and the Gynecology service consulted to evaluate the patient. Moreover, if a postmenopausal women presents with evidence for a TOA, then surgical evaluation is indicated because of the higher incidence of associated malignancy. TREATMENT ⦁ The large majority of small abscesses (<7 cm in diameter) resolves with antibiotic therapy alone broad spectrum antibiotics if the patient is stable and the abscess is less than 9 cm All patients with a high suspicion for a TOA need to be hospitalized and IV antibiotics immediately started. - treatment modalities include: antibiotic therapy, minimally invasive drainage procedures, invasive surgery, or a combination of these interventions ⦁ Cefoxitin (2 grams IV q6h) or cefotetan (2 grams IV q12h) + doxycycline (100 mg orally or IV q12h) ⦁ Ampicillin (2 grams IV q6h) + gentamicin (2 mg/kg IV loading dose, then 1.5 mg/kg IV q8h) +clindamycin (900 mg IV q8h) ⦁ Ampicillin/sulbactam (3 grams IV q6h) + doxycyline 100 mg IV or oral q12h) Antibiotic therapy alone is usually effective in about 70% of patients. However, if the patient does not meet these criteria or has any evidence of a ruptured TOA, then surgery is indicated – either a laparoscopy or laparotomy. Surgery involves the removal of the abscess cavity and irrigation of the peritoneal cavity with both aerobic and anaerobic cultures sent.

Answer 26

``` Primary Headaches (90%) = Tension, Migraine, Cluster Secondary Headaches (4%) = meningitis, SAH, intracranial HTN, hypertensive crisis, acute glaucoma ``` TTH = Tension Type Headache TTH = MC type of primary headache mean age of onset = 30's, peaks in 40's TTH = more common in women Thought to be due to mental stress. Have peripheral activation or sensitization of myofascial nocireceptors (pain receptors) that migrate through pain pathways in CNS Tension headaches lead to steady, pressure-like pain with a bilateral distribution. Tension headaches are characterized by a tightening feeling of the head and scalp, with pain potentially extending down the posterior neck and into the shoulders. The pain is frequently present on both sides of the head at the same time. The pain is typically mild to moderate, but may be severe. SYMPTOMS ⦁ * mild to moderate intensity * ⦁ ****BILATERAL**** ⦁ non-throbbing (non-pulsatile) - unlike migraine ⦁ ****DULL, TIGHT, BAND-LIKE/TIGHT CAP**** ⦁ Muscle tenderness in head/neck/shoulders ⦁ Poor concentration described as a constant pressure, as if the head were being squeezed in a cap The pain can radiate from the lower back of the head, neck, eyes, or other muscle groups in the body Typically affects the head bilaterally. They usually occur for a DURATION > 30 minutes, typically last 4-6 hours Causes constant daily headache Muscle tenderness in head/neck/shoulders Poor concentration ``` PRECIPITATING FACTORS ⦁ stress/mental tension ⦁ fatigue / lack of sleep ⦁ eye strain ⦁ bad posture ⦁ hunger ⦁ lack of caffeine ⦁ ** Not worsened with activity (unlike migraines) ** ⦁ ** No nausea, vomiting, or focal neurologic symptoms (no photophobia / phonophobia) - unlike migraines ** ``` EPISODIC vs CHRONIC TTH o Episodic tension headaches are usually associated with stress. Episodic = < 15 days / month o Chronic tension headaches are usually associated with contracted muscles. Chronic = 15+ days / month DIAGNOSIS ⦁ clinical TREATMENT ⦁ ****1ST LINE = NSAIDS - ibuprofen/naproxen, or APAP (acetaminophen) ⦁ 2nd line = caffeine + 1st line - caffeine can help increase effectiveness of NSAIDS / acetaminophen, but due to increase in SE, is reserved until patient has failed 1st line analgesic monotherapy ⦁ 3rd line = migraine meds if CI to 1st line (stomach ulcers, renal/liver failure, pregnant), or if not working = Triptans, TCAs (Elavil - Amytriptyline*), BBs, etc - can try muscle relaxers as well - higher chance of success with smoking cessation - use relaxation techniques, massage, avoid high-stress, get good sleep, improve posture/sleep posture, avoid eye strain/corrected vision ACUTE TREATMENT OF TTH (ER SETTING) ⦁ Ketorolac (Toradol) 30mg IM If using OTC meds to treat TTH = need to taper off; abruptly stopping could cause rebound HA - Medication-overuse headaches must be avoided by limiting use of abortive agents to no more than 2 days/week. TCAs can help with analgesic rebound headaches - also to avoid gastritis from chronic NSAID use PROPHYLAXIS ⦁ Amitriptyline - use with caution due to SE Patient will present as → a 25-year-old female presents with a headache. She describes the headache as a tightening, band-like quality on both sides of his forehead. It is non-throbbing, but feels like a "tight cap." She denies phonophobia or photophobia, nausea, or vomiting. On physical exam, you note pericranial muscle tenderness.

Answer 27

More common in men (4x MC) Predominantly occurs in young + middle-aged men **Trigeminal Hypothalamic Pathway** Cluster headaches are differentiated from trigeminal neuralgia by the duration of pain - trigeminal neuralgia = shooting pain that typically lasts about 1 min - cluster headache = lasts anywhere from 15min - 3hrs Clusters of attacks separated by periods of remission Symptoms usually remain on the same side / location during a cluster attacks SYMPTOMS ⦁ ****RECURRENT*** headaches that cluster together ⦁ typically last < 2 hrs (45-90 min) ⦁ Have 1 every other day to 8x/day x 6-8+ weeks ⦁ ****UNILATERAL**** ⦁ ****PERIORBITAL/TEMPLE PAIN**** ⦁ Pain = Excruciating, sharp, searing, stabbing ⦁ ****Eye/Nose symptoms = Ipsilateral rhinorrhea, lacrimation, periorbital pain, nasal congestion, conjunctival injection***** ⦁ *** Awakens patients from sleep *** Cluster headaches characteristically occur around the same time each day, often in the early hours of the morning Can be worse at night = often wakes patients up from sleep Attacks usually occur in series (cluster periods) lasting for weeks or months separated by remission periods usually lasting months or years. However, about 10–15% of patients have chronic symptoms without remissions ****HORNER'S SYNDROME**** = ptosis, miosis, anhidrosis (miosis = constriction) The duration of cluster headaches are, on average, 15 min - 3 hrs. many patients sit + rock back/forth or pace - active Patients often pace, rubbing their heads to try to alleviate the pain ``` TRIGGERS ⦁ alcohol ⦁ stress ⦁ glare ⦁ ingestion of specific foods ``` The exact etiology of cluster headaches is unknown, but triggers may include stress, allergens, alcohol, and the vasodilator nitroglycerin. DIAGNOSIS ⦁ MRI* (or CT) to rule out pituitary adenoma TREATMENT ⦁ 1ST LINE = OXYGEN - nonrebreather mask or cannula in upright position - 6-10 L (pance) or 12-15L/min (ppt/picmonic) x at least 15 min (just think 15L/min x 15 min!) - sometimes oxygen is enough ⦁ 2nd line = Triptans (cause vasoconstriction) - Can try Oxygen + Sumatriptan (SQ) 6mg - Sumatriptan 6 mg SQ: max 12 mg/24 hr with at least 1 hour between injections (max = 2 doses in 24hr period with 1 hr in between) or - Sumatriptan nasal spray: 20 mg. May repeat in 2 hours, max dose 40 mg/24 hr (max = 2 doses in 24hr period with 2 hrs in between) Triptan SE = nonischemic chest pain + distal paresthesias = don't give in stroke / CVD / uncontrolled HTN / pregnancy - Other options = Ergotamines (vasoconstriction) or intranasal lidocaine PROPHYLAXIS ⦁ CCB - ****VERAPAMIL 240mg QD**** - Other prophylactic meds = verapamil, ergotamine, lithium, methysergide, prednisone, topiramate and other corticosteroids, indomethacin, beta blockers, TCAs, and SSRIs SUMMARY Cluster headache is a neurological disorder characterized by recurrent, severe headaches on one side of the head, typically around the eye. There are often accompanying autonomic symptoms during the headache such as eye watering, nasal congestion and swelling around the eye, typically confined to the side of the head with the pain. The are typically treated with inhaled oxygen and sumatriptans. Patient will present as → a 45-year-old man comes to your office with a 4-week history of recurrent headaches that wake him up in the middle of the night. The headaches have been occurring every night and have been lasting approximately 1 hour. The headaches are described as a deep burning sensation centered behind the left eye. The headaches are excruciating (he rates them as a 15 on a 10-point scale) and are associated with watery eyes, “a sensation of heat and warmth in my face,” nasal discharge, and redness of the left eye.

Answer 28

Migraine = Severe headache, usually associated with Nausea, Vomiting and Light sensitivity Neuronal Dysfunction: The trigeminal nerve becomes more susceptible to stimulus/more sensitive to irritating agents and increased pain reception - Trigeminal nerve innervates blood vessels --> causes vasodilation --> HA ⦁ Migraines = affect women more than men ⦁ MC age = adolescent / early adults ⦁ Can be genetic (familial) *MC Type of Migraine = MIGRAINE WITHOUT AURA* TRIGGERS ⦁ *** MC = STRESS/EMOTIONAL STRESS (80%) *** ``` Other triggers = ⦁ hormonal variation (estrogen)/OCPs ⦁ not eating ⦁ weather ⦁ sleep disturbances ⦁ diet (MSG, chocolate, cheese) ``` 4 PHASES OF MIGRAINES 1) PRODROMAL PHASE - occurs in 60% of patients with migraines - Symptoms occur 24-48hrs before headache onset - Symptoms = euphoria, depression, irritability** - Can also have food cravings, constipation, neck stiffness, yawning 2) MIGRAINE AURA (classic) - only occurs in 25% of patients with migraines - Lasts < 1 hour - start to feel HA coming on during aura - Involves Positive and Negative symptoms o POSITIVE ⦁ visual (bright lights, see shapes/objects) ⦁ auditory (tinnitus/noises) ⦁ sensory (burning / pain / paresthesias) ⦁ motor (twitches / muscle jerks) ``` o NEGATIVE ⦁ loss of vision ⦁ loss of hearing ⦁ loss of feeling ⦁ inability to move a part of the body ``` * *MC Aura symptoms = Visual (positive and/or negative) - see bright lights, shapes/objects or have loss of vision - particularly in peripheral field just lateral to point of fixation) - Visual usually followed by sensory aura During aura, serotonin levels increase -> vasoconstriction 3) MIGRAINE HEADACHE ⦁ can last anywhere from 4-72 hours ⦁ Usually UNILATERAL, but can be bilateral. ⦁ Localized ⦁ **PULSATILE/THROBBING** ⦁ Can experience **NAUSEA / VOMITING / PHOTOPHOBIA / PHONOPHOBIA** ⦁ **Worsens with activity** - worse with physical activity, stress, lack or excess sleep, alcohol, specific foods, OCPs/menstruation During migraine, serotonin levels decrease-> vasodilation 4) POSTDROMAL PHASE - patients often feel drained or exhausted - Some report mild elation or euphoria - Sudden head movement causes pain in the location of antecedent headache DIAGNOSIS OF MIGRAINE - neuroimaging only done with atypical features / red flags: ⦁ "Worst" headache of my life / thunderclap HA (SAH) ⦁ "New" headache - new (>40) - never had HA before ⦁ Any neurological symptoms (confusion, AMS, papilledema, seizures) ⦁ previous HAs were different TREATMENT - treatment for migraines should be administered as early as possible - earlier administration improves efficacy ⦁ 1st line = NSAIDS / ASA / APAP (just like tension) - Ibuprofen / Naproxen / Ketorolac / APA / ASA - different OTCs may have different efficacy, so several should be tried before escalating treatment Triptans = 1st line if moderate to severe migraine, or if NSAIDS have failed - IV fluids and put patient in dark/quiet room can help ⦁ 2nd line****TRIPTANS**** (Sumatriptan/Imitrex) - Triptans = first line after NSAIDS have failed - DON'T give triptans with hemiplegic or brainstem aura - SE of triptans = chest tightness due to vasoconstriction + distal paresthesias Sumatriptan is a 5-HT1B/1D agonist in the cranial arteries. The drug binds to serotonin receptors in the brain, which triggers vasoconstriction, inhibits trigeminal activation (thought to be the cause of migraine pain) Can try adding NSAIDS or caffeine to triptans 2nd line = or Ergotamines MOA of triptans + ergotamines = serotonin 5HT-1 agonists ==> vasoconstriction - SE = chest tightness from constriction - CI = CAD / PVD / CVD / stroke / uncontrolled HTN / hepatic or renal disease / pregnancy ⦁ 3rd line = IV Phenothiazines: Metoclopramide, Promethazine, Prochlorperazine = Dopamine blockers - Indication = antiemetics for N/V - *** Give with BENADRYL *** to prevent EPS / dystonic reactions / parkinsonism symptoms due to decreased dopamine IF PREGNANT = can only give ACETAMINOPHEN American Academy of Neurology (AAN) and AHS have also recommended RIBOFLAVIN (B2) + MAGNESIUM to help reduce migraine frequency and headache days PROPHYLAXIS ⦁ BB (propranolol)*** or CCB ⦁ TCAs (Elavil) ⦁ Anticonvulsants (valproic acid, Topamax) - triptans = not indicated for prophylaxis Patient will present a → a 25-year-old female comes to your office with a 3-year history of recurrent headaches that have gotten worse during the past year. These headaches occur approximately twice per week. Before the headache, nausea, and severe vomiting begin, she experiences a “type of odd visual feeling or sight—flashing lights, almost like a pattern in front of my eyes.” Headaches usually lasts 24 to 36 hours. It is throbbing in nature and often “switches from one side to the other”. She needs to be in a dark room and finds noise bothersome when she has these headaches.

Answer 29

Cellulitis = - acute, spreading infection of dermal + subcutaneous tissues through a skin portal - can occur in all ages* ``` COMMON CAUSES (adults) ⦁ staph ⦁ group A strep (GABHS = Strep Pyogenes) ``` CAUSES (kids) ⦁ h. flu ⦁ strep pneumo Skin infection with underlying drainage, penetrating trauma, eschar, or abscess is most likely caused by STAPH; on the other hand Strep is the most likely pathogen when these factors (drainage, penetrating trauma, eschar, abscess) are not present. - hx of trauma - may be unaware of wound of entry - may include dog, cat or human bite - common in patients with diabetes or PVD, but can happen in anyone Common risk factors include recent surgery, trauma, or animal bite (dog / cat / insect) MC will have a hx of trauma MC site of cellulitis = lower leg - surgery may exacerbate spread of disease - particularly venous stripping ``` PHYSICAL EXAM: SIGNS / SYMPTOMS ⦁ warmth ⦁ erythema ⦁ edema ⦁ tenderness of affected area ⦁ Flat margins + NOT well-demarcated (unlike erysipelas) ``` Maceration of the web spaces on the feet may be seen in cases of uncomplicated cellulitis Cellulitis is an acute bacterial skin and skin structure infection of the dermis and subcutaneous tissue; commonly characterized by pain, erythema, warmth, and swelling. Margins are flat and not well demarcated - cellulitis with violaceous color + bullae suggests infection with strep pneumoniae if a pt comes in with cellulitis = take black sharpie and mark area affected - make sure not rapidly spreading, and that treatment is working COMPLICATIONS ⦁ Necrotizing Fasciitis - necrosis of subcutaneous tissue. ⦁ Sepsis ⦁ Endocarditis DIAGNOSIS ⦁ CULTURE = if purulent - no work up required for uncomplicated cases that meet the following criteria ⦁ small area of involvement ⦁ minimal pain ⦁ no systemic signs of illness (fever / chills / dehydration / altered mental status / tachypnea / tachycardia / hypotension ) ⦁ no risk factors for serious illness (eg, extremes of age, general debility, immunocompromised status). **IF COMPLICATED = SIGNS OF SYSTEMIC INVOLVEMENT** ⦁ CBC ⦁ CMP ⦁ blood cultures TREATMENT - staph + strep coverage X 7-10 days MILD ⦁ Keflex = 1st line (suspected MSSA) ⦁ Dicloxacillin - Clindamycin or Erythromycin if allergic to PCN If strep pyogenes = amoxicillin IV (MSSA) ⦁ Ceftriaxone (Rocephin) ⦁ Ampicillin - Sulbactam (Unasyn) ⦁ Ancef (Cephalexin) MRSA ⦁ bactrim, clinda, doxy Cat / Dog / Human bite = Augmentin ⦁ Cat 2nd line = Doxy (if allergic to PCN) ⦁ Dog / Human 2nd line = Clindamycin + Cipro or Bactrim If puncture wound (ex: through shoe) = cover for pseudomonas (cipro) COMPLICATED - hospitalization for IV antibiotics (to cover MRSA+) ⦁ Vanco ⦁ Zyvox (Linezolid) Patient will present as → a 64-year-old female with a 4 cm × 7 cm edematous, red, hot tender area on the left thigh. The lesion has gotten larger over the past 6 hours. She tells you she has also had a low-grade fever and some chills. On physical exam, there is a poorly demarcated 12 cm red and tender plaque on her right calf. Some parts resemble an orange peel. There is a superficial cut in the middle of the plaque.

Answer 30

Septic arthritis = Infectious arthritis = joint inflammation secondary to infection - usually due to bacterial infection of the joint - considered a medical emergency due to high risk of joint destruction All joint types (fibrous, cartilaginous, synovial) can get infected **** MC CAUSE = STAPH **** ex: in synovial joints - synovial fluid - helps to lubricate the joint and to absorb shock - the synovial membrane has vessels that supply the joint with nutrients + oxygen - the 2 bones that form at that joint are covered in articular cartilage - also absorbs shock + reduces friction during movement HOW DOES A JOINT BECOME INFECTED? 1) pre-existing infection in adjacent tissue (usually the bone = Osteomyelitis) --> spreads to articular cartilage --> spreads to joint 2) hematogenous spread = bacteria is somewhere else in the body (ex: lungs) --> travels via bloodstream --> joint 3) Trauma / puncture wound / surgery ex: if nail pierces through knee and into joint - septic arthritis could either be from the nail (ex: tetanus) or from the surface of the skin (ex: staph) Once bacteria gets into synovial joint ==> starts destroying the articular cartilage via TOXINS (ex: chondrocyte protease - enzyme that digests collagen in cartilage) Bacteria stimulates an immune response reaction ⦁ macrophages phagocytose the bacteria, and release cytokines (Interleukin - 1 + TNF-alpha) = signaling cytokines ⦁ IL-1 + TNF-alpha recruit more immune cells to site ⦁ mast cells release histamine --> vasodilation + increases vascular permeability ==> more blood comes into area --> INFLAMMATORY RESPONSE --> joint becomes red / swollen / warm ⦁ due to increased vascular permeability --> more fluid accumulates in joint space --> increased interarticular pressure --> compresses blood vessels supplying blood to joint --> necrosis of affected bones / cartilage --> joint destruction ``` RISK FACTORS ⦁ age ⦁ chronic debilitating disease ⦁ immunosuppressive drugs ⦁ IVDU ⦁ prosthetic joint / surgery ⦁ chronic arthropathies (RA / gout / osteoarthritis) ``` ``` SYMPTOMS ⦁ joint pain ⦁ red ⦁ swollen ⦁ warm ⦁ impaired ROM ⦁ systemic = fever / chills / diaphoresis / myalgia / malaise ``` - symptoms may vary depending on pathogen GONOCCOCAL ARTHRITIS - due to Neisseria gonorrhea - spreads hematogenously from cervix / urethra / pharynx - affects multiple joints - causes multiple SKIN LESIONS + TENOSYNOVITIS (inflammation of muscle tendons) Neisseria gonorrhoeae is the most common cause of infectious septic arthritis in young sexually active adults. BUT MAJORITY OF SEPTIC ARTHRITIS = NON-GONOCCOCAL ARTHRITIS = includes all other pathogens that cause septic arthritis - typically only 1 joint is affected (MC a knee) ⦁ *** MC CAUSE = STAPH AUREUS *** - can completely destroy the joint within days unless treated - Other causes: ⦁ Strep species (2nd most common) ⦁ mycobacterium tuberculosis ⦁ borrelia species (lyme dz) ⦁ * Group B strep *, H. flu in neonates ⦁ Pseudomonas in IVDU ⦁ staph epidermidis in prosthetics DIAGNOSIS OF SEPTIC ARTHRITIS ⦁ joint aspiration - collect joint fluid - purulent synovial fluid - elevated WBC (> 50,000) (>1100 = positive in prosthesis) - primarily PMNs (polymorphonuclear leukocytes = granulocytes = basophils + neutrophils + eosinophils) - positive gram stain / positive culture - lactate level > 10 (cell death --> release lactic acid) - elevated ESR / CRP ``` IMAGING ⦁ Xray ⦁ Ultrasound ⦁ CT or MRI - can show bone erosion + joint effusion - especially useful for hip or sacroiliac joints where aspiration of fluid is difficult ``` When the hip is affected, the leg is characteristically held in abduction, external rotation and flexion; this position provides the most comfort because it maximizes the joint space. ``` TREATMENT - Antibiotic therapy + pain medication ⦁ Staph = Nafcillin (MRSA = Vancomycin) ⦁ Gonococcal arthritis = Ceftriaxone ⦁ IVDU (pseudomonas) = Cipro or Levofloxacin ``` - Arthrocentesis - joint aspiration + washout - Arthrotomy + joint drainage - surgical Empiric IV antibiotics should be started that cover S. aureus, the most common cause of septic arthritis. - must be > 12 to have fluoroquinolones If MRSA is suspected, clindamycin or vancomycin are better options In neonates, antibiotics must also cover H. influenza, as this is a major cause of septic arthritis in those who are non-immunized.

Answer 31

Dura Mater = outermost protective layer of the brain Epidural = outside the dura Epidural hemorrhage = bleeding above the dura mater - bleeding between dura mater + skull ANATOMY - the brain is protected by MENINGES = 3 thin layers of tissue that cover the brain and spinal cord 1) dura mater = outerlayer 2) arachnoid mater = middle layer - subarachnoid space - houses CSF 3) pia mater = inner layer Pia + arachnoid mater = leptomeninges - between leptomeninges = subarachnoid space, which houses CSF (cerebrospinal fluid) CSF = clear / watery fluid that is pumped around the spinal cord and brain that functions to provide nutrients as well as cushion them from impact The dura mater has 2 layers: external + internal the internal dura mater lies above the arachnoid mater - subdural space = between internal dura mater + arachnoid mater the external dura mater adheres to the inner surface of the skull the 2 layers of the dura mater travel together, expect at meningeal folds, which help to divide sections of the brain CAUSES OF EPIDURAL HEMORRHAGE ⦁ *** MC cause = HEAD TRAUMA *** - the meningeal arteries are protected by the skull, but can be damaged by serious head trauma - MC site = PTERION = site where frontal, temporal, parietal, and sphenoid bones join - this site is located right above the MIDDLE MENINGEAL ARTERY MC site of skull fracture = TEMPORAL BONE = the most commonly affected in patients with skull fractures following blunt head trauma * ** MC ARTERY = MIDDLE MENINGEAL ARTERY *** - runs through foramen spinosum Actively bleeding artery = hemorrhage Collection of blood that results = hematoma Once a meningeal artery is torn, blood will pool between the skull and the external layer of the dura mater ==> epidural hemorrhage / hematoma The blood cannot cross the suture lines where the dura mater adheres, so appears as a BICONVEX or LENTICULAR shape If blood accumulates slowly, there may be a "lucid interval" in which several hours pass before onset of symptoms A LARGE epidural hematoma on one side can cause a "MIDLINE SHIFT" = displacement of the whole brain towards the opposite side of the skull A LARGE epidural hematoma can also cause an increase in intracranial pressure --> can also cause brain to shift or herniate Epidural hematoma can also cause ⦁ Supratentorial herniation = where the cerebrum is pushed against the skull or the tentorium (houses the cerebellum) ==> can compress arteries that lead to the brain --> Ischemic stroke! ⦁ Infratentorial herniation = cerebellum is pushed against the brainstem ==> can compress part of the brainstem --> can affect consciousness / respiration / heart rate Both supratentorial + infratentorial herniation can be lethal! SYMPTOMS OF EPIDURAL HEMORRHAGE ⦁ *** MC = LOSS OF CONSCIOUSNESS after head trauma - due to concussion *** slow epidural bleed ⦁ may have lucid interval - where patient improves temporarily right after initial trauma, but then deteriorates as hematoma grows Lucid interval initially = the brain is initially able to compensate for the extra intracranial volume through redistribution of the blood and cerebrospinal fluid ``` ⦁ Headache ⦁ Dizziness ⦁ Nausea / Vomiting ⦁ Focal neurological symptoms: such as muscle weakness or sensory deficit, depending on location ⦁ ** Ipsilateral pupil dilation ** ``` BASILAR SKULL FRACTURES are closely associated with epidural hematomas = because the middle meningeal artery and vein run beneath the pterion, a relatively weak area of the skull where the frontal, parietal, temporal, and sphenoid bones meet. ⦁ clear rhinorrhea ⦁ "halo sign" ⦁ raccoon eyes = periorbital ecchymosis ⦁ battle sign = bruising behind the ears ⦁ deficits in CN 3 / 4 / 6 PHYSICAL EXAM - assess pupillary response: Expansion of a hematoma can increase intracranial pressure and lead to an ipsilateral dilated pupil - assess GCS scale GCS < 8 confers a risk of ~80% of poor prognosis. Having multiple pathologies on CT scan confers a poorer prognosis - *** CUSHING'S TRIAD *** = signifies increased ICP 1) bradycardia 2) widened pulse pressure (systolic rises steeply, diastolic decreases or remains normal) 3) irregular respirations (often irregular and deep = Cheyne stokes or apneic) Cushing's Triad = 1) bradycardia 2) widened pulse pressure 3) irregular respirations DIAGNOSIS ⦁ CT without contrast - appears as hyper-dense mass (super white) - *** BICONVEX or LENTICULAR SHAPED *** = elliptical shape - epidural hematomas DO NOT cross suture lines ⦁ or MRI Lumbar puncture is contraindicated if increased intracranial pressure is suspected, such as in epidural hematomas, because it can cause herniation of the brain through the foramen magnum, compressing the brainstem and leading to respiratory arrest TREATMENT Due to its rapid expansion, an epidural hematoma is a neurosurgical emergency requiring drainage. ⦁ craniotomy - part of bone removed in order to remove blood accumulation below ⦁ burr hole - to drain fluid and relieve pressure if ICP continues to be elevated, but post-op and normal vitals = HYPERVENTILATION via mechanical ventilation can serve to temporarily decrease an elevated ICP (only lasts 1-24 hours) ⦁ can also try hypertonic saline (not NS!) ⦁ can try elevating the head of the bed 30 degrees (reverse Trendelenburg) ⦁ mannitol = preferred diuretic in increased ICP (would not use Lasix as monotherapy, but in conjunction to mannitol) ⦁ aggressive mechanical cooling can be attempted if increased ICP and patient has a fever Once hyperventilation no longer serves to decrease the ICP, the respiratory rate should be adjusted so that the patient's PaCO2 returns to normal. Patients classically present with a lucid interval after TBI, followed by LOC in an epidural hematoma *** stem will have patient start to feel fine, then HA *** Epidural hematoma will present with → transient loss of consciousness from an injury, then lucid period followed by increasing drowsiness, headache and unilateral (contralateral) weakness

Answer 32

out of 15 total points ``` minimum = 3 maximum = 15 ``` ``` EYE = Eye Opening (4) ⦁ 4 = spontaneous ⦁ 3 = to voice ⦁ 2 = to pain ⦁ 1 = none ``` ``` VERBAL = verbal response (5) ⦁ 5 = normal conversation ⦁ 4 = confused / disoriented conversation ⦁ 3 = words, but noncoherent ⦁ 2 = no words, only sounds ⦁ 1 = none ``` ``` MOTOR = motor response (6) ⦁ 6 = normal = obeys commands ⦁ 5 = localized to pain ⦁ 4 = withdraws to pain ⦁ 3 = decorticate posture - an abnormal posture that can include rigidity, clenched fists, legs held straight out, and arms bent inward toward the body with the wrists and fingers bend and held on the chest = flexed arms at chest ⦁ 2 = decerebrate - an abnormal posture that can include rigidity, arms and legs held straight out, toes pointed downward, head and neck arched backwards = extended arms at sides ⦁ 1 = none ``` Using the Glasgow Coma Scale Generally, brain injury is classified as: ⦁ Severe: GCS 3-8 (You cannot score lower than a 3) ⦁ Moderate: GCS 9-12 ⦁ Mild: GCS 13-15 If the patient's GCS score drops to 8 or below (severe), immediate action would be required; specifically, endotracheal intubation. ex: patient opens his eyes when his name is called, but has no verbal or motor response to painful stimuli = 3 + 1 + 1 = 5 ex: opens his eyes to pain, responds to speech with incoherent, isolated words, and tries to avoid a painful pinch to his nail-bed by pulling away from it. 2 + 3 + 4 = 9 es: You call the patient by his name and get no response. After rubbing your knuckles against his chest, he opens his eyes and closes them. You then ask him a question, the patient doesn't utter a word or sound. Finally, you place pressure over the patient's left index finger nail bed. He moves his hands away due to the stimulus = 2 + 1 + 4 = 7

Answer 33

Subdural = below the outermost protective layer of the brain (dura mater) Subdural hemorrhage = bleeding between the inner and outer layers of the dura mater = VENOUS BLEEDING (bridging veins) ANATOMY - the brain is protected by MENINGES = 3 thin layers of tissue that cover the brain and spinal cord 1) dura mater = outer layer 2) arachnoid mater = middle layer - subarachnoid space - houses CSF 3) pia mater = inner layer Pia + arachnoid mater = leptomeninges - between leptomeninges = subarachnoid space, which houses CSF (cerebrospinal fluid) CSF = clear / watery fluid that is pumped around the spinal cord and brain that functions to provide nutrients as well as cushion them from impact The dura mater has 2 layers: external + internal - internal dura mater lies above the arachnoid mater - subdural space = between internal dura mater + arachnoid mater the external dura mater adheres to the inner surface of the skull the 2 layers of the dura mater travel together, except at meningeal folds, which help to divide sections of the brain The subdural space plays a major role in venous blood drainage in the brain Subarachnoid space has numerous arteries that supply oxygen to the brain. The blood drains into superficial cerebral veins (bridging veins) that also sit in the subarachnoid space --> travel through the arachnoid mater --> subdural space --> penetrate the inner layer of the dura mater to drain into dural venous sinuses = located between the 2 layers of the dura mater eventually this blood in the dural venous sinuses drains into the internal jugular vein --> heart CAUSE OF SUBDURAL HEMORRHAGE due to rupture of the bridging veins --> hemorrhage ⦁ Head trauma (MC)- falls or shaken baby syndrome (babies have thin-walled bridging veins) ⦁ brain atrophy (elderly = brain shrinks in size --> bridging veins are stretched across a wider space ⦁ alcohol abuse (veins become thin-walled) ⦁ coup-contracoup (acceleration / deceleration injury - whiplash) Acute subdural hemorrhage = associated with trauma Chronic subdural hemorrhage = associated with mild trauma, cerebral atrophy, elderly, and alcoholism. - once a bridging vein is torn, blood pools into the subarachnoid space - since the bridging vein is under low pressure, the bleeding can be slow --> DELAYED onset of symptoms = may develop over days to weeks as hematoma gradually expands o Acute subdural hematoma = symptoms in 1-3 days = hyperdense o Subacute subdural hematoma = symptoms in 4days - 2 weeks = isodense o chronic subdural hematoma = > 2 weeks = hypodense Hematoma can compress the brain and cause INCREASED ICP (intracranial pressure) Large subdural hematoma on one side of the brain can cause MIDLINE SHIFT Increased intracranial pressure can also cause brain to herniate o Supratentorial herniation = brain pushed against the skull or the tentorium - can compress the arteries that nourish the brain --> ischemic stroke o Infratentorial herniation = cerebellum pushed against the brainstem - can compress brain stem which controls consciousness / heart rate / respirations SYMPTOMS ⦁ LOC (at injury or in days / weeks as it increases in size) ⦁ Headaches ⦁ Nausea / Vomiting ⦁ Neurological symptoms: muscle weakness / sensory problems / etc Chronic subdural hematomas present in the elderly after trauma with mental status changes, hemiparesis, headache, CN III or VI palsy, hemianopsia, and papilledema. Elderly patients on anticoagulation such as warfarin can develop subdural hematomas after even minor trauma. - *** CUSHING'S TRIAD *** = signifies increased ICP 1) bradycardia 2) widened pulse pressure (systolic rises steeply, diastolic decreases or remains normal) 3) irregular respirations (often irregular and deep = Cheyne stokes or apneic) - no fever (98.6 or 37) Cushing's Triad = 1) bradycardia (< 60) 2) widened pulse pressure 3) irregular respirations (likely elevated) DIAGNOSIS ⦁ CT without contrast - Acute = hyperdense mass (more white than surrounding brain tissue) - Chronic = hypodense mass (less white than surrounding brain tissue) - Acute-on-Chronic = old bleed formed hematoma, then started to re-bleed (mixed hyper + hypodense) - CRESCENT SHAPE / CONCAVE Subdural hemorrhage = between 2 layers of dura mater - between outer and inner dura mater - therefore subdural hematomas follow the contour of the brain --> CRESCENT SHAPE - DOES CROSS SUTURE LINES (unlike epidural) - do NOT perform LP - with increased ICP, can cause herniation - Guidelines suggest urgent surgical evacuation if the ICP is consistently >20 mmHg. TREATMENT ⦁ CRANIOTOMY = preferred surgical treatment of subdural hematoma ⦁ small subdural hematomas = burr hole drilled into brain, drained via catheter - burr holes = shown to have more complications and lower efficacy than craniotomy ⦁ large subdural hematomas = craniotomy - part of bone is removed in order to drain blood below GCS of 8 or less = Intubate Midline shift >5 mm suggests that surgical intervention may be beneficial for the patient, but minimal shifting may be corrected medically. if ICP continues to be elevated, but post-op and normal vitals = HYPERVENTILATION via mechanical ventilation can serve to temporarily decrease an elevated ICP (only lasts 1-24 hours) ⦁ can also try hypertonic saline (not NS!) ⦁ can try elevating the head of the bed 30 degrees (reverse Trendelenburg) ⦁ mannitol = preferred diuretic in increased ICP (would not use Lasix as monotherapy, but in conjunction to mannitol) ⦁ aggressive mechanical cooling can be attempted if increased ICP and patient has a fever Have a high clinical suspicion for subdural hematoma in an elderly patient with history head trauma and altered mental status. Subdural hematoma will present as → an elderly patient with a history of multiple falls who is now presenting with neurological symptom

Answer 34

Concussion = Mild TBI (traumatic brain injury) Usually starts with hitting the head, but a large part of the brain gets injured rather than a small specific area Concussions do not cause obvious brain injury that can be seen on imaging, such as bleeding Concussion clinically describes mild brain injury with or without loss of consciousness following sudden trauma of the head. ``` Most concussions = due to ⦁ falls ⦁ MVA ⦁ recreational activities / sports ⦁ abuse ``` 2 types of concussion injuries 1) Coup-Contrecoup 2) Torque COUP-CONTRECOUP - coup injury = initial contact or blow injury to head - forms initial contusion (bruise) - contrecoup = when brain strikes opposite side of skull from momentum of initial coup injury TORQUE - rotation of the head either in or out of its original plane - ex: hook punch - causes head and neck to twist against the brainstem, stretching the brainstem - *** RETICULAR FORMATION *** = network of nerves within brainstem that control level of consciousness - with torque injury, reticular formation gets stretched + damaged --> may cause LOC COUP-CONTRECOUP vs TORQUE - torque usually results in more serious concussions, and more often causes a loss of consciousness With either type of concussion, damage occurs on a microscopic scale at the level of the neuron, rather than causing visible damage to a specific part of the brain - after a concussion, there is an increased demand for blood supply due to increased EPSPs (excitatory post-synaptic potential), but there is actually a decreased amount of blood supply after injury --> glucose starvation of neuron cells in brain - can last for a few hours to a few days Pathophysiology is still being clarified, but brain dysfunction is thought to involve excitotoxicity, which is neuronal damage caused by excessive release of excitatory neurotransmitters, particularly glutamate. - Secondary Impact Syndrome or repeated concussions in this state = very problematic, can lead to cerebral edema ``` SYMPTOMS OF CONCUSSION o Initial ⦁ confusion* ⦁ amnesia* (retrograde or antegrade) ⦁ may have LOC - these symptoms usually improve within 1-2 days ``` o Symptoms that appear a little later ⦁ Headache ⦁ Dizziness ⦁ Nausea / Vomiting ⦁ Light sensitivity ⦁ may have tinnitus / blurred or double vision ⦁ mood changes: emotional instability Signs of increased ICP = persistent vomiting, worsening headache, increasing disorientation, and changing levels of consciousness DIAGNOSIS ⦁ based on history + symptoms ⦁ CT - normal (study of choice) - no focal neurologic deficits If > 2 and GCS = 15 = only do head CT if signs of basilar fracture or if AMS (altered mental status) TREATMENT ⦁ rest ⦁ ensure that patient has completely recovered prior to returning to activity ⦁ no bright-lights / screens for a few days All patients with concussion should be observed for 24 hours. - Patient does not need to be admitted for monitoring - can be outpatient + return to ER if condition worsens Patients with concussion should be admitted to the hospital if their Glasgow coma scale is less than 15. Single concussion: if + LOC or symptoms of concussion lasting more than 15 minutes NOT to return to play sports until asymptomatic for at least one week. Repeat concussions: if associated with either loss of consciousness or symptoms for more than 15 minutes NOT to return to play sports for that season ⦁ Complete rest until symptom-free ⦁ Begin gradual reintroduction of activity as long as symptom free ⦁ Do each step generally 24 hours apart: light aerobic exercise; sport-specific exercise; noncontract training drills; full-contact training; game play ⦁ Stop all activity until again asymptomatic for 24 hours, if any signs or symptoms recur (i.e., exertional headache, visual disturbance, or disequilibrium). Restarting return-to-play plan at last step when patient was asymptomatic Patient will present as → a 16-year-old male who briefly lost consciousness following a football collision and after regaining consciousness had an episode of nausea and vomiting.

Answer 35

``` ⦁ Suspected open skull FX ⦁ Signs of basilar skull FX ⦁ ≥ 2 episodes of vomiting ⦁ ≥ 65 years old ⦁ Amnesia >≥ 30 minutes prior to impact ⦁ MVA with ejection ⦁ Pedestrian struck by car ⦁ Fall from ≥ 3 feet ⦁ Underlying bleeding disorder ⦁ Anticoagulant use ⦁ Seizure activity ⦁ Focal neurological deficit ⦁ ETOH involvement ```

Answer 36

Amitriptyline (TCA) toxicity Life threatening effects of TCAs 1) Coma 2) Convulsions 3) Cardiac arrhythmias Patients often develop features of the anticholinergic toxidrome such as delirium, mydriasis, dry mucous membranes, tachycardia, hyperthermia, mild hypertension, urinary retention, and slow GI motility. CNS toxicity can include lethargy, coma, myoclonic jerks, and seizures. Sinus tachycardia is the most common cardiovascular manifestation of toxicity. Patients can also develop widening of the QRS complex, premature ventricular contractions, and ventricular arrhythmias ANTIDOTE = ** SODIUM BICARBONATE **

Answer 37

ST segment elevation in lead aVR greater than 1 mm or greater than the elevation seen in the ST segment of V1 should prompt concern for occlusion of the left main coronary artery. The finding of ST elevation in aVR that is greater than that seen in VI can distinguish occlusion of the left main coronary artery from the left anterior descending artery with a sensitivity and specificity of approximately 80%. Other ECG findings consistent with left main occlusion include horizontal ST depression in leads I, II, and V4-6.

Answer 38

Early symptoms begin with nausea, vomiting, CNS depression. Late manifestations include anion gap metabolic acidosis, hypocalcemia, and kidney failure (secondary to deposition of calcium oxalate crystals in the renal tubules). patients with ethylene glycol poisoning can have elevations in their serum lactate concentration from acidosis. It can be diagnosed by ethylene glycol blood concentrations. Osmolar gap may also be used as a surrogate marker. TREATMENT = ** FOMEPIZOLE ** = competitive inhibitor of alcohol dehydrogenase - used to be ethanol

Answer 39

OPHTHO EMERGENCY!!! - every minute counts! Irrigation must be started immediately!!! Alkali burns = worse that acids! - due to liquefactive necrosis = alkaline chemicals denature proteins + collagen --> thrombosis of vessels - Ex: fertilizers, household cleaners, drain cleaners Acidic burns - coagulative necrosis = H+ precipitates the protein barrier - ex: cleaners, batteries Chemical injuries to the eye represent one of the true ophthalmic emergencies While almost any chemical can cause ocular irritation, serious damage generally results from either strongly basic (alkaline) compounds or acidic compounds. ALKALINE burns = more common + more DANGEROUS Bilateral chemical exposure is especially devastating, often resulting in complete visual disability. o ACID CHEMICAL BURN ⦁ results in ** protein coagulation ** ⦁ limited depth of injury o ALKALINE CHEMICAL BURN ⦁ results in ** liquefaction necrosis ** ⦁ lipophilic ⦁ penetrates faster than acidic burns ⦁ can rapidly damage cornea / iris / lens ⦁ can result in blindness TREATMENT Immediate, prolonged irrigation, followed by aggressive early management and close long-term monitoring, is essential to promote ocular surface healing and to provide the best opportunity for visual rehabilitation ⦁ 1ST = remove any particulate material --> Immediate irrigation with NS or LR - LR is ideal due to its pH of 6-7.5 = closer to the pH of tears (7.1) than NS (4.5 - 7.0), and LR is less irritating to the eyes - initial step even before complete exam when a patient presents with a chemical eye injury - irrigate x 30 minutes, or at least 2 L of fluid - A lid speculum should be placed and topical anesthesia applied - Irrigation may be administered by a handheld bottle or through IV tubing with an irrigation lens ⦁ 2ND = check pH with a pH strip + check visual acuity after irrigation - irrigation discontinued when the pH reaches 7.0 - 7.3 Any particulate matter should be removed prior to irrigation if it is a reactive substance such as ammonium hydroxide crystals since fluid may dissolve these causing more injury. The upper lid should be everted to check for any particulate matter ⦁ 3RD = give MOXIFLOXACIN + cycloplegic agent (ex: atropine drops) ⦁ 4TH = Ophtho f/u

Answer 40

A dislocated shoulder occurs when the humerus separates from the scapula at the ** GLENOHUMORAL JOINT ** that connects humeral head to glenoid fossa The shoulder joint has the greatest range of motion of any joint in the body, and is thus particularly susceptible to subluxation (partial dislocation) and dislocation. Approximately half of major joint dislocations seen in emergency departments involve the shoulder. MECHANISM: ⦁ blow to an ABDUCTED, EXTERNALLY rotated arm that is EXTENDED - can also be due to FOOSA (fall onto outstretched arm) - contact sports in younger patients - falls in older patients Dislocations can occur from a trauma (95%) or from laxity of the ligaments (5%) ⦁ Patients often report hearing or feeling a pop during the incident*** ``` SYMPTOMS ⦁ significant pain ⦁ limited ROM ⦁ swelling ⦁ obvious deformity ⦁ arm is ABDUCTED + EXTERNALLY ROTATED ⦁ can palpate humeral head inferiorly ⦁ ** LOSS OF DELTOID CONTOUR** ⦁ => " SQUARED OFF SHOULDER " - appears box-like due to glenoid bone sticking out ``` humeral head can often be palpated anteriorly beneath the clavicle remember that ABs are anterior and important for EXTERNAL appearance (Anterior = ABduction + External rotation) Anterior dislocation = MC type of shoulder dislocation COMPLICATIONS ⦁ Axillary nerve injury (C5-C6 fibers) ⦁ Axillary artery injury ⦁ Rotator cuff damage MC torn rotator cuff tendon = supraspinatus tendon - is commonly torn with anterior shoulder dislocation DIAGNOSIS ⦁ Xray - Axillary + Y view - see humeral head ANTERIOR + INFERIOR to glenoid fossa - may have ⦁ HILL-SACHS lesion = groove on humeral head = compression fracture from impact against glenoid ⦁ BANKART lesion = fracture of inferior rim of glenoid or *injury to glenoid labrum* - soft tissue injury TREATMENT = * Manual Reduction * - closed reduction followed by sling immobilization for 2-6 weeks - PT - but must rule out axillary nerve injury first (pinprick sensation over the deltoid) Patient will present as → an 80-year-old woman arrives at the emergency room with severe right shoulder pain and immobility. She fell down the steps outside her house and landed on her right side two hours prior to presentation. On exam, her right arm is abducted and externally rotated. She has decreased sensation to touch over the lateral aspect of her right shoulder. Radiographs demonstrate an anterior shoulder dislocation.

Answer 41

A dislocated shoulder occurs when the humerus separates from the scapula at the ** GLENOHUMORAL JOINT ** The shoulder joint has the greatest range of motion of any joint in the body, and is thus particularly susceptible to subluxation (partial dislocation) and dislocation. Approximately half of major joint dislocations seen in emergency departments involve the shoulder. MECHANISM: ⦁ forced ADDUCTION, + INTERNAL rotation ``` Posterior shoulder dislocations are rare and typically seen after ⦁ ** seizures ** = MC ⦁ ** electrocution ** ⦁ car accidents ⦁ trauma ``` ``` SYMPTOMS ⦁ significant pain ⦁ limited ROM ⦁ swelling ⦁ obvious deformity ⦁ arm is held ADDUCTED + INTERNALLY rotated ``` Anterior shoulder = FLAT Humeral head is prominent the anterior shoulder will appear square with a flat coracoid process, and the humeral head may be palpated posteriorly beneath the acromion process. DIAGNOSIS ⦁ Xray - Axillary + Y view TREATMENT = * Manual Reduction * - closed reduction followed by sling immobilization for 2-6 weeks - PT

Answer 42

Dislocation occurs when the ball–shaped head of the femur comes out of the cup–shaped acetabulum set in the pelvis. Dislocation of the hip is a common injury to the hip joint. This may happen to a varying degree. MC in females A dislocated hip is a condition that can either be congenital or acquired. True orthopedic emergency!! CAUSE ⦁ MC = Trauma -MVA - fall from height Anterior hip dislocation = usually secondary to forced hip abduction MC = ** POSTERIOR HIP DISLOCATION ** (90%) CLINICAL MANIFESTATIONS ⦁ Anterior = may be externally rotated ``` COMPLICATIONS ⦁ ** Avascular Necrosis ** - reduced with early closed reduction < 6 hours ⦁ * Femoral nerve / artery injury * ⦁ DVT ⦁ Bleeding ``` FEMORAL NERVE INJURY - loss of sensation over thigh - weakness of quadriceps - loss of knee DTR FEMORAL ARTERY INJURY - hematoma - loss of pulses - pallor Vs Sciatic nerve injury (posterior hip dislocation complication) = loss of sensation in posterior leg/foot, loss of plantar flexion / dorsiflexion, loss of ankle DTR DIAGNOSIS ⦁ Xray = 1st line! - no fracture - An anteriorly dislocated femoral head will appear LARGER than the contralateral side on AP film TREATMENT - emergent reduction under conscious sedation ⦁ Closed reduction within 6 hours (to prevent avascular necrosis) CI to reduction = concurrent femoral neck fracture ⦁ PT ** If patient presents with hip pain, shortened leg, externally rotated + abducted = more likely hip fracture than anterior hip dislocation (not very common)

Answer 43

Dislocation occurs when the ball–shaped head of the femur comes out of the cup–shaped acetabulum set in the pelvis. Dislocation of the hip is a common injury to the hip joint. This may happen to a varying degree. MC in females A dislocated hip is a condition that can either be congenital or acquired. True orthopedic emergency!! CAUSE ⦁ MC = Trauma -MVA (ex: knee hits dashboard) - fall from height Posterior hip dislocations are most commonly associated with high-energy trauma such as motor vehicle collisions, falls from significant height, and high impact sports. Artificial hips can dislocate with less force. Posterior hip dislocations account for 90% of all hip dislocations. Posterior dislocations occur when a large axial load is transmitted through a FLEXED KNEE - ex: ****when the knee comes into contact with the dashboard in a crash**** MC = ** POSTERIOR HIP DISLOCATION ** (90%) Given the large amount of force needed to dislocate the femoral head, the majority of dislocations are associated with other injuries. ``` CLINICAL MANIFESTATIONS o Posterior ⦁ Severe hip pain ⦁ Inability to bear weight ⦁ hip deformity ⦁ limited ROM ⦁ ** Shortened leg ** ⦁ INTERNALLY ROTATED + ADDUCTED ⦁ with hip / knee slightly flexed ``` A detailed neurovascular exam should be conducted to rule out sciatic nerve injury. COMPLICATIONS ⦁ ** Avascular Necrosis ** - reduced with early closed reduction < 6 hours ⦁ * Sciatic nerve injury * (or superior / inferior gluteal nerve injury) ⦁ DVT ⦁ Bleeding ⦁ Recurrent dislocations ⦁ Arthritis SCIATIC NERVE INJURY - loss of sensation in posterior leg + foot - loss of plantar flexion + dorsiflexion - loss of ankle DTR DIAGNOSIS ⦁ Xray = 1st line! - no fracture - A posteriorly dislocated femoral head will appear SMALLER than the contralateral side on AP film TREATMENT - emergent reduction under conscious sedation ⦁ Closed reduction within 6 hours (to prevent avascular necrosis) CI to reduction = concurrent femoral neck fracture ⦁ PT

Answer 44

- a condition that affects pregnant women - occurs after 20 weeks gestation - in some cases, can develop up to 6 weeks after delivery MC occurs in final trimester CLINICAL MANIFESTATIONS ⦁ New onset Hypertension ⦁ Proteinuria (marker of kidney damage) ⦁ can cause damage to other organs as well (such as brain + liver) ***HYPERTENSION + PROTEINURIA*** WIDE-RANGE OF SYMPTOMS ⦁ asymptomatic or mild vs life-threatening PREECLAMPSIA + SEIZURES = ECLAMPSIA*** ``` RISK FACTORS FOR PREECLAMPSIA ⦁ first pregnancy ⦁ multiple gestation (twins / triplets / etc) ⦁ mothers > 35 ⦁ hypertension ⦁ diabetes ⦁ obesity ⦁ family hx of preeclampsia ``` PATHOPHYSIOLOGY Cause = develop of an abnormal placenta Normally in pregnancy, spiral arteries dilate to 5-10x their size and develop into large utero-placental arteries in order to deliver large quantities of blood to the developing fetus 1) UTERO-PLACENTAL ARTERIES BECOME FIBROUS / NARROWED - In Pre-eclampsia, these utero-placental arteries become fibrous --> narrow, so less blood gets to the placenta - a poorly perfused placenta can lead to intrauterine growth restriction + even fetal death 2) HYPO-PERFUSED PLACENTA RELEASES PRO-INFLAMMATORY PROTEINS- - Placenta is hypo-perfused --> releases pro-inflammatory proteins - these proteins enter maternal circulation --> cause the damage to endothelial cells that line blood vessels --> become dysfunctional 3) *** DAMAGED ENDOTHELIAL CELLS *** IN BLOOD VESSELS - causes vasoconstriction - also causes kidneys to retain more sodium - -> Hypertension! ** VASOCONSTRICTION + SODIUM RETENTION IN KIDNEYS --> HYPERTENSION ** 4) *** MATERNAL VASOSPASM *** - pro-inflammatory proteins can also cause local vasospasm, and therefore start to affect specific organs ⦁ reduced blood flow to kidneys --> glomerular damage --> oliguria (decreased urine output) + proteinuria (sign of glomerular damage) ⦁ reduced blood flow to retina --> blurred vision / flashing lights / scotomas (blurry spot in vision) ⦁ reduced blood flow to liver --> severe liver injury + swelling --> elevated LFTs + stretches the capsule around the liver --> RUQ pain 5) MICRO-THROMBI FORMATION IN VASCULATURE - Endothelial cell injury leads to formation of lots of tiny thrombi in micro-vasculature - uses up lots of platelets --> thrombocytopenia ± DIC - as RBCs try to navigate around clots in vessels, eventually run into clots and lyse --> hemolysis --> HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) HELLP syndrome develops in 10-20% of patients with severe pre-eclampsia / eclampsia 6) INCREASED VASCULAR PERMEABILITY - endothelial damage increases vascular permeability ==> water leaks out of vessels and into tissues - due to lack of protein in blood from proteinuria, there is lower osmotic pressure in vessels, so even more fluid leaks out of vasculature into tissues ==> Generalized Edema (legs / face / hands) ==> Pulmonary Edema (cough / SOB) ==> Cerebral Edema (headaches / confusion / seizures) - PRESENCE OF SEIZURES = NOW ECLAMPSIA CLASSIC TRIAD OF PRE-ECLAMPSIA 1) Hypertension 2) Proteinuria 3) Edema must have HTN + proteinuria to diagnose preeclampsia Preeclampsia is caused by abnormal placental spiral arteries leading to endothelial dysfunction, vasoconstriction and ischemia. ``` POSSIBLE SYMPTOMS ⦁ HTN ⦁ proteinuria ⦁ edema ⦁ headache ⦁ visual symptoms ⦁ oliguria ⦁ confusion ⦁ cough ⦁ SOB ⦁ thrombocytopenia ``` DIAGNOSIS OF PRE-ECLAMPSIA ⦁ Systolic BP > 140mmHg ⦁ Diastolic BP > 90mmHg o Mild Preeclampsia = BP ≥ 140/90 ⦁ Proteinuria: > 300mg/24 hours or +1 on dipstick The diagnosis of mild preeclampsia requires 2 serial blood pressure readings of >140/90 mmHg over 6 hours or more, and > 0.3 g/24hrs of protein in the urine. o Severe pre-eclampsia = BP ≥ 160/110 ⦁ Proteinuria: > 500mg/24 hours or +3 on dipstick - these extreme BPs can lead to hemorrhagic stroke or placental abruption (placenta prematurely detaches from uterine wall) Preeclampsia is considered severe with blood pressure of >160/110 mmHg, urinary protein of >0.5g/day, or if there are signs of end-organ damage such as visual disturbance, hepatocellular injury, thrombocytopenia, oliguria (<500mL produced per day), fetal growth restriction, or pulmonary edema. ⦁ Oliguria = < 500mL/day Abdominal pain, nausea, retrosternal chest pain, and headache are common symptoms of preeclampsia with severe features ``` COMPLICATIONS - Patients who have had preeclampsia have increased risk of developing ⦁ hypertension later in life ⦁ ischemic heart disease ⦁ stroke ⦁ venous thromboembolism. ``` TREATMENT o Mild Pre-eclampsia ⦁ DELIVERY OF FETUS + PLACENTA**** - depends on gestational age + severity of disease - Delivery at 37 weeks gestation - May deliver at 34-36 weeks if necessary ``` - If < 34 weeks = Conservative treatment ⦁ daily weights ⦁ weekly BP ⦁ weekly dipstick ⦁ bedrest ``` - If < 34 weeks = STEROIDS to mature lungs (betamethasone) o Severe Pre-eclampsia ⦁ DELIVERY OF FETUS + PLACENTA**** - prompt delivery = only cure + Hospitalization ⦁ *** MAGNESIUM SULFATE *** to prevent eclampsia (seizures) - can be given x 24-48 hours ⦁ BP MEDS if severe HTN = HYDRALAZINE** (others = labetalol, nifedipine) If symptoms develop after delivery, treatment = manage symptoms, which will slowly subside on their own Sodium nitroprusside is a medication used in severe hypertensive emergency in pregnancy, where first-line medications have failed to lower the blood pressure.

Answer 45

ECLAMPSIA = Pre-eclampsia + SEIZURES or COMA = life threatening for mother + fetus ``` SYMPTOMS ⦁ abrupt tonic-clonic seizures x 1-2 min followed by post-ictal state - may have ⦁ headache ⦁ visual changes ⦁ cardiorespiratory arrest ``` Patient meets all criteria for preeclampsia (HTN + Proteinuria + Seizures or Coma) PREECLAMPSIA + SEIZURES = ECLAMPSIA*** ``` RISK FACTORS FOR PREECLAMPSIA / ECLAMPSIA ⦁ first pregnancy ⦁ multiple gestation (twins / triplets / etc) ⦁ mothers > 35 ⦁ hypertension ⦁ diabetes ⦁ obesity ⦁ family hx of preeclampsia ``` PATHOPHYSIOLOGY Cause = development of an abnormal placenta Normally in pregnancy, spiral arteries dilate to 5-10x their size and develop into large utero-placental arteries in order to deliver large quantities of blood to the developing fetus 1) UTERO-PLACENTAL ARTERIES BECOME FIBROUS / NARROWED - In Pre-eclampsia, these utero-placental arteries become fibrous --> narrow, so less blood gets to the placenta - a poorly perfused placenta can lead to intrauterine growth restriction + even fetal death 2) HYPO-PERFUSED PLACENTA RELEASES PRO-INFLAMMATORY PROTEINS- - Placenta is hypo-perfused --> releases pro-inflammatory proteins - these proteins enter maternal circulation --> cause the damage to endothelial cells that line blood vessels --> become dysfunctional 3) *** DAMAGED ENDOTHELIAL CELLS *** IN BLOOD VESSELS - causes vasoconstriction - also causes kidneys to retain more sodium - -> Hypertension! ** VASOCONSTRICTION + SODIUM RETENTION IN KIDNEYS --> HYPERTENSION ** 4) *** MATERNAL VASOSPASM *** - pro-inflammatory proteins can also cause local vasospasm, and therefore start to affect specific organs ⦁ reduced blood flow to kidneys --> glomerular damage --> oliguria (decreased urine output) + proteinuria (sign of glomerular damage) ⦁ reduced blood flow to retina --> blurred vision / flashing lights / scotomas (blurry spot in vision) ⦁ reduced blood flow to liver --> severe liver injury + swelling --> elevated LFTs + stretches the capsule around the liver --> RUQ pain 5) MICRO-THROMBI FORMATION IN VASCULATURE - Endothelial cell injury leads to formation of lots of tiny thrombi in micro-vasculature - uses up lots of platelets --> thrombocytopenia ± DIC - as RBCs try to navigate around clots in vessels, eventually run into clots and lyse --> hemolysis --> HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) HELLP syndrome develops in 10-20% of patients with severe pre-eclampsia / eclampsia 6) INCREASED VASCULAR PERMEABILITY - endothelial damage increases vascular permeability ==> water leaks out of vessels and into tissues - due to lack of protein in blood from proteinuria, there is lower osmotic pressure in vessels, so even more fluid leaks out of vasculature into tissues ==> Generalized Edema (legs / face / hands) ==> Pulmonary Edema (cough / SOB) ==> Cerebral Edema (headaches / confusion / seizures) - PRESENCE OF SEIZURES = NOW ECLAMPSIA CLASSIC TRIAD OF ECLAMPSIA 1) Hypertension 2) Proteinuria 3) Seizures ``` POSSIBLE SYMPTOMS ⦁ HTN* ⦁ proteinuria* ⦁ seizures* ⦁ edema ⦁ headache ⦁ visual symptoms ⦁ oliguria ⦁ confusion ⦁ cough ⦁ SOB ⦁ thrombocytopenia ``` DIAGNOSIS OF PRE-ECLAMPSIA / ECLAMPSIA o Mild Preeclampsia = BP ≥ 140/90 ⦁ Proteinuria: > 300mg/24 hours or +1 on dipstick The diagnosis of mild preeclampsia requires 2 serial blood pressure readings of >140/90 mmHg over 6 hours or more, and > 0.3 g/24hrs of protein in the urine. o Severe pre-eclampsia = BP ≥ 160/110 ⦁ Proteinuria: > 500mg/24 hours or +3 on dipstick - these extreme BPs can lead to hemorrhagic stroke or placental abruption (placenta prematurely detaches from uterine wall) Preeclampsia is considered severe with blood pressure of >160/110 mmHg, urinary protein of >0.5g/day, or if there are signs of end-organ damage such as visual disturbance, hepatocellular injury, thrombocytopenia, oliguria (<500mL produced per day), fetal growth restriction, or pulmonary edema. ⦁ Oliguria = < 500mL/day Abdominal pain, nausea, retrosternal chest pain, and headache are common symptoms of preeclampsia with severe features ⦁ Seizures = is now diagnosed as eclampsia ``` COMPLICATIONS - Patients who have had preeclampsia have increased risk of developing ⦁ hypertension later in life ⦁ ischemic heart disease ⦁ stroke ⦁ venous thromboembolism. ``` TREATMENT 1) ABCDEs 2) MAGNESIUM SULFATE for seizures - 2nd line = Lorazepam - only if refractory to mag sulf 3) Once patient stabilized ==> Delivery of Fetus 4) BP Meds: HYDRALAZINE, Labetalol Magnesium sulfate is the first-line medication for the prevention of primary and recurrent eclamptic seizures.

Answer 46

HELLP syndrome is a manifestation of preeclampsia with hemolysis, elevated liver enzymes, and low platelets. HELLP syndrome = preeclampsia + thrombotic microangiopathy involving the liver characterized by hemolysis, elevated liver enzymes, and low platelet count. PATHOPHYSIOLOGY Normally in pregnancy, spiral arteries dilate to 5-10x their size and develop into large utero-placental arteries in order to deliver large quantities of blood to the developing fetus 1) UTERO-PLACENTAL ARTERIES BECOME FIBROUS / NARROWED - In Pre-eclampsia, these utero-placental arteries become fibrous --> narrow, so less blood gets to the placenta - a poorly perfused placenta can lead to intrauterine growth restriction + even fetal death 2) HYPO-PERFUSED PLACENTA RELEASES PRO-INFLAMMATORY PROTEINS- - Placenta is hypo-perfused --> releases pro-inflammatory proteins - these proteins enter maternal circulation --> cause the damage to endothelial cells that line blood vessels --> become dysfunctional 3) DAMAGED ENDOTHELIAL CELLS IN BLOOD VESSELS - causes vasoconstriction - also causes kidneys to retain more sodium - -> Hypertension! ** VASOCONSTRICTION + SODIUM RETENTION IN KIDNEYS --> HYPERTENSION 4) LOCAL VASOSPASM - pro-inflammatory proteins can also cause local vasospasm, and therefore start to affect specific organs ⦁ reduced blood flow to kidneys --> glomerular damage --> oliguria (decreased urine output) + proteinuria (sign of glomerular damage) ⦁ reduced blood flow to retina --> blurred vision / flashing lights / scotomas (blurry spot in vision) ⦁ reduced blood flow to liver --> severe liver injury + swelling --> elevated LFTs + stretches the capsule around the liver --> RUQ pain (HELLP) 5) MICRO-THROMBI FORMATION IN VASCULATURE - Endothelial cell injury leads to formation of lots of tiny thrombi in micro-vasculature - uses up lots of platelets --> thrombocytopenia - as RBCs try to navigate around clots in vessels, eventually run into clots and lyse --> hemolysis --> HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) HELLP syndrome develops in 10-20% of patients with severe pre-eclampsia / eclampsia 6) INCREASED VASCULAR PERMEABILITY - endothelial damage increases vascular permeability ==> water leaks out of vessels and into tissues - due to lack of protein in blood from proteinuria, there is lower osmotic pressure in vessels, so even more fluid leaks out of vasculature into tissues ==> Generalized Edema (legs / face / hands) ==> Pulmonary Edema (cough / SOB) ==> Cerebral Edema (headaches / confusion / seizures) - PRESENCE OF SEIZURES = NOW ECLAMPSIA ``` DIAGNOSIS ⦁ HTN (> 140/90) ⦁ proteinuria (> 0.3g/day or +1) ⦁ hemolytic anemia (low hct and/or hemoglobin) - normal hematocrit (men) = 38-50 - normal hematocrit (women) = 34-45 - normal hemoglobin (men) = 14-18 - normal hemoglobin (women) = 12-16 ⦁ thrombocytopenia (platelets will be < 100,000) - normal = 150,00 - 450,000 ⦁ elevated LDH level (cell damage) - normal = 140-330 ⦁ elevated total bilirubin (> 1.2) - due to hemolysis ⦁ elevated AST / ALT (increase by > 70) - normal AST = 5-40 - normal ALT = 7-56 ⦁ presence of schistocytes on peripheral smear ``` TREATMENT ⦁ Immediate induction of labor with plan for vaginal delivery

Answer 47

Inflammation of the meninges caused by bacteria ``` Meninges = 3 protective layers around the brain + spinal cord ⦁ dura mater = outermost ⦁ arachnoid mater = middle - subarachnoid space ⦁ pia mater = innermost ``` Meningitis = specifically inflammation of the 2 inner meninges, also called the Leptomeninges Between the leptomeninges = subarachnoid space where CSF is located CSF = clear / watery fluid that is pumped around the spinal cord and brain that functions to provide nutrients as well as cushion them from impact CSF WBC count = up to 5 (no RBCs) ``` In 1 deciliter of CSF ⦁ 70% lymphocytes ⦁ 30% monocytes ⦁ remaining few = PMNs - PMNs (polymorphonuclear leukocytes = granulocytes = basophils + neutrophils + eosinophils) ⦁ proteins (15-50 mg) ⦁ glucose (45-100 mg) = about 2/3 of glucose found in same volume of blood ⦁ Pressure: < 200 mmH20 = < 15mmHg - normal opening pressure = 5-20 cm ``` TOTAL AMOUNT OF CSF IN BODY = about 150mL - is constantly replenished - 500mL produced each day - excess is reabsorbed into blood For any nutrients to enter or leave the CSF = must go through tightly-regulated BBB (blood-brain barrier) BBB = blood vessels in the brain - endothelial cells in these blood vessels are so tightly bound to one another that they prevent leakage and only allow certain molecules to slip through them Meningitis = NOT the inflammation of the brain itself (encephalitis), but the inflammation of the 2 inner leptomeninges surrounding the brain + spinal cord Both can occur together, however, which is called meningoencephalitis CAUSES / TRIGGERS OF MENINGITIS ⦁ autoimmune disease (lupus) ⦁ adverse medication reaction (intrathecal therapy - med injected directly into CSF) ⦁ *** MC = INFECTION *** HOW IS INFECTION TRANSMITTED TO CSF + MENINGES 1) Direct spread - pathogen gets into skull or spinal column and then penetrates the meninges, eventually getting to CSF - sometimes the pathogen goes through overlying skin or up through nose - MC = anatomical defect that allows pathogen through ⦁ congenital = Spina bifida ⦁ acquired = skull fracture - CSF leaking through sinuses 2) Hematogenous spread - pathogen spreads through blood and through endothelial cells that make up BBB, and into CSF - either by binding to surface receptors or finding area of damage in BBB Once pathogen is in CSF ==> can start multiplying! small amount of WBCs in CSF --> release cytokines --> recruit more WBCs --> may end up with thousands of WBCs in 1 microliter of CSF > 5 WBCs = enough to signify meningitis DIAGNOSIS FOR BACTERIAL MENINGITIS - Pressure rises > 200 mmH20 / > 5-20 cm - CSF appearance = Turbid - Glucose levels (50-80) = *decreased* (< 40) - Protein levels (18-58) = *increased* (>200) - WBC count (0-5) = *increased* (100 - 100,000) - PMNs (1%) = predominantly neutrophils (> 80%/ > 90%) - gram stain positive The additional immune cells attract more cells to the area --> start causing local destruction as they try to control the infection Bacteria + Virus = usually cause acute meningitis Fungi = usually cause chronic meningitis BACTERIAL CAUSES o < 1 month ⦁ MC = Group B strep (strep agalactiae) = 70% ⦁ Listeria monocytogenes* ⦁ E. coli ⦁ strep pneumo - Tx = Ampicillin (covers listeria) + Cefotaxime or Aminoglycoside (also used in 1-3 months old) o 1 month - 18 years ⦁ MC = Neisseria meningitidis (petechial rash) ⦁ strep pneumo* ⦁ h. flu - Tx - 1-3 months old = Ampicillin (covers listeria) + Cefotaxime or Aminoglycoside - > 3 months - 18 = Ceftriaxone + Vanco ``` o 18 - 50 y/o ⦁ MC = Strep pneumo ⦁ Neisseria meningitidis (petechial rash) ⦁ listeria monocytogenes ⦁ h. flu - Tx = Ceftriaxone + Vanco ``` o > 50 y/o ⦁ Strep pneumo ⦁ listeria monocytogenes - Tx = Ampicillin + Ceftriaxone +/- Vanco Tick-borne: Borrelia burgdorferi (lyme dz) meningitis ** start empiric antibiotics immediately! - don't wait for LP ** SYMPTOMS - CLASSIC TRIAD OF MENINGITIS SYMPTOMS ⦁ headache ⦁ fever / chills (95%) ⦁ nuchal rigidity (neck stiffness) OTHER SYMPTOMS ⦁ photophobia ⦁ phonophobia ⦁ N / V Can develop AMS / Seizures ** start empiric antibiotics immediately! - don't wait for LP ** DIAGNOSIS o Physical Exam ⦁ *** KERNIG'S SIGN *** = laying on back, lift 1 leg up, flexed at 90 at the knee. Slowly straighten the leg out at the knee to where leg is straight up --> back pain! ⦁ *** BRUDZINSKI SIGN *** = laying flat on back, patient flexes head forward --> causes patient to automatically bend both legs at the knee with feet still touching floor o CT to rule out mass effect BEFORE getting LP o LUMBAR PUNCTURE = ** definitive diagnosis ** - needle penetrates into subarachnoid space, take CSF - analyze pressure / WBCs / Protein / Glucose ⦁ neutrophils ⦁ decreased glucose (< 45) ⦁ increased protein (> 200) ⦁ increased CSF pressure (> 5-20 cm) ⦁ turbid color / cloudy ** start empiric antibiotics immediately! - don't wait for LP ** o PCR - can be used to find specific causes, such as HIV, enteroviruses, HSV, TB, etc - if suspect particular cause = can test for that ⦁ western blot - for TB ⦁ thin blood smear - for malaria BACTERIAL TREATMENT - depends on underlying cause o < 1 month (MC = group B strep) - Tx = Ampicillin (covers listeria) + Cefotaxime or Aminoglycoside (also used in 1-3 months old) o 1 month - 18 y/o (MC = Neisseria) - 1-3 months = - Tx = Ampicillin (covers listeria) + Cefotaxime or Aminoglycoside - > 3 months = - Tx = Ceftriaxone + Vanco o 18 - 50 y/o (MC = strep pneumo - Tx = Ceftriaxone + Vanco o > 50y/o (MC = strep pneumo) - Tx = Ampicillin + Ceftriaxone +/- Vanco POST-EXPOSURE PROPHYLAXIS ⦁ Cipro 500mg PO x 1 dose ⦁ Alternative = Rifampin 600mg PO q12h x 2 days

Answer 48

Inflammation of the meninges NOT caused by bacteria, but caused by virus / fungus / TB / etc. ``` Meninges = 3 protective layers around the brain + spinal cord ⦁ dura mater = outermost ⦁ arachnoid mater = middle - subarachnoid space ⦁ pia mater = innermost ``` Meningitis = specifically inflammation of the 2 inner meninges, also called the Leptomeninges Between the leptomeninges = subarachnoid space where CSF is located CSF = clear / watery fluid that is pumped around the spinal cord and brain that functions to provide nutrients as well as cushion them from impact CSF WBC count = up to 5 (no RBCs) ``` In 1 deciliter of CSF ⦁ 70% lymphocytes ⦁ 30% monocytes ⦁ remaining few = PMNs - PMNs (polymorphonuclear leukocytes = granulocytes = basophils + neutrophils + eosinophils) ⦁ proteins (15-50 mg) ⦁ glucose (45-100 mg) = about 2/3 of glucose found in same volume of blood ⦁ Pressure: < 200 mmH20 = < 15mmHg - normal opening pressure = 5-20 cm ⦁ WBC count (normal) = up to 5 ``` TOTAL AMOUNT OF CSF IN BODY = about 150mL - is constantly replenished - 500mL produced each day - excess is reabsorbed into blood For any nutrients to enter or leave the CSF = must go through tightly-regulated BBB (blood-brain barrier) BBB = blood vessels in the brain - endothelial cells in these blood vessels are so tightly bound to one another that they prevent leakage and only allow certain molecules to slip through them Meningitis = NOT the inflammation of the brain itself (encephalitis), but the inflammation of the 2 inner leptomeninges surrounding the brain + spinal cord Both can occur together, however, which is called meningoencephalitis CAUSES / TRIGGERS OF MENINGITIS ⦁ autoimmune disease (lupus) ⦁ adverse medication reaction (intrathecal therapy - med injected directly into CSF) ⦁ *** MC = INFECTION *** HOW IS INFECTION TRANSMITTED TO CSF + MENINGES 1) Direct spread - pathogen gets into skull or spinal column and then penetrates the meninges, eventually getting to CSF - sometimes the pathogen goes through overlying skin or up through nose - MC = anatomical defect that allows pathogen through ⦁ congenital = Spina bifida ⦁ acquired = skull fracture - CSF leaking through sinuses 2) Hematogenous spread - pathogen spreads through blood and through endothelial cells that make up BBB, and into CSF - either by binding to surface receptors or finding area of damage in BBB Once pathogen is in CSF ==> can start multiplying! small amount of WBCs in CSF --> release cytokines --> recruit more WBCs --> may end up with thousands of WBCs in 1 microliter of CSF > 5 WBCs = enough to signify meningitis DIAGNOSIS FOR VIRAL MENINGITIS - Opening Pressure (5-20cm) = Normal or mild increase - CSF appearance = Clear - Glucose levels (50-80) = *normal* - Protein levels (18-58) = *normal or mild increase* - WBC count (0-5) = *slight increase* (10-300) - Predominantly LYMPHOCYTES - gram stain = negative DIAGNOSIS FOR FUNGAL + TUBERCULOSIS MENINGITIS - Opening Pressure (5-20cm) = Normal or mild increase - CSF appearance = Fibrin webs - Glucose levels (50-80) = *decreased* - Protein levels (18-58) = *increased* - WBC count (0-5) = *slight increase* (10-200) - Predominantly LYMPHOCYTES - gram stain = negative The additional immune cells attract more cells to the area --> start causing local destruction as they try to control the infection Bacteria + Virus = usually cause acute meningitis Fungi = usually cause chronic meningitis o VIRAL CAUSES ⦁ **Enterovirus** = MC (*MC = Echovirus*, Coxsackie) ⦁ Arboviruses (arthropod borne viruses - via insects) ⦁ HSV ⦁ HIV ⦁ Mumps o FUNGAL CAUSES ⦁ Cryptococcus ⦁ Coccidioides - mainly affect immunocompromised SYMPTOMS - CLASSIC TRIAD OF MENINGITIS SYMPTOMS ⦁ headache ⦁ fever / chills (95%) ⦁ nuchal rigidity (neck stiffness) OTHER SYMPTOMS ⦁ photophobia ⦁ phonophobia ⦁ N / V Viral symptoms not as intense as bacterial meningitis symptoms - Viral meningitis = associated with NORMAL cerebral function - not commonly associated with focal neurological deficits or seizures (no AMS / Seizures) ``` DIAGNOSIS - 1) CT scan to rule out intracranial mass - 2) LP - CSF analysis Virus = ⦁ Lymphocytes ⦁ normal glucose ⦁ mildly elevated protein ``` TREATMENT = supportive care ⦁ antipyretics ⦁ IV fluids ⦁ antiemetics PROGNOSIS = good usually self-limiting, lasts about 7-10 days - increased fatality in neonates

Answer 49

Trichomoniasis is a common cause of vaginitis. most common non-viral STD worldwide It is a common sexually transmitted infection, and is caused by the single-celled protozoan PARASITE** - Trichomonas vaginalis ⦁ Bacteria = Trichomonas vaginalis (T. vaginalis) ⦁ PEAR SHAPED FLAGELLATED PROTOZOA ⦁ sexually transmitted Produces mechanical stress on host cells and then ingesting cell fragments after cell death. Trichomoniasis is primarily an infection of the UROGENITAL TRACT MC site of infection = urethra and vagina in women ``` SYMPTOMS ⦁ vulvar pruritus ⦁ vulvovaginal erythema ⦁ itching ⦁ burning ⦁ dysuria ⦁ dyspareunia ⦁ post-coital bleeding ``` ⦁ MALODOROUS VAGINAL DISCHARGE - copious, malodorous discharge - FROTHY YELLOW-GREEN DISCHARGE - discharge is worse with menses ⦁ STRAWBERRY CERVIX (cervical petechiae) Vaginal pH > 5 (normal vaginal pH = 3.8 - 4.5) ``` DIAGNOSIS ⦁ wet mount = mobile protozoa (trichomonads) = "CORKSCREW" motility - FLAGELLA **** ⦁ elevated WBC count ⦁ vaginal pH 5-6 ⦁ UA = positive for WBCs ``` *** MOBILE WET PREP *** TREATMENT ⦁ Metronidazole (Flagyl) - either 2g oral x 1 dose or 500mg bid oral x 7 days - safe to use in pregnancy! ⦁ Tinidazole **** MUST TREAT PARTNER **** COMPLICATIONS - perinatal complications - increased HIV transmission

Answer 50

Ipratropium bromide is inhaler of choice for COPD (anticholinergic bronchodilator) Treatment: Short acting bronchodilators for mild disease, long acting bronchodilators +/- inhaled corticosteroids for moderate to severe disease, Smoking cessation and supplemental O2 (O2 is single most important medication in long term) Antibiotics for acute exacerbations Flu and pneumococcal vaccines are a must Defined as a chronic cough that is productive of phlegm occurring on most days for 3 months of the year for 2 or more consecutive years without an otherwise-defined acute cause Chronic Bronchitis = Blue Bloaters (2º to chronic hypoxia) Common in Smokers (80% of COPD patients) Physical exam: wheezes, rales, and rhonchi PFT's: FEV1/FVC ratio less than 0.7 Chest radiograph: peribronchial and perivascular markings ↑ HGB and HCT common because of chronic hypoxic state ↑ pulmonary HTN with RVH, distended neck veins, hepatomegaly

Answer 51

Pneumothorax = Air within the pleural pace ANATOMY - lungs are surrounded by visceral pleura - then pleural space - then parietal pleura Within the pleural space = normally have lubricating fluid that reduces friction as the lungs expand and contract 2 forces that create a slight vacuum within the pleural space = 1) muscle tension from the diaphragm and chest wall as they expand outward = balanced with 2) elastic recoil of the lungs that are pulled inward ==> This creates a negative water pressure within the pleural space (-5) compared to pressure of 0 in both lungs + thoracic cavity In pneumothorax, air gets between the visceral and parietal pleura PATHOPHYSIOLOGY ⦁ Pneumothorax forms when the seal of the pleural space gets punctured and air moves in ⦁ this makes the pressure in the pleural space = 0 ⦁ since the negative pleural pressure is lost ==> the 2 opposing forces no longer pull on one another ==> ⦁ lungs pull inward and collapse COLLAPSED LUNG - limited ability to exchange air --> decreased amount of oxygen available for the rest of the body - -> build up of CO2 in the body because of decreased ability to release air TYPES OF PNEUMOTHORAX 1) PRIMARY SPONTANEOUS PNEUMOTHORAX ⦁ no underlying lung disease ⦁ occurs in "tall thin young males" - usually in 20s ⦁ positive family hx ⦁ can happen from **smoking**, diving, high altitude flying, or holding breath MC cause of primary spontaneous pneumothorax = Rupture of subpleural apical blebs due to high negative intrapleural pressures - air leaks from alveoli --> creates air bullae on lung - if bullae breaks, air can fill pleural space ``` 2) SECONDARY SPONTANEOUS PNEUMOTHORAX ⦁ with an underlying lung disease - asthma - COPD - emphysema - lung cancer - CF** - HIV related - pneumocystis - TB - Marfan's syndrome / Ehlers Danlos** ``` Patients with Marfan syndrome are prone to recurrent pneumothoraces. 3) TRAUMATIC PNEUMOTHORAX ⦁ trauma or chest injury - *rib fracture / stab wound / GSW rips through parietal pleura, allowing air to enter from outside directly into pleural space 4) IATROGENIC PNEUMOTHORAX ⦁ "medically caused" - medical interventions that went wrong, such as chronic mechanical ventilation (can cause barotrauma to lungs), or some sort of procedure - CPR, thoracentesis, ventilation, subclavian line placement, rapid pre-oxygenation rate An overly rapid pre-oxygenation rate prior to intubation can cause a pneumothorax After placing a central venous catheter (CVC), a chest radiograph should be obtained immediately to ensure adequate line placement and to assess for complications before the line is used Pneumothorax formation may occur during the supraclavicular approach of a brachial plexus block 5) TENSION PNEUMOTHORAX (MC after trauma** or infection) ⦁ essentially the same as any other pneumothorax, however, what makes it tension is that air in the pleural space cannot exit AT ALL - a one-way valve is created, allowing air to flow into pleural space, however, flap of tissue only allows air in + prevents air from getting out --> continues to expand - over time, so much air in pleural space can start compressing the heart and other lung, and starts shifting large structures such as the trachea (tracheal deviation) + mediastinal shift - can prevent heart from filling up properly --> reduced cardiac output - can prevent other lung from expanding properly --> reduced oxygen ⦁ most serious type --> goes into severe respiratory distress, to where patient can die ⦁ medical emergency = don't have time to diagnose via cxr, like others - falling O2 sats, hypotension, tracheal deviation CATAMENIAL PNEUMOTHORAX = occurs during menstruation (ectopic endometrial tissue in pleura) SYMPTOMS OF PNEUMOTHORAX ⦁ dyspnea / SOB ⦁ pleuritic chest pain (pain while breathing) ⦁ decreased breath sounds on affected side ⦁ unequal respiratory expansion ⦁ ** HYPERRESONANCE ** on percussion ⦁ Decreased tactile fremitus ⦁ Decreased egophany ⦁ JVD (jugular veins distended) = tension ⦁ hypotension + tachypnea + tachycardia = tension JVD = due to increased pressure on the collapsed lung, blood backs up on right side of heart (cannot send as much blood to lungs) --> backs up right side of heart --> JVD (pressure in pulmonary artery = really high!) Hyperresonance = indicates that too much AIR is present in the lungs (pneumothorax / asthma / emphysema) Dullness to percussion = indicates abnormal lung density / consolidation (atelectasis, tumor, plural effusion, pneumonia, fibrous tissue, hemothorax) Egophony is an increased resonance of voice sounds heard when auscultating the lungs, often caused by lung consolidation and fibrosis - due to enhanced transmission of high-frequency sound across fluid / tissue. - normal lungs (filled with air), do not readily transmit sounds, while consolidated lung tissue more readily transmits sounds - Egophany = decreased with air (pneumothorax - increased with fluid / excess tissue (consolidation) = pneumonia / pleural effusion - *** Although in pleural effusion = egophony is only heard above the effusion in an upright patient increased Tactile fremitus = indicates denser tissue / consolidation decreased tactile fremitus = air or fluid in pleural space(pneumothorax, effusion) Tactile fremitus increases in intensity whenever the density of lung tissue increases, such as consolidation or fibrosis - causes of increased tactile fremitus include: Pneumonia, Lung tumor or mass, Pulmonary fibrosis, Atelectasis. Tactile fremitus will decrease when a lung space is occupied with an increase of fluid or air (pleural effusion, pneumothorax and emphysema) DIAGNOSIS ⦁ CXR = initial test for all pneumothoraces except tension (emergency!) - absent vascular markings due to air - air (black) - may see outline of collapsed lung - may see hyperexpanded diaphragm - tracheal deviation to other side = tension - mediastinal shift (heart pushed to other side) = tension ⦁ CT = ** still considered gold standard ** - but xray more commonly used in practice because it is cheaper, faster, and has less radiation exposure TREATMENT ⦁ if "small " pneumothorax and not tension = can be managed with just oxygen - small = < 2-3 cm or <15-20% of diameter between visceral and parietal pleura = OBSERVE x at least 6 hrs, then repeat CXR to affirm no progression - f/u in 24-48 hours - often spontaneously resolves within 10 days - Tx = ** HIGH FLOW OXYGEN ** (10L/min) - shown to increase air resorption 3-4x faster than 1.25% every day - If patients remain stable for 4-6 hours, they can be released with follow-up in several days. Patients should be instructed to immediately seek medical attention should they become short of breath. For otherwise healthy, young patients with a small primary spontaneous pneumothorax (<3 cm between the lung and the chest wall on chest X-ray), observation alone may be appropriate. The intrinsic resorption rate is approximately 1-2% a day and is accelerated with the administration of 100% oxygen. Many physicians observe these patients for 6 hours and then repeat the chest X-ray. If the repeat chest X-ray shows no increase in the size of the pneumothorax, the patient can be discharged with follow-up in 24 hours. Air travel and underwater diving (which cause changes in atmospheric pressure) must be avoided until the pneumothorax completely resolves. ⦁ Chest tube (thoracostomy) if large pneumothorax or if severe symptoms - 4th-5th or 5th-6th ICS - mid axillary line ⦁ Needle Decompression (14G) = if TENSION PMX* - followed by chest tube - 2nd ICS (between 2nd + 3rd rib) at the midclavicular line - hear gush of air RECURRENT PNEUMOTHORACES ex: tall thin young males who have had recurrent primary spontaneous pneumothoraces can have PLEURODESIS done = via Video-assisted thoracoscopic surgery or Thoracotomy Pleurodesis = a procedure that scars the lung tissue so that it adheres to the parietal pleura, providing a sturdier barrier in that portion of the lung wall and obliterating the pleural space lung tissue is scarred either via an irritant (talc powder) or through mechanical abrasion, in order for it to adhere tightly to the parietal pleura, thereby eliminating the pleural space. SPONTANEOUS PNEUMOTHORAX Patient will be a young, tall, thin, man PE will show decreased breath sounds, decreased fremitus, hyperresonance to percussion CXR will show the absence of lung markings along lung periphery Treatment is: < 20% in a healthy patient: observation with oxygen administration > 20%: chest tube thoracostomy ON TEST - if not a tension pneumothorax = get an xray first - if tension pneumothorax = needle decompression first

Answer 52

In order to diagnose AMS, the patient must have a recent gain in altitude which occurred at least several hours ago, a headache, and one of the following additional symptoms: gastrointestinal upset, generalized weakness, fatigue, dizziness, lightheadedness, or insomnia. due to low partial pressure of oxygen at high altitudes The headache is generally BITEMPORAL and THROBBING. Headaches are generally worse at night and when moving to an upright position. The pathophysiology of AMS is not fully understood, but is thought to be caused by hypoxia which leads to intracranial vasodilation and cerebral edema. Insomnia is caused by nocturnal, periodic breathing. The cornerstone of management of AMS is to halt ascent until symptoms improve. Headaches can be treated with acetaminophen or ibuprofen. Supplemental oxygen may also reduce symptoms. Acetazolamide can be used to stimulate breathing and can be helpful for insomnia. It is a carbonic anhydrase inhibitor which causes a renal bicarbonate diuresis. This causes a metabolic acidosis which stimulates increased ventilation and thereby improves arterial oxygenation. If symptoms do not improve or worsen with conservative management, the patient should descend to lower altitudes. 1) stop ascent 2) supportive: fluids / analgesia / antiemetic 3) acetazolamide / dexamethasone 4) descent Acetazolamide = CI in patients with sickle cell + sulfonamide allergies

Answer 53

is the most severe form of AMS and manifests when cerebral edema becomes profound enough to cause global cerebral dysfunction. Signs of high-altitude cerebral edema (HACE) include ataxia, confusion, and altered mental status. It can progress to brain-stem herniation and death. Management of HACE includes 1) immediate descent 2) supplemental oxygen 3) acetazolamide / steroids. Portable hyperbaric chambers can be used as a temporizing measure if descent cannot be immediately achieved.

Answer 54

= Acute inflammation of the gallbladder MC CAUSE = gallstone lodged in cystic duct stones = MC made up of cholesterol MC in women than men Prevalence increases with age Higher in Native American population 3 F's = FERTILE + FAT + FORTY = Classic patient Bile is made in the liver, stored in the gallbladder the hepatic ducts descend and meet with the cystic duct to form the common bile duct - the pancreatic duct and the common bile duct drain into the duodenum through Ampulla of Vater via Sphincter of Oddi PATHOPHYSIOLOGY 1) gallstones present in gallbladder 2) person eats food 3) small intestine secretes CCK (cholecystokinin) into blood --> makes its way into the gallbladder --> signals gallbladder to secrete bile to aid in digestion of food 4) the gallbladder contracts --> gallstone gets lodged in cystic duct 5) flow of bile is blocked by gallstone in cystic duct - -> builds up in gallbladder 6) Gallbladder continues to squeeze / contract, but is blocked, and CCK continues to trigger gallbladder to secrete bile. Gallbladder gets stretched --> irritation of nerves in gallbladder + cystic duct --> pain! 7) Bile remaining in Gallbladder for prolonged time becomes an IRRITANT --> gallbladder mucosa starts secreting mucus + inflammatory enzymes --> inflammation / distention / more pressure --> RUQ pain 8) May start to have some bacterial growth in gallbladder (MC = E. Coli, Others = Klebsiella, Enterococci, Bacteroides fragilis, clostridium) 9) Bacteria can start invading through gallbladder wall --> peritonitis --> Rebound tenderness 10) bacterial invasion --> triggers immune response --> leukocytosis + neutrophils SUMMARY: 90% of acute cholecystitis cases = caused by GALLSTONES - trapped bile becomes concentrated and causes irritation + pressure build-up in gallbladder - -> can lead to bacterial infection - -> can lead to perforation - usually follows a large or fatty meal SYMPTOMS ⦁ Pain - initially MID EPIGASTRIC ⦁ Pain then moves to RUQ - dull / achy pain ⦁ precipitated by fatty foods / large meal ⦁ Pain may radiate to scapula or shoulders ⦁ Nausea / Vomiting ⦁ Anorexia ⦁ Fever ⦁ Rebound tenderness ⦁ Guarding ⦁ Enlarged, palpable gallbladder ⦁ Murphy's sign = positive! ⦁ Jaundice (not common, but may be seen if choledocholithiasis present) Murphy's Sign: Patient exhales, then apply deep pressure to RUQ, will have severe pain upon inhalation - when taking a deep breath, the diaphragm expands downwards and pushes gallbladder down - if pressure is in place after exhalation, then upon inhalation when diaphragm contracts downwards, the gallbladder is pinned in place --> PAIN! --> patient will quickly stop breathing in further + Boas sign = referred pain to the right subscapular / right shoulder area due to phrenic nerve irritation (vs Kehr's sign = referred pain to LEFT subscapular area due to phrenic nerve irritation, but seen with splenic rupture instead) 1 of 2 things can happen 1) gallstone moves back into gallbladder on its own --> resolves cholecystitis = happens in majority of cases! = Biliary Colic (RUQ pain, but no fever / WBC, no jaundice) 2) stone doesn't fall back into gallbladder, and pressure continues to build up due to increased mucus / bacteria / WBCs --> pressure can eventually cause gallbladder to start compressing on blood vessels supplying gallbladder with blood --> no blood / oxygen supply --> ischemia --> gangrenous cell death - gallbladder walls may also weaken due to pressure + bacteria --> RUPTURE --> sharp pain, and if left untreated, could cause sepsis - if gets this bad = patient may need cholecystectomy COMPLICATIONS OF ACUTE CHOLECYSTITIS ⦁ chronic cholecystitis ⦁ mucocele ⦁ empyema ⦁ Mirizzi's Syndrome = gallstone also obstructs hepatic duct --> jaundice ⦁ Perforation ⦁ Gallbladder - Duodenal fistula formation (allows gallstones to cause gallstone ileus at terminal ileum) --> gastric outlet obstruction ⦁ Choledocholithiasis (formation of gallstone in common bile duct) ⦁ Cholangitis (from choledocholithiasis or cholelithiasis by obstructing common bile duct --> infection) ⦁ Pancreatitis (if gallstone moves down to obstruct pancreatic enzymes from getting through pancreatic duct to duodenum ⦁ Obstructive jaundice (bile backflow to liver due to stone in common bile duct) DIAGNOSIS ⦁ ***HIDA*** = GOLD STANDARD TEST ⦁ Ultrasound = initial test ⦁ CT = alternative to ultrasound + can detect complications Ultrasound - can detect stones, stone sludge, and mucus buildup in gallbladder or cystic duct - if stone is lodged in common bile duct though = a lot more difficult to see on ultrasound - includes murphy's sign test HIDA SCAN (cholescintigraphy) = Most Specific! - radioactive tracer = attached to HIDA (acid) and injected into patient - HIDA is taken up by hepatocytes and gets excreted into the bile - can watch tracer drain down hepatic ducts and into gallbladder + common bile duct; will see if obstruction is present - if cholecystitis present = will not see gallbladder LABS ⦁ CBC = leukocytosis with left shift (excess neutrophils) ⦁ may have elevated Alkaline Phosphatase (ALP) ⦁ may have elevated AST / ALT (liver) - AST = 10-40 - ALT = 7-56 ⦁ may have elevated total bilirubin (0.3-1.0) (increased direct or conjugated bilirubin) (liver) (direct = 0.1 - 0.3) (indirect = 0.2-0.8) ⦁ may have elevated Lipase / Amylase (pancreas) - would be slightly elevated, not in 1000s (pancreatitis) ALP (20-140) = an enzyme found high in liver + bile ducts, so when bile backs up and increases pressure on the ducts in the liver, liver cells lining the ducts can get damaged --> release ALP Lipase (0-160)= enzyme secreted by pancreas that hydrolyzes fats. When pancreas is inflamed or damaged --> elevated Lipase (lipase more sensitive than amylase) Amylase (40-140) = enzyme also secreted by pancreas that digests carbs (starch --> sugars). When pancreas is inflamed or damaged --> elevated Amylase TREATMENT - NPO - IV fluids - Pain meds (NSAIDS or narcotics) - antibiotics (Ceftriaxone + Metronidazole) ⦁ Laparoscopic Cholecystectomy ⦁ emergency surgery may be necessary if gangrene, perforation, ischemia, pancreatitis, inflammation of common bile duct occurs Early cholecystectomy is generally preferred, best done during the first 24-48 hours following symptoms - laparoscopic preferred over open Prophylactic cholecystectomy for asymptomatic cholelithiasis is generally not recommended

Answer 55

- shock = decreased blood flow to the whole body - circulatory failure --> cellular damage and possibly multi-organ failure if not treated immediately Shock is like ischemia (decreased blood flow to tissue), but on a global scale Shock = body's tissues aren't getting enough blood, and therefore aren't getting enough oxygen Blood is delivered to tissues because of blood pressure - enough pressure circulating blood throughout the body ``` Blood pressure = resistance to flow x cardiac output 1) resistance to flow - determined by ⦁ vessel length ⦁ blood viscosity ⦁ vessel diameter ``` 2) cardiac output (amount of blood pumped by the heart out to the body per minute) ⦁ cardiac output = HR (bpm) X SV (volume per beat) ⦁ stroke volume = EDV (amt of blood in LV after diastole) - ESV (amount of blood left over in LV after contraction or systole) HYPOVOLEMIC SHOCK - low blood volume that leads to shock - can either be non-hemorrhagic or hemorrhagic Loss of blood or fluid volume due to hemorrhage or fluid loss that leads to shock Hypovolemic shock divided into Hemorrhagic and Non-hemorrhagic. 1) HEMORRHAGIC HYPOVOLEMIC SHOCK - loss of blood volume from bleeding - loss of about 20% of blood volume (about 1L) = could be enough to cause hypovolemic shock ⦁ GI bleed ⦁ AAA rupture ⦁ massive hemoptysis ⦁ trauma ⦁ ectopic pregnancy ⦁ postpartum hemorrhage etc. ``` NON-HEMORRHAGIC HYPOVOLEMIC SHOCK - loss of fluid volume is NOT from bleeding ⦁ severe dehydration ⦁ severe vomiting ⦁ bowel obstruction ⦁ pancreatitis ⦁ severe burns ⦁ DKA (osmotic diuresis due to hyperglycemia) ``` PATHOPHYSIOLOGY 1) lack of blood volume --> decreased EDV 2) decreased EDV --> decreased SV 3) decreased SV --> decreased CO 4) decreased CO --> decreased BP Loss of blood or fluid volume --> increased heart rate, vasoconstriction (increased SVR), hypotension, and decreased CO The body's response to hypovolemia = peripheral vasoconstriction, increased cardiac activity, sodium + water retention, and increased cortisol/catecholamines When cardiac output decreases, catecholamines are released (Epinephrine / Ne), ADH (posterior pituitary), and Angiotensin II are released RAAS: renin released from kidneys when renal blood flow is reduced --> renin enters circulation and converts angiotensinogen from liver to angiotensin I. Angiotensin I is converted to Angiotensin II via ACE (lungs - endothelial cells) - Angiotensin II = triggers release of aldosterone (sodium and therefore water reabsorption), and also triggers vasoconstriction --> increase in blood volume and therefore blood pressure Catecholamines, ADH, and Angiotensin II release in attempt to cause vasoconstriction of blood vessels and increase blood volume SYMPTOMS ⦁ hypotension (without volume = low pressure) ⦁ Tachycardia ⦁ cool / clammy skin (blood provides heat) ⦁ decreased CO --> oliguria / anuria ⦁ pale / cool dry extremities ⦁ slow capillary refill: > 2 seconds ⦁ decreased skin turgor ⦁ dry mucous membranes ⦁ altered mental status ⦁ doesn't usually cause profound respiratory distress Tachycardia, hypotension, oliguria, and cool, clammy skin can all be signs of hypovolemic shock. ``` DIAGNOSIS ⦁ vasoconstriction (increased SVR) ⦁ hypotension ⦁ decreased CO (anuria / oliguria) ⦁ decreased pulmonary capillary pressure ``` LABS ⦁ increased Hgb / Hct = due to dehydration - decreased hgb / hct = late sign in hemorrhagic shock ⦁ decreased CVP (central venous pressure) / PCWP (pulmonary capillary wedge pressure) TREATMENT ⦁ ABCDEs ⦁ 2 large bore IVs or a central line ⦁ NS or LR - monitor urine output to assess success of volume resuscitation ⦁ control source of hemorrhage if present ⦁ RBC transfusion if severe hemorrhage

Answer 56

- shock = decreased blood flow to the whole body - circulatory failure --> cellular damage and possibly multi-organ failure if not treated immediately Shock is like ischemia (decreased blood flow to tissue), but on a global scale Shock = body's tissues aren't getting enough blood, and therefore aren't getting enough oxygen SEPTIC SHOCK = due to pathogens in the blood - endotoxins directly cause damage to endothelial cells in blood vessels - cause blood vessels to release vasodilators (nitric oxide) + activate the complement pathway in the blood + mast cell release of histamine (another vasodilator) - activate macrophages + neutrophils --> inflammation - make blood vessels leaky / increase capillary permeability TNF-α is the major mediator of septic shock.It is released when toll-like receptors on the surface of macrophages bind bacterial lipopolysaccharide, activating the signaling cascade allowing for its release SYMPTOMS ⦁ hypotension (without volume = low pressure) ⦁ warm/ flushed skin (blood provides heat) initially late = cool clammy skin ⦁ normal or high oxygen saturation Tachypnea, tachycardia, hypotension, and high white blood cell count are together suggestive of septic shock. Need to treat with fluids to increase SVR, because vasodilation has caused distributive type shocks to have decreased SVR Venous lactate clearance has been shown to be an effective measure for guiding sepsis resuscitation efforts and is less invasive than central venous oxygen saturation or central venous pressure

Answer 57

- shock = decreased blood flow to the whole body - circulatory failure --> cellular damage and possibly multi-organ failure if not treated immediately Shock is like ischemia (decreased blood flow to tissue), but on a global scale Shock = body's tissues aren't getting enough blood, and therefore aren't getting enough oxygen CARDIOGENIC SHOCK - shock caused by trauma or condition with the heart that is preventing it from pumping enough blood to the body Impaired cardiac contractility and overall pump failure - heart is unable to generate sufficient cardiac output to maintain tissue perfusion * ** MC CAUSE = Acute MI *** - while MI causes ischemia to heart tissue itself, this in turn can cause the damaged heart muscle to not be able to adequately perfuse the body due to weak contractions (decreased SV -> decreased CO) ``` OTHER CAUSES ⦁ acute MI (most common) ⦁ cardiac tamponade ⦁ blunt cardiac trauma ⦁ air embolus ⦁ tension pneumothorax ⦁ arrhythmias ⦁ massive PE ⦁ Other causes include myocarditis, valve dysfunction, and congenital heart disease ``` Free wall rupture is a complication that occurs within 72 hours of MI Cells produce lactic acid when they metabolize carbohydrates anaerobically -- without oxygen. During high-intensity exercise, muscles expend energy so rapidly that they outrun the circulatory system's ability to provide them with oxygen. As they rely more on anaerobic metabolism, they produce lactic acid, which can accumulate in the bloodstream SYMPTOMS ⦁ altered mental status ⦁ hypotension (without volume = low pressure) ⦁ tachycardia ⦁ cool / clammy skin (blood provides heat) ⦁ low oxygen saturation (due to low BV) ⦁ elevated lactic acid production (acidosis) PHYSICAL EXAM ⦁ JVD ⦁ low urine output ⦁ systolic BP < 90 TREATMENT ⦁ fluids ⦁ Cautious volume infusion (250- to 500-mL bolus of 0.9% saline) may be tried while auscultating the chest frequently for signs of fluid overload ⦁ Vasopressors (vasocontrict in ER setting) - ex: Dobutamine, Norepinephrine ⦁ Oxygen ⦁ surgical repair of structural disorders

Answer 58

- shock = decreased blood flow to the whole body - circulatory failure --> cellular damage and possibly multi-organ failure if not treated immediately Shock is like ischemia (decreased blood flow to tissue), but on a global scale Shock = body's tissues aren't getting enough blood, and therefore aren't getting enough oxygen ANAPHYLACTIC SHOCK - allergic reaction that causes dangerously low BP

Answer 59

- shock = decreased blood flow to the whole body - circulatory failure --> cellular damage and possibly multi-organ failure if not treated immediately Shock is like ischemia (decreased blood flow to tissue), but on a global scale Shock = body's tissues aren't getting enough blood, and therefore aren't getting enough oxygen NEUROGENIC SHOCK - damaged CNS can't control the body's BP Neurogenic shock is a distributive type of shock resulting in hypotension, occasionally with a slowed heart rate, that is attributed to the disruption of autonomic pathways within the central nervous system. SYMPTOMS ⦁ Hypotension ⦁ ** BRADYCARDIA ** ``` CAUSES OF NEUROGENIC SHOCK ⦁ spinal cord injury ⦁ trauma ⦁ severe stress or pain ⦁ anesthesia widespread vasodilation --> decreased CO, decreased PCWP, and decreased SVR ```

Answer 60

Shock = inadequate organ perfusion + tissue oxygenation to meet the body's oxygenation requirements **often associated with Hypotension (but not always) Shock = determined by either 1) low cardiac output 2) low systemic vascular resistance (SVR) SVR = the resistance to blood flow through the circulatory system - peripheral vasoconstriction increases SVR - vasodilation decreases SVR ``` 4 main types of shock ⦁ Hypovolemic ⦁ Cardiogenic ⦁ Obstructive ⦁ Distributive ``` HYPOVOLEMIC = loss of blood/ fluid volume --> shock ex: hemorrhage CARDIOGENIC = myocardial dysfunction leads to reduced cardiac output --> shock ex: MI OBSTRUCTIVE = obstruction to circulation --> shock ex: cardiac tamponade DISTRIBUTIVE = maldistribution of blood flow from essential organs to nonessential organs ex: septic shock ex: anaphylactic shock ex: neurogenic shock PATHOPHYSIOLOGY OF SHOCK 1) Inadequate tissue perfusion - inability to meet the body's metabolic oxygen requirements --> anaerobic respiration --> lactic acid production --> metabolic acidosis + organ dysfunction 2) Nervous system activation - in an attempt to improve systemic oxygen delivery ⦁ Vasoconstriction (to increase SVR) ⦁ Tachycardia (to increase cardiac output) ⦁ increased NE / Dopamine / Cortisol release ⦁ RAAS activation to increase volume (+ vasoconstriction) 3) Systemic Effects of Shock ⦁ Metabolic Acidosis - lack of oxygen, so cells turn to anaerobic metabolism --> produces lactic acid byproduct ⦁ MODS = Multiorgan Dysfunction Syndrome - consequences of shock on organ systems - includes lungs / kidneys / heart / brain dysfunction, as well as DIC ⦁ MSOF = Multisystem Organ Failure - if condition persists ``` GENERAL SYMPTOMS OF SHOCK ⦁ acutely ill ⦁ altered mental status ⦁ decreased pulses ⦁ tachycardia ⦁ cool / mottled / clammy skin ⦁ warm / flushed skin if distributive shock ⦁ hypotension: Systolic BP < 110 - may be normotensive initially ``` ``` DIAGNOSTIC TESTS ⦁ CBC ⦁ CMP ⦁ Lactate ⦁ Coag studies ⦁ Cultures ⦁ ABG - others depending on etiology ``` GENERAL MANAGEMENT OF SHOCK ⦁ Airway (may need intubation) ⦁ Breathing (mechanical ventilation + sedation decreases the work of breathing, reducing the oxygen demand associated with tachypnea) ⦁ Circulation: isotonic crystalloids (NS / LR) ⦁ Oxygen (monitor lactate levels) ⦁ Endpoint of resuscitation = urine output, CVP, MAP

Answer 61

Mesenteric ischemia = not enough blood supply to the small intestine --> injury of small intestine It can come on suddenly, known as acute mesenteric ischemia, or gradually, known as chronic mesenteric ischemia ACUTE MESENTERIC ISCHEMIA - often presents with sudden severe pain Acute mesenteric ischemia is often caused by embolic occlusion of the superior mesenteric artery. - Symptoms may come on more slowly in those with acute on chronic disease. Acute mesenteric ischemia is associated with pain out of proportion with physical findings, and red currant-jelly stools Occlusive acute mesenteric ischemia is treated with surgery. CHRONIC MESENTERIC ISCHEMIA - abdominal pain after eating - unintentional weight loss - vomiting - being afraid of eating In patients with chronic mesenteric ischemia, revascularization of the affected arteries should be pursued, or medical management used if risks outweigh benefits. In an older person with hypercholesterolemia, postprandial epigastric pain, food aversion and weight loss, consider chronic mesenteric ischemia as a diagnosis. Chronic mesenteric ischemia is often caused by ATHEROSCLEROSIS of the celiac, superior mesenteric, or inferior mesenteric arteries. TREATMENT Medical therapy with NITRATES can provide short-term relief for pain in patients with chronic mesenteric ischemia.

Answer 62

Mesenteric Ischemia = insufficient blood flow to the small intestine --> ischemia CAUSES OF ISCHEMIA ⦁ thrombus (A-fib, MI) ⦁ embolus (atherosclerosis) ** MC due to occlusion ** ** case = will often have patient with A-fib, MI or CHF - could also be tumor, intussusception, hernia, volvulus that compresses on vasculature and occludes blood flow A complication of volvulus and intussusception is small bowel ischemia where arteries that supply the small intestine becomes compressed. NON-OCCLUSIVE CAUSES ⦁ shock (decreased blood flow) ⦁ cocaine (vasospasm) MC ARTERY = ** PROXIMAL SUPERIOR MESENTERIC ARTERY ** The artery that branches off the aorta and supplies most of the small intestine is the superior mesenteric artery. The 3 major mesenteric arteries branching off of the abdominal aorta are the celiac, superior mesenteric and inferior mesenteric arteries that supply the foregut, midgut, and hindgut, respectively. The superior mesenteric artery supplies blood to the distal duodenum to the proximal 2/3 of the transverse colon The inferior mesenteric artery supplies the distal 1/3 of the transverse colon to the upper portion of the rectum and is the smallest mesenteric vessel. The splenic flexure is considered a watershed area and is more susceptible to ischemia during poor arterial flow due to inferior mesenteric ischemia. - splenic flexure = corner between transverse + descending colon (hepatic flexure = corner between ascending + transverse colon) The celiac artery supplies blood to the lower esophagus, stomach, duodenum, liver, pancreas, and spleen This lack of perfusion causes bowel ischemia + potentially necrosis if left untreated Usually, the first layer of the intestine damaged in gastrointestinal ischemia or infarction is the MUCOSAL LAYER. HALLMARK SYMPTOMS ⦁ severe abdominal pain that is out of proportion to their physical exam ⦁ Nausea / Vomiting ⦁ Bloody stools - bloody diarrhea Bloody diarrhea = caused by - damage to small intestine is caused by both tissue hypoxia + reperfusion injury 1) hypoxia --> tissue ischemia + necrosis 2) reperfusion injury = if tissue that has been damaged is reperfused => oxidative stress, and causes even more damage caused by neutrophil activation --> releases free radicals + buildup of toxic byproducts after periods of ischemia - this damage leads to sloughing of cells + blood into intestinal lumen --> blood in stool DIAGNOSIS o Labs ⦁ increased WBC (with increased bands = immature WBCs) ⦁ metabolic acidosis ⦁ elevated lactate o Imaging ⦁ ** CT Angiography = definitive*** (without contrast) ⦁ Xray = thumb-printing sign = due to thickened bowel walls from bowel wall edema - initial test ⦁ Colonoscopy Pneumatosis Intestinalis = air within bowel wall = indicates severe disease ``` TREATMENT ⦁ ** SURGICAL REVASCULARIZATION ** = angioplasty with stenting or bypass - surgical resection if bowel not salvageable ⦁ fluids ⦁ antibiotics ⦁ anticoagulation (heparin) or urokinase thrombolytic ⦁ emergency surgery in severe cases ``` Patient will present as → a 71-year-old male with a history of atrial fibrillation with a sudden onset of severe abdominal pain occurring 10 minutes after eating. Physical exam findings are relatively benign, and the patient has only minimal pain with palpation of the abdomen. Stool guaiac is positive and blood tests reveal leukocytosis with an elevated lactate and LDH.

Answer 63

- same pathophysiology of ischemic bowel disease caused by MESENTERIC ATHEROSCLEROSIS of the GI tract Atherosclerosis --> inadequate perfusion, especially at the SPLENIC FLEXURE (inferior mesenteric artery) during POST-PRANDIAL STATES SYMPTOMS ⦁ *** Chronic dull abdominal pain *** that is WORSE AFTER MEALS ⦁ Weight loss (due to anorexia / fear of eating)*** Postprandial epigastric pain usually within the first hour after eating Pain will resolve in 2-3 hours "Mesenteric angina" Usually will present as recurrent cramping with postprandial pain in a patient with a history of PVD, smoker or DM DIAGNOSIS ⦁ *** CT angiography = gold standard *** ⦁ Xray = initial test TREATMENT ⦁ bowel rest ⦁ surgical revascularization (angioplasty with stenting or bypass

Answer 64

ischemic colitis is the result of mesenteric ischemia MC due to systemic hypotension or atherosclerosis that involve the superior + inferior mesenteric arteries ==> that leads to ischemia of bowel MC Location = "watershed" areas with decreased collaterals = Splenic flexure + Rectosigmoid junction SYMPTOMS ⦁ severe abdominal pain ⦁ MC = LLQ pain (splenic flexure / rectosigmoid jnct) ⦁ *** BLOODY DIARRHEA *** (sloughing of colon) DIAGNOSIS ⦁ Colonoscopy - see segmental ischemic changes in areas of low perfusion (would be CT Angiogram to diagnose mesenteric ischemia, but colonoscopy if specifically diagnosing ischemic colitis) TREATMENT ⦁ revascularization - restore perfusion + observe for signs of perforation

Answer 65

PLEURAL EFFUSION - The abnormal accumulation of fluid in the pleural space - generally the entrance + exit of fluid into pleural space is about equal - fluid accumulation occurs when there is either an increase in entry fluid or decrease in exit fluid - there are capillaries in visceral and parietal pleura through which interstitial fluid leaks out and into pleural space; lymphatic vessels then drain the pleural fluid in an equal balance *** MC cause of pleural effusions overall = CHF *** ``` MOST COMMON CAUSES OF PLEURAL EFFUSION ⦁ heart failure (MC transudative) ⦁ bacterial pneumonia (exudative) ⦁ PE (exudative) ⦁ Malignancy (MC exudative) ⦁ viral infections (not as common as bacterial) (exudative) ⦁ cardiac surgery (exudative) ⦁ pancreatitis (exudative) ``` - can be either TRANSUDATIVE issue = too much fluid leaks out of capillaries either due to INCREASE IN HYDROSTATIC PRESSURE or DECREASE IN ONCOTIC PRESSURE - or can be EXUDATIVE issue = too much fluid leaks out of capillaries due to INFLAMMATION of pulmonary capillaries --> damage makes them more leaky - creates larger spaces in capillary membrane for fluid to leak out TRANSUDATIVE PLEURAL EFFUSION (increased fluid) ``` o TRANSUDATIVE EFFUSIONS ⦁ heart failure (CHF) ⦁ cirrhosis ⦁ nephrotic syndrome ⦁ atelectasis ``` ⦁ CHF - increased in hydrostatic pressure = the force that blood exerts on the walls of the vessels (blood pressure - pushing force) - due to increased volume - Heart failure: heart can't effectively pump blood to body, so blood backs up into the lungs --> increased hydrostatic pressure in pulmonary vessels, which forces fluid out of pulmonary capillaries and into the pleural space ⦁ Cirrhosis ⦁ Nephrotic Syndrome - decrease in oncotic pressure = if there is a decrease in solute concentration in pulmonary vessels, fluid will leak into pleural space with higher oncotic pressure, as solutes cannot cross capillary walls - Cirrhosis = not making enough proteins --> low oncotic pressure in vessels - Nephrotic syndrome = proteins lost in urine --> low oncotic pressure in vessels - Mechanism of Transudative Effusions ⦁ increased hydrostatic pressure (CHF) ⦁ decreased oncotic pressure (albumin - cirrhosis or nephrotic syndrome) ⦁ increased negative intrapleural pressure (atelectasis) ⦁ ascites o Transudative fluid = clear EXUDATIVE PLEURAL EFFUSION (increased fluid) - inflammation of capillaries --> larger spaces in capillary membrane, allowing fluid, immune cells and large proteins + enzymes (LDH) to leak out of capillaries and into pleural space ⦁ **infection (pneumonia) = MC exudative** ⦁ malignancy ⦁ trauma ⦁ inflammatory conditions (SLE, RA, sjogrens - autoimmune conditions) o Exudative fluid = cloudy (full of immune cells) o EXUDATIVE EFFUSIONS ⦁ malignancy ⦁ inflammatory processes (trauma, autoimmune, infection) - Mechanism = increased vascular permeability due to infection or inflammation LYMPHATIC PLEURAL EFFUSION (decreased drainage) - chylothorax = lymphatic fluid accumulates in the pleural space due to an disruption in the **thoracic duct** - prevents drainage ⦁ damage to thoracic duct during surgery ⦁ tumors in mediastinum that compress thoracic duct o Lymphatic fluid = filled with fat looks like *milk* - high in triglycerides ``` MEDICATIONS THAT CAN LEAD TO PLEURAL EFFUSION ⦁ Methotrexate ⦁ Amiodarone ⦁ Phenytoin ⦁ Nitrofurantoin ⦁ Beta blockers ``` BETty sold her FUR coat for METH/AM/PHEtamines - beta blockers - nitroFURantoin - METHotrexate - AMiodarone - PHEnytoin TYPES OF PLEURAL EFFUSION OR ASSOCIATED CONDITIONS o Empyema = infection of pleural space o Parapneumonic = pleural effusion secondary to bacterial pneumonia o Hemothorax = gross blood (from chest trauma or malignancy) o Chylothorax = lymph fluid due to impaired lymphatic drainage If pneumonia + fever -->shows effusion on CXR but will not drain from thoracentesis = suspect EMPYEMA = will need surgical removal ****biggest way to distinguish between transudative + exudative fluid = is that exudative fluid will have high amounts of protein + LDH from leaking out of inflamed damaged capillaries - use LIGHT CRITERIA- exudative if > 1 of the following ⦁ fluid protein : serum protein > 0.5 ⦁ fluid LDH : serum LDH > 0.6 ⦁ fluid LDH > 2/3 of upper limit of serum LDH - exudative also has high cholesterol level > 45 ``` SYMPTOMS ⦁ Asymptomatic - small effusion may go unnoticed ⦁ dyspnea / SOB ⦁ cough ⦁ pleuritic chest pain *** ⦁ fever (infection) ⦁ hemoptysis ⦁ weight loss (malignancy) ``` - large effusions ==> pain with inhalation (pleurisy) and SOB, worse when laying flat PHYSICAL EXAM ⦁ decreased breath sounds ⦁ dullness to percussion (unlike pneumothorax) ⦁ decreased tactile fremitus (like pneumothorax) - can have so much fluid accumulate that it causes pneumothorax / pushes trachea over / mediastinal shift - if effusion is large enough, can put pressure on lungs and push trachea to other side (like tension pneumothorax) DIAGNOSIS ⦁ CXR (standing + laying flat) = INITIAL TEST - standing = fluid will settle in costophrenic angle (bottom is white) - laying flat = will settle all over chest wall, creating a layering effect (whole side is white) - ***BLUNTING OF COSTOPHRENIC ANGLES *** - *** positive menisci sign *** - lateral decubitus films = best ⦁ can detect smaller effusions ⦁ can differentiate loculations + empyema (whether fluid shifts when laying down or not) ⦁ CT scan can help determine lung disorders and presence of loculation ⦁ Ultrasound can determine presence of loculation and fibrin stranding; also aids in thoracentesis procedure ⦁ THORACENTESIS + ANALYSIS OF PLEURAL FLUID = **** DIAGNOSTIC TEST OF CHOICE ***** ``` PLEURAL FLUID ANALYSIS ⦁ differential cell count ⦁ cytology ⦁ protein (helps determine transudate vs exudate) ⦁ LDH (helps determine transudate vs exudate) ⦁ gram stain ⦁ culture ⦁ pH ⦁ glucose ``` EXUDATIVE EFFUSION WILL HAVE HIGH AMOUNTS OF PROTEIN + LDH IN PLEURAL FLUID LIGHT'S CRITERIA: EXUDATE IF >/= 1 o fluid protein : serum protein > 0.5 o fluid LDH : serum LDH > 0.6 o fluid LDH > 2/3 the upper normal limit of serum LDH pleural fluid protein needs to be more than half of serum protein ``` ALTERNATIVE CRITERIA: TRANSUDATE IF ⦁ LDH % = 45% ⦁ cholesterol = 45 mg/dL ⦁ protein = 2.9 g/dL ``` EXUDATE IF ⦁ LDH% = > 45% ⦁ cholesterol > 45 mg/dL ⦁ protein > 2.9 g/dL TREATMENT - the treatment of underlying conditions may often resolve pleural effusions (don't drain all of them!) ⦁ thoracentesis if needed - Thoracentesis = diagnostic + therapeutic - not all pleural effusions need to be drained with a needle (thoracentesis); often will resolve on their own SMALL EFFUSIONS from CHF - may be treated with diuretics or sodium restriction - Remove fluid via thoracentesis (max amount removed at one time = 1.5L - don't want to remove too much, because relieving too much pressure at once can lead to compensatory pulmonary edema) - thoracentesis guided via ultrasound - needle inserted above rib to avoid vasculature / nerve underneath ribs - may have placement of chest tube for continued drainage Hemothorax, with persistent bleeding is an indication for thoracotomy. If on initial placement of the chest tube 1000-1500cc of blood drains or if the chest tube continues to drain over 200cc/hr over 4-5 hours, it is unlikely that the bleeding will stop with a chest tube, or systolic pressure < 70 Emergency thoracotomy = at 5th intercostal space - chronic effusion may require pleurodesis (induced scarring - with talc or doxycycline) - empyema may require surgical removal - can be too thick to be drained via thoracentesis hemothorax can cause mediastinal shift and can lead to collapse Patient presents as → a 58-year-old female who returns to the hospital with chest pain and difficulty breathing several weeks after being discharged following a myocardial infarction requiring immediate cardiac catheterization. She has been coughing up frothy sputum for the past three days. The patient complains of a sharp pain that worsens during inspiration. Physical exam reveals decreased tactile fremitus, dullness to percussion and diminished breath sounds on the left side

Answer 66

2 main types of Stroke ⦁ Hemorrhagic stroke ⦁ Ischemic stroke Hemorrhagic stroke = when an artery ruptures and bleeds within the brain Ischemic stroke = when an artery gets blocked 2 types of Hemorrhagic strokes ⦁ Subarachnoid hemorrhage ⦁ Intracerebral hemorrhage Intracerebral hemorrhage = bleeding within cerebrum Subarachnoid hemorrhage = bleeding between pia mater and arachnoid mater SUBARACHNOID HEMORRHAGE - can be lethal! - bleeding that pools between the arachnoid mater and the pia mater --> increased ICP - prevents enough blood from flowing into the brain BLOOD SUPPLY OF THE BRAIN - brain receives blood from the left + right INTERNAL CAROTID ARTERIES as well as the left + right VERTEBRAL ARTERIES - left + right vertebral arteries come together to form the BASILAR ARTERY ==> branches provide blood flow to the cerebellum + brainstem - the basilar artery also branches into the right + left POSTERIOR CEREBRAL ARTERIES which provide blood to the occipital lobe and part of the temporal lobe + thalamus - the left + right carotid arteries flow into the left + right MIDDLE CEREBRAL ARTERIES which provide blood to the lateral portions of the frontal / parietal / temporal lobes of the brain - the left + right carotid arteries also branch into the left + right ANTERIOR CEREBRAL ARTERIES which provide blood to the medial portions of the frontal + parietal lobes CIRCLE OF WILLIS = right/left internal carotid arteries + middle cerebral arteries + anterior cerebral arteries + anterior communicating artery + posterior cerebral arteries + posterior communicating arteries - allow blood to get to various parts of the brain if blockage occurs ``` CAUSES OF SUBARACHNOID HEMORRHAGE ⦁ 1) MC = Berry Aneurysm - rupture - can rupture with increased ICP - Marfans = predisposed to aneurysms - MC aneurysm in brain = berry aneurysm of anterior cerebral arteries ``` The most common site of saccular aneurysm rupture causing subarachnoid hemorrhage is at the junction of the anterior communicating artery and anterior cerebral artery. ⦁ 2) Trauma ⦁ 3) AVM - lack of capillaries between artery + vein = replaced by abnormally tangled vessels that directly connect high pressures of arteries with veins that are not built for high pressures --> rupture Once SAH is occurring --> starts putting pressure on skull, nearby tissues and compressing nearby blood vessels - less blood is flowing downstream to rest of brain - healthy tissue can die with direct pressure + lack of oxygen within a few hours * * another complication = blood vessels sitting in a pool a blood can start to vasoconstrict (VASOSPASM) ** - if this occurs in the circle of willis = will reduce blood flow to brain --> further ischemic injury Subarachnoid hemorrhage has an increased risk of developing communicating or obstructive hydrocephalus. ``` SYMPTOMS ⦁ sudden onset of severe "THUNDERCLAP" HEADACHE - worst headache of my life ⦁ may have LOC ⦁ Nuchal rigidity (neck stiffness)*** ⦁ photophobia*** ⦁ N / V** ⦁ vision changes ⦁ confusion / delirium ``` Subarachnoid hemorrhage (SAH) patients will commonly report having another sudden, severe headache one to three weeks prior. These are known as "sentinel headaches" and are thought to be caused by a minor hemorrhage. ``` DIAGNOSIS ⦁ CT FIRST without contrast*** = if CT negative but high suspicion => ⦁ LP - Xanthochromia (RBCs) - Increased CSF (ICP) ``` TREATMENT ⦁ Emergent surgery! - coiling or clipping of aneurysm - supportive = bed rest / lower ICP / adjust BP - CCB (*Nicardipine or Nimodipine) - can help prevent vasospasm from setting in