Clin Med Exam 4 Study Guide.docx

CLIN MED EXAM 4 Study Guide (60 Questions, 3/4 EC questions) 1.

CAT BITES: MC pathogen: P. Multocida, Tx: Amoxicillin/Clavulanate, Cefuroxime, Doxycycline

2.

DOG BITES: MC type: Crush-type bite a. MC pathogen: Pasturella multocida (within 24hrs), Staph/Streptococcus (>24hrs) b. Body areas that are MC infected d/t dog bites: HANDS c. Which type of bite is associated w/ “high” (increased rate? Most serious?) i. Factors that increase the rate of infection include: i. Victim >50 years old ii. Delay in seeking treatment >24 hours iii. Hand wounds (face/scalp/trunk are considered low risk) iv. Deep puncture wounds ii. Infection d/t organisms inoculated into the depth of the wound by the animal’s teeth

3.

HUMAN BITES: MC bites overall** MC in hands/upper extremities (60-75%) a. MC pathogen: Eikenella corrodens (susceptible to penicillin) b. MGMT – know when to approximate a large bite but also that you normally do not close these i. Non-clenched fist human bite wounds should be left open after examination and irrigation. If widely open, may close loosely to approximate tissues ii. Face, head, and neck- can be closed after copious irrigation

4.

BROWN RECLUSE SPIDER: a. CLINICAL PRESENTATION: Bites are initially painless; MC manifestation is mild erythematous lesion (may become firm & heal with little or no scarring) First 24 hours i. Erythema ii. Blister formation iii. Bluish discoloration 3-4 days iv. May become necrotic w/ eschar formation by the end of the first week b. May cause systemic involvement (MC in PEDS) i. Usually within 48 hours of bite i. Fevers, chills, N/V, myalgias, arthralgias, petechiae & hemolysis ii. Hemolysis may be severe causing hemoglobinuria, renal failure, DIC, & death

5.

ANAPHYLACTIC SHOCK: Generalized systemic allergic reaction (single or multiple stings) a. CLINICAL PRESENTATION: Painful (Bee sting) b. Local reaction (MC): Pain, slight erythema, edema, and pruritis at sting site. No systemic s/sx c. Toxic reaction: History of multiple stings, may resemble anaphylaxis. MC presents as N/V/D. Lightheadedness and syncope are common. No urticaria or bronchospasm i. Initial symptoms of anaphylaxis include i. Itchy eyes ii. Facial flushing iii. Generalized urticaria iv. Dry cough ii. Symptoms intensify rapidly with i. Chest constriction, throat constriction, tongue swelling ii. Wheezing, dyspnea, laryngeal stridor, cyanosis iii. Abdominal cramps, diarrhea iv. Vertigo, syncope v. Involuntary bowel or bladder action vi. Nausea, vomiting, fever, chills vii. Shock d. MGMT: Remove stinger & place ice for local reaction i. Anaphylaxis management: i. Epinephrine 1:1000, 0.3-0.5 mg IM in adults a. Epinephrine 0.01 mg/kg in children b. Never more than 0.3 mg ii. Diphenhydramine, H2 blocker, Steroids, Inhaled B agonists

6.

CHEST PAIN: a. CLINICAL PRESENTATION: i. Ischemic: causes of chest pain include; i. Myocardial Infarction (MI) ii. CAD (Angina pectoris) iii. Aortic Stenosis iv. Coronary Vasospasm v. Hypertrophic Cardiomyopathy. ii. Non-ischemic: causes of chest pain include; i. Pericarditis, ii. Dissecting Aortic iii. Aneurysm, iv. Mitral Valve Prolapse. b. Myocardial Infarction (MI) MC sx is DIAPHORESIS (78%) then CHEST PX (64%) then NAUSEA (52%), SOB (47%), UNROCOGNIZED/ASX (25%) i. MI’s may go unrecognized, sometimes symptoms are delayed for many hours. ii. Anterior MI’s i. often present with chest pain and dyspnea due to left ventricular involvement. iii. Inferior MI’s i. Often present with chest pain ii. N & V iii. Diaphoresis iv. Singultus (hiccups) due to possible Vagus nerve involvement iv. Lateral MI’s i. often present with chest pain and left arm pain. c. Ischemic Symptoms: Coronary artery disease (CAD) or (Angina pectoris) caused by insufficient myocardial oxygen supply on demand. i. Pain is transient or episodic. Frequently described as heavy pressure occurring after exertion/stress or emotional upset. ii. Associated sx: Diaphoresis, N/V, weakness, CAD chest pain often relieved by nitroglycerin. d. Labs: ECG: ACS includes ST-elevation/depression, Q-waves, T-wave inversion. Initial ECG is often NOT diagnostic in patients with ACS

7.

STROKE: 87% of strokes are ischemic a. CLINICAL PRESENTATION: i. Embolism: Occurs w/o warning, patient has hx of cardiovascular disease ii. In thrombosis: Dizzy spells or sudden memory loss, no pain, may ignore symptoms iii. In cerebral hemorrhage: May have warning like dizziness and ringing in the ears (tinnitus) violent headache, with nausea and vomiting iv. Sudden-onset CVA i. Usually most severe ii. Loss of consciousness iii. Face becomes red iv. Breathing is noisy and strained v. Pulse is slow but full and bounding vi. Elevated BP vii. May be in a deep coma b. COMMON STROKE Symptoms: i. Weakness/paralysis ii. Numbness, tingling, decreased sensation iii. Vision changes iv. Speech problems v. Swallowing difficulties/drooling vi. Loss of memory vii. Vertigo (spinning sensation) viii. Loss of balance/coordination ix. Personality changes x. Mood changes (depression/apathy) xi. Drowsiness, lethargy, or loss of consciousness xii. Uncontrollable eye movement/eyelid drooping.

c.

RF: > 55y, African-American, Having diabetes, family hx of stroke i. Medical stroke RISKS: previous stroke, previous TIA,  cholesterol,  BP, heart disease, A-fib, carotid artery dz ii. LIFE RISKS: Smoking, overweight, alcohol d. Labs/Imaging: Magnetic resonance angiography (MRA) or cerebral angiography i. To identify presence of cerebral hemorrhage ii. abnormal vessel structures iii. vessel ruptures iv. regional perfusion of blood flow in the brain ii. Lumbar puncture i. Used to assess presence of blood in the CSF iii. Carotid endarterectomy i. Performed to open the artery by removing atherosclerotic plaque iv. Interventional radiology i. Performed to treat cerebral aneurysm e. MGMT, rehab i. Monitor for changes in the patient’s level of consciousness (increased intracranial pressure sign). Elevate the patient's head to reduce ICP and to promote venous drainage. ii. Institute seizure precautions. iii. Maintain a non-stimulating environment. iv. Assist with communication skills if the patient’s speech is impaired. v. Encourage PROM every 2 hr to the affected extremities and AROM every 2 hr to the unaffected extremities. vi. Elevate the affected extremities to promote venous return and to reduce swelling. vii. Maintain a safe environment to reduce the risks of falls. viii. Scanning technique (turning head from side to side) when eating and ambulating to compensate for hemianopsia f. THROMBOLYTIC THERAPY: Contraindications of thrombolytic therapy; when to rx/ NOT rx g. ABSOLUTE contraindication: evidence of intracranial hemorrhage on CT scan h. Also, anything that increases the risk of intracranial hemorrhage (pt has hx of stroke w/i 3months) i. If a patient has a clinical presentation suggestive of a subarachnoid bleed: i. Severe headache ii. Orbital pain iii. Vision loss iv. Dizziness v. A previous subarachnoid bleed i. EVEN W/ NORMAL CT SCAN THE ABOVE ARE STILL C/I j. Arterial puncture at a non-compressible site within the previous week. k. Recent head trauma or active head bleed 8.

ISCHEMIC STROKE: happens when the blood flow to part of the brain stops for a short period of time. a. TIA: transient ischemic attack, this “mini-stroke”, sudden and short-lived attack b. CLINICAL PRESENTATION PPP: often lasts <24hrs i. Internal Carotid artery: Amaurosis fugax monocular vision loss- temporary “lamp shade down on one eye” weakness in contralateral hand. i. Other sx; sudden headache, speech changes, confusion ii. Vertebrobasilar: brainstem/cerebellar sx (gait & proprioception, dizziness, vertigo)

9.

ANGINA: a. CLINICAL PRESENTATION: Chest pain b. Ddx, r/o Ddx’s i. c. Labs: EKG if suspect potential MI

10. PULMONARY EMBOLISM: a. CLINICAL PRESENTATION: VIRCHOWS TRIAD: Venostasis, hypercoagbility, vessel wall inflammation. Dyspnea MC symptom: * tachypnea MC sign. * i. Abrupt onset of pleuritic chest px (intense sharp px), dyspnea, hemoptysis ii. Symptoms: Dyspnea, wheezing, cough, pleuritic chest pain, non-pleuritic chest pain, hemoptysis, sweats, syncope, back pain, shoulder pain, upper abdominal pain, or asymptomatic iii. Signs: Tachypnea, Tachycardia, Rales, cardiac gallop, phlebitis or DVT, edema, Cyanosis, Diaphoresis iv. Patients may be asymptomatic. v. History classic triad: dyspnea (80%), pleuritic chest pain (70%) & hemoptysis. Classic presentation: post-op patient with sudden tachypnea (70%), tachycardia. ± cough or hemoptysis. vi. If massive PE ±syncope, hypotension, pulseless electrical activity. - Factor V Leiden MC predisposing condition. b. Physical exam: The pulmonary exam is usually normal. * May have rales or a pleural friction rub. Homan's sign (calf pain with dorsiflexion is a classic but nonspecific sign). c. DIAGNOSTIC STUDIES/Labs: i. CXR: Hampton’s Hump, Westermark Sign ii. EKG: S1Q3T3 iii. D-dimer (90% sensitivity, many false +’s) iv. ABG (used to calculate the A-a gradient) v. GOLD STSANDARD: Pulmonary Angiography vi. Spiral CT (used in ER) vii. VQ scan if allergy to IVP dye: Only r/o PE in patients with low clinical suspicion. viii. Helical CT scan (CT-PA): best initial test for suspected PE. * More sensitive for proximal emboli. positive if intraluminal defect is seen. May demonstrate other etiologies. d. MGMT: Stabilize the pt: O2, IVF bolus, maintain BP (PE can lead to decreased CO), heparin, LMWH (enoxaparin), TPA or stretkinase e. Disposition from the ED: i. Admission to hospital if clinically unstable ii. (ICU) if stable (Telemetry) 11. ARDS life threatening acute hypoxemic respiratory failure. MC develops in critically ill patients a. CLINICAL PRESENTATION: Acute dyspnea & hypoxemia. Multi-organ failure if severe. SEVERE REFRACTORY HYPOXEMIA is hallmark, NOT responsive to 100% O2 (refractory hypoxemia) i. Sx: Cough, progressively worsening dyspnea ii. Signs: Tachypnea, cyanosis, fever, rales (pulmonary edema) b. Labs/Imaging: Order blood panel (CBC, BMP or CMP, PT/PTT, possibly blood cx) and UA i. No definitive lab test to diagnose ARDS ii. CBC may show leukocytosis, anemia, and/or thrombocytopenia iii. ABG: May show respiratory alkalosis (indicating respiratory distress), hypoxia iv. BILATERAL INFILATRATES** on CXR w/ WHITE OUT pattern (CXR resembles CHF) ARDS characteristically spares the costophrenic angles v. Absence of cardiogenic pulmonary edema/CHF vi. Cardiac catheterization of pulmonary artery (Swan-Ganz) pulmonary capillary wedge pressure. This is used to differentiate from cardiac pulmonary edema. 12. PNEUMOTHORAX: Air in pleural space. Increasing positive pleural pressure causes collapse of lung. a. CLINICAL MANEFESTATIONS: i. Chest px: usually pleuritic, UNILATERAL, non-exertional & sudden; dyspnea. ii. Sx: Acute onset of pleuritic pain (90-95%), dyspnea (80%) iii. Signs: Decreased/absent breath sounds on affected side (85%), adventitious breath sounds (crackles, wheezes) on affected side, tachypnea (RR>24), tachycardia (HR>120) b. PHYSICAL EXAMINIATION: i. Increased hyperresonance to percussion, decreased fremitus, decreased breath sounds (over affected side) ii. Unequal respiratory expansion, tachycardia, tachypnea iii. Tension pneumothorax: Increased JVP, pulsus paradoxus, hypotension, displaced trachea, hypoxia, hypotension c. MANAGEMENT: CXR (expiratory is better), chest CT, US i. Observation: In primary spontaneous if small. Observe for at least 6 hours then repeat CXR to affirm progression ii. Chest tube placement: If large or severe symptoms iii. Needle aspiration: IMMIDIATE needle thoracostomy (DO NOT do x-ray first) If tension pneumothorax followed by chest tube placement. Needle placed in 2nd intercostal space @ midclavicular line of affected side i. Avoid pressure changes like high altitudes, smoking, unpressurized aircraft and scuba diving.

13. SEXUAL ASSAULT/ABUSE: Drug Facilitated – ETOH MC a. Sexual assault: Inappropriate touching, child molestation, voyeurism (gaining sexual pleasure from watching others when they are naked or engaged in sexual activity), stalking, vaginal/anal/oral penetration, sexual intercourse with no consent, attempted rape, rape

14. BURNS: RULE OF NINE: ONLY deep partial thickness and FULL thickness are included a. PARKLAND FORMULA i. 4cc/kg/% TBSA burn, half over FIRST 8hrs, then the other half over the NEXT 16hrs ii. Example: 4ml x 70kg x 22.5% = 6,300cc i. 6,300cc/ 2 = 3,150cc ii. 3,150cc/ 8hrs = 393.7cc/hr iii. 3,150cc/ 16hrs = 196.875cc/hr b. CLASSIFICATION (1st, 2nd, 3rd, 4th degrees) i. Presentation (appearance, pain, etc.) ii. 1st Degree: Superficial, epidermal layer only, pink-red, painful & slightly edematous. Heals w/ peeling of dead skin in 7 days. iii. 2nd Degree: SUPERFICIAL PARTIAL thickness, involves the epidermis and the papillary layer of dermis. Extremely painful burns/ BLISTERS. Healing 14-21 days i. DEEP PARTIAL thickness: extend to reticular layer, can damage sweat/hair glands. HALLMARK is skin white and difficult to distinguish between full thickness. May have blisters. Healing 3-6weeks, scarring iv. 3rd Degree Full thickness: involves entire dermal layers. Presents as insensate/white/charred. HALLMARK is thrombosed vessels, PAINLESS and leathery. Healing only with scar formation/skin grafts. v. 4th Degree: Involves structures deep to the dermis, nerve, tendon, muscles, or bone. Areas are charred. Requires surgical debridement, amputation of reconstruction. c. MGMT Rehabilitation: Third degree burns (When you would consider referring d/t complications of thrombosis) can have devastating physical and psychological effects on patients. i. Burn rehabilitation often includes: i. Physiotherapy (Important in PEDs d/t increased physical and psychological vulnerability, crucial to growth/demands of elasticity), occupational therapy, & psychiatric therapy. ii. Wound MANAGEMENT: i. Debridement of tissue ii. Escharotomy: used for CIRCUMFERENTIAL BURNS, frees body of tourniquet effect iii. SILVADENE is better topical ABX than silver nitrate (more penetration)

15. ABDOMINAL PAIN: MCC of abdominal px is nonspecific px > appendicitis >biliary tract a. Know how to examine the abdomen i. FAR COLDER i. Frequency ii. Associated sx iii. Radiation iv. Character v. Onset vi. Location vii. Duration viii. Exacerbating factors ix. Relieving factors ii. Physical examination: Vitals, appearance, auscultation, palpation iii. CLINICAL PRESENTATION: i. RUQ: Liver, GB, lung, bowel, renal ii. LUQ: Cardiac, gastric, esophageal, bowel, renal iii. RLQ: Urologic, GYN, bowel, renal iv. LLQ: Urologic, GYN, bowel, renal iv. MGMT: LABS/IMAGING i. Abdominal x-ray – Evaluates stomach, liver, spleen, small and large intestines. Assesses for radiopaque stones (calcium oxalate, calcium phosphate, struvite stones) foreign bodies, look for free air if perforation is suspected. ii. EGD (esophagogastroduodenoscopy) – flexible fiber optic tube with camera to evaluate the upper GI tract (esophagus, stomach, duodenum) Evaluates ulcers, diagnose and treats GI bleeds, biopsy lesions, removes foreign objects (food) DIAGNOSTIC TEST OF CHOICE – peptic ulcer disease/Mallory Weiss iii. Colonoscopy – diagnose and treat lower GI bleeds, biopsy suspicious lesions/polyps, evaluate and treat inflammatory bowel diseases. iv. ERCP – upper GI scope + x rays to diagnose and treat disorders of the bile or pancreatic ducts (gallstones, obstructions, tumors, infection (cholangitis). COMPLICATIONS** – PANCREATITIS, perforation, hemorrhage. v. MRCP – Magnetic resonance cholangiopancreatography (MRCP) imaging to visualize the biliary and pancreatic ducts in a non-invasive manner. This procedure can be used to determine if gallstones are lodged in any of the ducts surrounding the gallbladder. vi. CT Scan abdomen and pelvis – diagnose and confirm disorders (appendicitis, kidney stones, pancreatitis, lesions on organs, AAA) Quick test that gives you broad/specific information. 16. APPENDICITIS: MCC fecalith, TX: Appendectomy a. CLINICAL PRESENTATION: Periumbilical/epigastric px, loss of appetite/not eating, low grade fever, px moves to RLQ w/ N/V. i. Rovsing sign: RLQ px w/ LLQ palpation ii. Obturator sign: RLQ px w/ internal & external hip rotation, bent knee iii. Psoas sign: RLQ px w/ right hip flexion/extension (raise leg vs resistance) iv. McBurney’s: 1/3 the distance from the anterior superior iliac spine (ASIS) and navel 17. HERNIA: Protrusion of contents of the abdominal cavity through the inguinal canal a. CLINICAL PRESENTATION: If pt is asymptomatic, could be strangulated. i. Incarcerated: irreducible, swelling or fullness @ hernia site which enlarges w/ ABD pressure and/or standing. Not able to return contents back into ABD cavity. Nausea/vomiting if bowel obstruction present. ii. Strangulated: Surgical emerg, ischemia, SEVERLY PAINFUL BM causing PT to refrain from having regular BM. b. MGMT: Surgery over watchful waiting (Inguinal usually requires surgical repair) i. Open vs Laparoscopic, Mesh or no mesh i. Open: Lichtenstein, Plug and patch ii. Lap: TEP totally extraperitoneal repair, TAPP Transabdominal properitoneal repair iii. Suture: Simple or Component iv. Mesh i. Synthetic: extruded monofilament, Expanded polytetrafluoroethylene ePTFE, Gortex ii. Biologic c. Femoral Hernia – MC in female d. Direct/Indirect Hernia – know the anatomy and what differentiates them i. INDIRECT: MC passage through INTERNAL inguinal ring down inguinal canal (MAY PASS INTO SCROTUM). MC in peds/young adults ii. DIRECT: passage through EXTERNAL inguinal ring at Hassel Bach triangle (RARELY ENTERs SCTROTUM) i.

Hesselbachs: (RIP): Rectus abdominus (medial), Inferior epigastric vessels (lateral), & Pouparts ligament (inferiorly)

18. HEAD TRAUMA & BRAIN INJURY: a. CLINICAL PRESENTATION: i. CSF rhinorrhea, otorrhea (Glucose test, ring test, beta-2 transferrin) ii. Battle Sign (mastoid ecchymosis) (bruising behind the ear) iii. Raccoon eyes (periorbital ecchymosis) iv. Hemotympanum (blood in tympanic membrane) v. Vertigo

b.

Epidural hematoma i. CLINICAL PRESENTATION: i. LOC followed by lucid interval and then subsequent neurologic demise ii. Fixed and dilated pupil on side of lesion develops with contralateral hemiparesis iii. herniation usually occurs within hours iv. may fully recover if evacuation before herniation / development of deficits ii. Imaging: MRI of head: Lens shaped, does not cross sutures (collects in potential space between skull and dura), classically described with injury to middle meningeal artery iii. MGMT: Immediate surgical intervention required, Low mortality if treated prior to herniation or neurologic defects iv. Rehabilitation: According to the time passed from the initial injury i. Acute (3-12m) a. Main goal: Preventing complications of immobility i. Passive ROM exercises ii. Positioning (sitting or semi sitting) b. Sensory and proprioceptive stimulation. ii. Post-Acute (12-24m) and Long term (>24m) a. Behavior management specialized severe and moderate behavioral problems. b. Outpatient therapy. c. Home health services. d. Independent living programs. e. Community re-entry programs. f. Social care institutions. g. Brain injury support groups. h. Day rehabilitation.

19. INTOXICATION: a. Identify the agent b. MGMT Narcan (Naloxone 0.4 up to 2mg)