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Oral medicine Case presentation

Transcript: personal data 0856200 Family History Refrences Radiographic Findings The 3 children with documented donor osteoblast engraftment had a median 7.5-cm increase in body length (range, 6.5-8.0 cm) 6 months after transplantation compared with 1.25 cm (range, 1.0-1.5 cm) for age-matched control patients. These patients gained 21.0 to 65.3 g total body bone mineral content by 3 months after treatment or 45% to 77% of their baseline values. With extended follow-up, the patients' growth rates either slowed or reached a plateau phase. Bone mineral content continued to increase at a rate similar to that for weight-matched healthy children, even as growth rates declined. These results suggest that BMT from HLA-compatible donors may benefit children with severe OI. Further studies are needed to determine the full potential of this strategy Need Oral Radiographe for further investigation on the Maxilla and Mandible ( osteopenea) Genatic counseling Give Oral Hygiene and balanced diet instructions Follow up Clinical responses to bone marrow transplantation in children with severe osteogenesis imperfecta 3 Years Old Dental History Treatment Bisphosphonates Low impact exercises such as swimming In more severe cases, surgery to place metal rods into the long bones ADEL RADWAN Male Atrophic red area on the dorsal surface of the tongue surrounded by an elevated whitish border Regular Check up Extra-Oral Examenation Preclinical models have shown that transplantation of marrow mesenchymal cells has the potential to correct inherited disorders of bone, cartilage, and muscle. The report describes clinical responses of the first children to undergo allogeneic bone marrow transplantation (BMT) for severe osteogenesis imperfecta (OI), a genetic disorder characterized by defective type I collagen, osteopenia, bone fragility, severe bony deformities, and growth retardation. Five children with severe OI were enrolled in a study of BMT from human leukocyte antigen (HLA)–compatible sibling donors. Linear growth, bone mineralization, and fracture rate were taken as measures of treatment response. The 3 children with documented donor osteoblast engraftment had a median 7.5-cm increase in body length (range, 6.5-8.0 cm) 6 months after transplantation compared with 1.25 cm (range, 1.0-1.5 cm) for age-matched control patients. These patients gained 21.0 to 65.3 g total body bone mineral content by 3 months after treatment or 45% to 77% of their baseline values. With extended follow-up, the patients' growth rates either slowed or reached a plateau phase. Bone mineral content continued to increase at a rate similar to that for weight-matched healthy children, even as growth rates declined. These results suggest that BMT from HLA-compatible donors may benefit children with severe OI. Further studies are needed to determine the full potential of this strategy. Osteogenesis Imperfecta diagnosed at 6 weeks of age Bronchopneumonia Multiple Bone Fractures Bisphosphanate Treatment Ca injections every 6 months Medical History Geographic Tongue The classic symptoms include: •Blue tint to the whites of their eyes (blue sclera) •Multiple bone fractures •Early hearing loss (deafness) Because type I collagen is also found in ligaments, persons with OI often have loose joints (hypermobility) and flat feet. Some types of OI also lead to the development of poor teeth. Symptoms Large Head Bilateral Flexed extremities Short Bilateral Humerus THANK YOU Provisional Diagnosis The 3 children with documented donor osteoblast engraftment had a median 7.5-cm increase in body length (range, 6.5-8.0 cm) 6 months after transplantation compared with 1.25 cm (range, 1.0-1.5 cm) for age-matched control patients. These patients gained 21.0 to 65.3 g total body bone mineral content by 3 months after treatment or 45% to 77% of their baseline values. With extended follow-up, the patients' growth rates either slowed or reached a plateau phase. Bone mineral content continued to increase at a rate similar to that for weight-matched healthy children, even as growth rates declined. These results suggest that BMT from HLA-compatible donors may benefit children with severe OI. Further studies are needed to determine the full potential of this strategy Chief Complaint Insignificant Description of the Lesion Oral Medicine Case Presentation Intra-Oral Examination sister - Died at 6 months of age (OI) 10y brother - OI and Blue sclera Osteogenesis imperfecta (OI) is a congenital disease, meaning it is present at birth. It is frequently caused by defect in the gene that produces type 1 collagen, an important building block of bone. There are many different defects that can affect this gene. The severity of OI depends on the specific gene defect. OI is an autosomal dominant disease. That means if you have one copy of the gene, you will have the disease. Most cases of OI are inherited from a parent, although some cases are the result of new genetic mutations. A person with OI has a 50% chance of

Internal Medicine Case Presentation

Transcript: ~8weeks prior to admission ER visit diagnosed with pneumonia and treated with a 5 day course of levaquin and prednisone CT of her chest showed ill defined bilateral patchy densities in the lungs and mild bronchiectasis. ~6wks prior to admission visited PCP and seemed to be improving. ~4wks prior to admission ER visit again for worsening dyspnea, xray remained unchanged, started on a 14 day course of prednisone and levaquin and again began to improve. 2 days prior to admission PCP Visit with worsening fatigue and dyspnea started on levaquin and prendnisone a 3rd time Xray showed Bilateral infiltrates in the mid and lower lung fields but, a comparison was not made between prior studies. Day of admit - PCP visit with further worsening of fatigue and dyspnea O2 sat mid 80's on RA so..... 1. Macrobid 100 MG Capsule 1 capsule qhs x 5yrs 2.Vitamin E 400 intl units CAP 1 cap(s) PO once a day 3.CoQ-10 100 MG Capsule 2 capsule with a meal Once a day 4.Aspir-81 81 MG Tablet Delayed Release 2 tablets Once a day 5.Potassium Chloride 10 MEQ Tablet ER 1 tablet 4 times a day 6.Levothyroxine Sodium 100 MCG 1 tablet Once a day 7.Toprol XL 25 MG ERT 1 tab Once a day, 8.Norvasc 5 MG TAB 1 tab Once a day, 9.Lisinopril 40 MG TAB 1 tab Once a day, 10.Oxybutynin Chloride 5 MG 1 tablet Once a day before breakfast/ takes when Vesicare doesn't work (currently taking instead of Vesicare) 11.Levaquin 500 MG Tablet 1 tablet Once a day for last 2 days General: Denied fevers. Skin: Denied lesions, rashes other than those noted in HPI. HEENT: Denied changes in vision nasal congestion, ear pain. Cardio: Denied Chest pain. Pulm: per HPI GI: Denied Nausea, vomiting or diarrhea GU: Denied Dysuria, hematuria. Musculoskeletal: Denied pain in extremities. Iatrogenic Colitis Mnemonic for Crohns Dz for Boards GIFTS for Crohns Dz Granulomas Ileum (most common location) Fistulas/ Fissures Transmural layers (all affected) Skip lesions Common Antibiotics Causing C. difficile Colitis: Father- Cerebral Aneurysm D 60’s Mother CVA D 81, Brother MI 58 Sister DM2 Pathophysiology of Ischemic Colitis Assessment: Clinical Sx: chronic watery, non-bloody diarrhea with nml colonoscopy results Etiology: contaminated water/ food caused by unwashed hands or soiled hands reaching the mouth Lives at home with family. Lifelong nonsmoker Denied drugs or alcohol use. No recent travel or exposure to asbestos or other irritating chemicals during her lifetime(is a retired secretary). Labs: increased lactate, LDH, CPK indicates tissue damage in colon, WBC above 20,000 + metabolic acidosis + GI Sx Imaging: 1st test- CT with contrast Definite dx- colonoscopy is required to dx ischemic colitis Ulcerative Colitis vs. Crohns disease Clinical Sx: GI Sx, Colitis, malnutrition, rectal prolapse, reactive arthritis, CNS, may also cause HUS-Hemolytic Uremic Syndrome (via Shiga-toxin similar to E.coli 0157:H7) SocialHx STUDY: more than 1000 patients with ischemic colitis demonstrated that Left Colon was involved in more than 75% of patients, with majority of lesions affecting the Splenic Flexure. Rectum was involved in only 5% of patients, which can be explained because of collateralization of IMA with systemic circulation through other vessels Gram negative, rod-shaped Retrospective study: 313 patients with ischemic colitis- patients with Left colon ischemic colitis less likely to require surgery & had a shorter length of stay than any other pattern of ischemic colitis. Allergies/Sensitivities Fidaxomicin- Macrolide, bactericidal (vs. Vanc/ Metro are bacteriostatic), approved in 2011 Study: Phase 3 randomized trial 629 patients with C. difficle colitis, clinical cure rates with Fidaxomicin 200 PO bid vs. Vancomycin 125 PO qid were similar but less recurrence with Fidaxomicin Shigella dysenteriae colitis Treatment: IVF and ususally conservative therapy Abx decreases duration of Sx by ~2days 1. Levofloxacin 500 mg PO qd X 3 days or 2. Ciprofloxacin 500 mg PO bid X 3 days or 3. Azithromycin 500 mg PO qd X 3 days or 4. Ceftriaxone IV 1gm 1d X 5 days Fidaxomicin versus vancomycin for Clostridium difficile infection. Louie TJ, Miller MA, Mullane KM, Weiss K, Lentnek A, Golan Y, Gorbach S, Sears P, Shue YK, OPT-80-003 Clinical Study GroupSON Engl J Med. 2011;364(5):422. Final Diagnosis: Hypersensitivity Pneumonitis/pulmonary toxicity from nitrofurantonin or other unknown source vs mixed connective tissue disorder Vitals: BP 140/90, P105, R 26, T36.6, 96% on 6L via Nasal cannula. General: Alert and oriented x3, no acute distress. Skin: Pale petechiae over bilateral lower extremities and back, barely noticeable. No other rashes or worrisome lesions Eyes: Pupils equal round and reactive to light. Extraocular muscles intact. Sclera non-icteric HENT: atraumatic, normocephalic, mucosa moist and pink. Neck: No JVD, No palpable lymph nodes. Cardiovascular: Normal rhythm slightly tachycardic. No murmurs,rubs or gallops. Pulmonary: Normal respiratory effort, not using accessory muscles. Mildy tachepnic

medicine case presentation

Transcript: personal data Chief complaint Past Medical History extra oral examination normal Skin : Eye : Ear : Nose : TMJ : Intra Oral Examination Labial mucosa ventral surface of the tongue Floor of the Mouth Description of the lesion Long standing , Soft , elevated , rounded , yellowish lesion of 1-2 cm in diameter on the lingual frenum ; and non tender and move around with very little finger pressure Differential diagnosis Mucocele Ranula Dermoid cyst lipoma Salivary gland tumor Diagnosis lipoma treatment plan No treatment is usually necessary for a lipoma. However, if the lipoma is in a location that bothers you, is painful or is growing, might recommend that it be removed. Lipoma treatments include: Surgical removal Steroid injections Liposuction This treatment uses a needle and a large syringe to remove the fatty lump. lipoma slowly enlarging, soft, smooth-surfaced mass of the submucosal tissues when superficial there is a yellow surface discoloration When well-encapsulated tumors freely movable beneath the mucosa Usually found in the buccal mucosa And rare in the floor of mouth Oral Medicine Case Presentation female fatima ahmed mohamed samy mohamed shuweil mohamed hamdy mohamed tantawy presented by Dilated lingual veins in the ventral surface of the tongue Most lipomas are removed surgically 55 married _ve What is lipoma ?? benign mesenchymal ,slowly growing , neoplasm composed of mature Adipocytes usually surrounded by a thin capsule They are the most common soft tissue tumors and about 20% of the cases occur in the head and neck region However only 1% to 4% of cases involve the oral cavity Oral lipoma represents 0.5% to 5% of all benign oral cavity neoplasms and lesions involving the floor of the mouth are quite rare . 55 years old female patient was coming for making a removable partial denture and during the routine extra oral and intra oral examination we have found this lesion . marital status Past Dental History buccal mucosa but doesn't completely eliminate the tumor. by cutting them out adress . name abo soliman normal History of Multiple teeth Extraction due to Caries and Pain . Recurrences after removal are uncommon . This treatment shrinks the lipoma Age : Sex :

Integrative Medicine Case Presentation

Transcript: NutriEval Beaumont Labs Fermenatble Oligosaccharides, Disaccharides, Monosaccharides, and Polyols "65y.o. female is in for a follow up for digestion. She has lost weight and feels wonderful Ben, her son, has had anxiety and it has been better, so her her stress is better. This is the first time that her gut has been balanced in her life.Overall she feels good." Plan: Go to PCP for HRT Continue to increase Yoga or other forms of exercise- In the future we will assess mercury level if sleep is not 100% and you are not feeling 100% Follow up in 4-6 months for the Nutra Eval and we can go over results Fatigue Medications: Align brand probiotic Calm brand magnesium supplement Citrucel fiber supplement Sleep: Hx of Sleep apnea initiates sleep, but difficulty with maintenance. wakes often. reports palpitations, joint pains. Diet: All Organic, all home-made, includes ample spinach and berries, supplements with protein powder Our Patient Differential for GI Bleed/Abdominal Pain Colon Cancer Diverticulitis Ischemic Bowel Inflammatory Bowel Crohn's Colitis Dysbiosis Food Allergy Hemorrhoids, Anal Fissure Synthesized in sunlight and available in few foods common deficiency Decreased with Statins, NSAIDs Joint Pain Vitamin D GI Upset, Constipation Updates: Family History Mother: OA, HTN, CAD, Schizophrenia Father: OA, HTN, ETOH abuse, DM2, CAD s/p PCI & CABG. Sister: RA Sister: Glaucoma Brother: OA No known family Hx of Colon, Prostate, ovarian, or breast Cancer. DLD, CVA, enhances absorption of Calcium, Iron, Magnesium, Phosphate, Zinc Hormonal Properties in calcium homeostasis and metabolism Antioxidant Supports Mood Beaumont Labs Follow Up on Labs Visit 4 PTH: 35 pg/mL [9-69] Calcium: 9.5 [8.5-10.5] We begin with lifestyle and dietary modification (eg, exclusion of gas-producing foods; a diet low in fermentable oligo-, di-, and monosaccharides and polyols [FODMAPs]; and in select cases, lactose and gluten avoidance) Integrative Medicine Case Presentation moving, son w/ rehab, relationship w/ husband strained Vitamin D Deficiency Sleep having palpitations laying supine sleep study showed central sleep apnea C-pap does not work Still waking through the night Digestive System improved greatly "better than it has ever been her entire life" Stress much better, has decided to sell house and move to a much smaller house Elimination Diet Eliminate Dairy, Gluten, Sugar 1 month, add each independently 3 days apart Labs NutraEval CBC, CMP Relaxation Work on Letting go of control Couples retreat exercise 3x/week Supplements Adren-All 2 QAM Adren-Vive2 QPM Follow up on Sleep, inflammation, blood work, digestion, diet, supplements, afternoon fatigue Plan: Non-Celiac Gluten Sensitivity Participants were randomly assigned to groups given a 2-week diet of reduced FODMAPs, and were then placed on high-gluten (16 g gluten/d), low-gluten (2 g gluten/d and 14 g whey protein/d), or control (16 g whey protein/d) diets for 1 week 66 y/o Female with PMH AVNRT s/p ablation 2001, sleep apnea, presents with complaint of rectal bleed, joint pain, fatigue, stress, sleep problems. She reports constipation relieved with Miralax, worsening with stress. Denies bloating or flatulence. Hx benign colon polyps. Last scoped 2009 Reports episodes of abdominal pain and bleeding, 3-4x/yr, pain relieved with defecation. Pt concerned about ischemic bowel disease. FODMAPS Visit 3 OA,HTN,DM2, CAD, Galactosemia UpToDate Visit 2 Craig Erbach, OMS-IV Dairy: got constipated No issue with gluten Sugar makes inflammation worse Energy: better after lunch feeling better overall Evidence in Mouse Models Gut-Brain Connection Ectopic Pregnancy Lifestyle Anger and Emotion management consider returning to work consider having fillings removed Increase weight bearing exercise Supplements 5000 IU Vitamin D3 Osteoben TID AdrenAll2 QAM Adrenvivie2 QPM Probiotic to Lactoprime QD Multi: with high B content with trace minerals Metabolic Synergy TID INcrease Magnesium to 2 tsp per day sleep disturbance, apnea Plan: Summary

Case Presentation- DME Medicine

Transcript: 81 year old female PC: dizziness followed by Collapse 11 days ago Whilst sitting, initially light headed followed by vertigo Sudden onset Hot and sweating No nausea or vomiting, headaches, chest pain, difficulty breathing On standing patient saw black and slumpped back into chair Whitnessed by neighbour and son - patient looked grey Staring ahead but unresponsive for 30 minutes No incontinence, seizures, tongue biting After event, the patient had no recollection of event No confusion Episodes of vertigo becoming more frequent FH: Mother died at 60- heart attack Father died at 83- gastric cancer SH: None smoker Whisky 3 units a day=21 week OBS Pulse:72 RR:16 Temp:36.1 BP: 94/40 GCS:15 O2 sat: 100% Alert- frequent episodes of vertigo during examination Slight tremor in R hand Neurological exam: -Pronator drift: normal -Tone + clonus: normal in both sides -Power: 5/5 -Reflexes: UL and LL both ellicited -Coordination: tremor on finger nose -Sensation: normal on both sides UL and LL Cranial nerves: I-XII normal- No nystagmus, no double vision no ataxia. CV: Nothing of note, HS I-II-0, no murmurs GI: Mass felt R Side PMH Blood ++ Protein + Nitrites + Leukocytes +++ (cc) photo by Metro Centric on Flickr Urinary infection Medication More info on head lump: CT showed: Broad base attachment to meningies No associated brain odema No midline shift or signs of hydrocephalus Meningioma right frontal lobe, 3.3x3.4cm syncope secondary to GI bleed Budapest San Francisco FBC 7.5 Urea 14.0 Cr 200 ALT 23 Examination Stockholm DME Case Presentation (cc) photo by jimmyharris on Flickr Plan 75mg OD (cc) photo by Franco Folini on Flickr ROS -Black stools 1 week ago (no abdo pain, hameatemisis) Double click to crop it if necessary Meningioma ?? urine dipstick Clopidogrel 8 mg OD 80mg OD 500mg OD 40 mg OD 5 mg OD 15 mg OD 100mg OD 250mg OD Current cellulitis Prior 2 weeks lump (referral) -Paroxysmal palpatations -CKD -Essential hypertension -Angina History Investigations Worsening renal function secondary to poor oral intake Bloods 5+7= (cc) image by anemoneprojectors on Flickr Place your own picture behind this frame! (cc) photo by Metro Centric on Flickr Transfuse Hb aim for 10 Iv fluids 8 hourly gaps Stop temporary frusemide, losartan Strict fluid balance chart U/S kidneys OGD (stop clopidogrel until then) CT abdomen Brain MRI Dose Important Details Surgical history Left mastectomy 16 years ago for breast Ca hysterectomy 9 years NKDA Doxazosin Furosemide Methyldopa Atorvastatin Amlodopine Mirtazapine Losartan Cefalexin Flucloxacillin and amoxocillin Differentials

Internal Medicine Case Presentation

Transcript: Review of Systems WBC: 18.4 RBC: 5.08 HGB: 13.4 HCT: 42.4 MCV: 83.5 MCH: 26.5 PLT: 353 NEUT: 83 LYMPH: 9 MONO: 8 swelling worse returns to UPH CT scan performed sinusitis orbital/periorbital cellulitis transferred to ASEM Surgeries Blood transfusions Accidents 2 weeks prior to admission: Sodium: 137 Potassium: 4.0 Chloride: 99 CO2: 31.2 BUN: 6 Creat: 0.8 Gluc: 124 Calcium: 9.3 Albumin: 3.4 Bronchial Asthma last exacerbation (2003) Chicken Pox (2011) Social History Childhood illnesses Diagnosis Treatment Immunizations "Se me hinchó el ojo izquierdo y no lo puedo abrir hace 3 dias" worsening headache eyelid swelling inability to open his eye taken to UPH, Toradol and Benadryl given Group I: preseptal cellulitis, and group II is orbital cellulitis. The remaining groups are all abscesses: group III is subperiosteal abscess, group IV is intraorbital abscess, and group V is cavernous sinus thrombosis (septic abscess). headaches facial tenderness dizziness returned to PCP prescribed:Amoxicillin, Mucinex, Loratidine Up to date by hx Vital Signs: T: 36.8 P: 89 R: 18 BP: 117/58 General: AAOx3, in no acute distress Head: atraumatic, normocephalic, tender to palpation in frontal area no bulges or masses, normal hair distribution. ENT: MOM, no pharyngeal exudates, clear TM Most common route of infection ethmoid sinusitis subperiosteal abscess 15-59% orbital abscess 24% vision loss cavernous sinus thrombophlebitis brain abscess CT - confirmation of clinical suspicion MRI- also helpful Venography- include when CST is suspected Complications Family History Feature Preseptal Cellulitis Orbital Cellulitis Proptosis - + Motility + +/- Pain on motion - + Orbital pain - + Vision Normal May be decreased Pupillary reaction + ± Chemosis Rare Common Corneal sensation + May be decreased Ophthalmoscopy Normal May be abnormal Systemic signs Mild Commonly severe 19 y/o M patient with past medical hx of Bronchial Asthma and allergic to ASA presents with swelling, redness of his left upper and lower eyelids since 3 days ago Past Medical History Laboratories 1 week prior to admission: Eyes: PERRLA, EOMI.Left upper and lower eyelid swelling and erythema, no eye proptosis, exudates, erythema or hemorrhages.Mild swelling starting in right eyelids. Sinuses: Tenderness upon palpation of maxillary and frontal sinuses Nodes: Non palpable or tender 6. RESPIRATORY: + hx of BA, URI symptoms past 2 weeks. - cough, dyspnea, orthopnea, history of tuberculosis or emphysema. 7. CARDIAC: -chest pain, tightness, palpitations and exercise intolerance. 8. GI: - N/V, constipation, diarrhea, heartburn, bloody stools, abdominal pain, food intolerance, changes in bowel habits. 9. GENITOURINARY: - polyuria, nocturia, incontinence, dysuria. 10. EXTREMITIES: - pain, loss of muscle strength, loss of sensation or difficulty moving Multivitamin by Mariana Mercader Pérez MS4 Preseptal Cellulitis Orbital Cellulitis HZV/VZV infection involving eye Tumors Trauma Insect bites Graves disease Cavernous sinus thrombosis Severe conjunctivitis Vasculitis Mucormycosis/ Aspergillosis Aspirin Medications ESR: 49 CRP: 142.7 BC: negative 48h Epidemiology Day of Admission Chief Complaint Evaluated by Ophta and ENT services Admitted to IM to treat with IV Antibiotics Any questions 3 days prior to admission: 1. GENERAL: + fever. - chills, night sweats, recent weight changes, fatigue, lethargy, dizziness, changes in appetite, difficulty sleeping or rashes. 2. HEAD: +headaches. -trauma to head, lightheadness. 3. EYES: + L eye redness, swelling, discomfort, tenderness to palpation, lacrimation. -pain on L eye motion, blurry vision, photophobia and decreased perception of colors; diplopia, floaters, use of contact lenses, recent trauma, blindness, or similar symptoms in the past. 4.EAR, NOSE, THROAT: - otorrhea, tinnitus, vertigo, hearing loss, rhinorrhea, epistaxis, dysphagia, odynophagia or hoarseness. 5. NECK: - lumps, enlarged nodes, tender nodes or difficulties in ranges of motion. Mother: Asthma Hospitalizations 2011 UPH Spontaneous Pneumothorax Chest tube Chicken Pox Pneumoniae bleeding pus secretion N/V use of contact lenses sick contacts pets similar previous episodes Imaging Physical Exam Allergies 11. HEMATOLOGIC: - anemia, easy bruising or bleeding. 12. ENDOCRINE: - polydipsia, polyphagia or polyuria, no history of thyroid disorders, recent weight changes, abdominal striae, difficulty concentrating, or any other endocrine abnormalities. 13. NEURO-PSYCHIATRIC: - seizures, paralysis, loss of consciousness, gait disturbances, speech, memory deficits, hallucinations, tremors, poor balance, loss of sensation or muscle strength and sphincter dysfunction. IV Antibiotics: None Vancomycin with 1 of the following: Ceftriaxone Cefotaxime Piperacillin-tazobactam Ampicillin-sulbactam For a total of at least two to three weeks HPI Surgery: abscess > 10mm HPI Father DMII HTN OSA Spina Bifida Oculta Genitalia and Rectum: not evaluated; patient refused exam. Extremities: BL upper and lower

Internal Medicine Case Presentation - Ivanna

Transcript: 8weeks prior to admission ER visit diagnosed with pneumonia and treated with a 5 day course of levaquin and prednisone CT of her chest showed ill defined bilateral patchy densities in the lungs and mild bronchiectasis. 6wks prior to admission visited PCP and seemed to be improving. 4wks prior to admission ER visit again for worsening dyspnea, xray remained unchanged 2 days prior to admission PCP Visit with worsening fatigue and dyspnea a 3rd time Xray showed Bilateral infiltrates in the mid and lower lung Day of admit - PCP visit with further worsening of fatigue and dyspnea 1. Macrobid 100 MG Capsule 1 capsule qhs x 5yrs 2.Vitamin E 400 intl units CAP 1 cap(s) PO once a day 3.CoQ-10 100 MG Capsule 2 capsule with a meal Once a day 4.Aspir-81 81 MG Tablet Delayed Release 2 tablets Once a day 5.Potassium Chloride 10 MEQ Tablet ER 1 tablet 4 times a day 6.Levothyroxine Sodium 100 MCG 1 tablet Once a day 7.Toprol XL 25 MG ERT 1 tab Once a day, 8.Norvasc 5 MG TAB 1 tab Once a day General: Denied fevers. Skin: Denied lesions, rashes other than those noted in HPI. Cardio: Denied Chest pain. Pulm: per HPI GI: Denied Nausea, vomiting or diarrhea GU: Denied Dysuria, hematuria. Musculoskeletal: Denied pain in extremities. Iatrogenic Colitis Mnemonic for Crohns Dz for Boards GIFTS for Crohns Dz Granulomas Ileum (most common location) Fistulas/ Fissures Transmural layers (all affected) Skip lesions Common Antibiotics Causing C. difficile Colitis: Father- Cerebral Aneurysm D 60’s Mother CVA D 81, Brother MI 58 Sister DM2 Pathophysiology of Ischemic Colitis Clinical Sx: chronic watery, non-bloody diarrhea with nml colonoscopy results Etiology: contaminated water/ food caused by unwashed hands or soiled hands reaching the mouth Lives at home with family. Lifelong nonsmoker Denied drugs or alcohol use. No recent travel or exposure to asbestos or other irritating chemicals during her lifetime (is a retired secretary). Labs: increased lactate, LDH, CPK indicates tissue damage in colon, WBC above 20,000 + metabolic acidosis + GI Sx Imaging: 1st test- CT with contrast Definite dx- colonoscopy is required to dx ischemic colitis Ulcerative Colitis vs. Crohns disease Clinical Sx: GI Sx, Colitis, malnutrition, rectal prolapse, reactive arthritis, CNS, may also cause HUS-Hemolytic Uremic Syndrome (via Shiga-toxin similar to E.coli 0157:H7) SocialHx STUDY: more than 1000 patients with ischemic colitis demonstrated that Left Colon was involved in more than 75% of patients, with majority of lesions affecting the Splenic Flexure. Rectum was involved in only 5% of patients, which can be explained because of collateralization of IMA with systemic circulation through other vessels Gram negative, rod-shaped Retrospective study: 313 patients with ischemic colitis- patients with Left colon ischemic colitis less likely to require surgery & had a shorter length of stay than any other pattern of ischemic colitis. Allergies & Sensitivities Fidaxomicin- Macrolide, bactericidal (vs. Vanc/ Metro are bacteriostatic), approved in 2011 Study: Phase 3 randomized trial 629 patients with C. difficle colitis, clinical cure rates with Fidaxomicin 200 PO bid vs. Vancomycin 125 PO qid were similar but less recurrence with Fidaxomicin Shigella dysenteriae colitis Treatment: IVF and ususally conservative therapy Abx decreases duration of Sx by ~2days 1. Levofloxacin 500 mg PO qd X 3 days or 2. Ciprofloxacin 500 mg PO bid X 3 days or 3. Azithromycin 500 mg PO qd X 3 days or 4. Ceftriaxone IV 1gm 1d X 5 days Fidaxomicin versus vancomycin for Clostridium difficile infection. Louie TJ, Miller MA, Mullane KM, Weiss K, Lentnek A, Golan Y, Gorbach S, Sears P, Shue YK, OPT-80-003 Clinical Study GroupSON Engl J Med. 2011;364(5):422. Final Diagnosis Hypersensitivity Pneumonitis/pulmonary toxicity from nitrofurantonin or other unknown source vs mixed connective tissue disorder Vitals: BP 140/90, P105, R 26, T36.6, 96% on 6L via Nasal cannula. General: Alert and oriented x3, no acute distress. Skin: Pale petechiae over bilateral lower extremities and back, barely noticeable. No other rashes or worrisome lesions Eyes: Pupils equal round and reactive to light. Extraocular muscles intact. Sclera non-icteric HENT: atraumatic, normocephalic, mucosa moist and pink. Neck: No JVD, No palpable lymph nodes. Cardiovascular: Normal rhythm slightly tachycardic. No murmurs,rubs or gallops. Pulmonary: Normal respiratory effort, not using accessory muscles. Mildy tachepnic R 24-26 and talked in short sentences. Rhonchi in lower and middle right lung fields louder on expiration and faint Rhonchi heard on Lower left left lung field Abdomen: No hepatospenomegaly. Non-distended. Non-tender. Bowels tones present in all quadrants Musculoskeletal: 2+ edema to bilateral lower extremities and scattered very small petechiae. No clubbing or Cyanosis. Treatment of Pseudomembranous colitis Treatment Gold standard dx is cytotoxin assay for C. difficile (results in 48 hrs, 100% sensitive, 99% specific)

TRANSFUSION MEDICINE: case presentation

Transcript: Blood Bank anti-G antibody reacts like a mixture of anti-D and anti-C antibodies. . . pregnancy complications take-home POINTS: Classic case anti-G antibody formation: D and C are both present when a D-negative mother has antibodies that look like anti-D along with anti-C in the antibody screen that is a routine part of prenatal care, the laboratory must ask a very important question: C is present without D G3: current G2: 2015 FT NSVD G1: 2014 SAB D-negative donors are not routinely screened for the presence or absence of the C antigen. In this case, not surprising for formation of anti-C but if unaware of G, the added anti-D specificity would make no sense. most people are G-positive distinguish between anti-G and both anti-C and anti-D by pulling one antibody out of the serum by using red cells with the corresponding antigen (adsorption) then isolated the anti-G by the use of a second adsorption procedure sometimes called “G-differentiation.” Knowing whether a patient has anti-D or should have RhIG to prevent future anti-D formation is an important distinction to make in determining a prenatal patient’s clinical treatment course. Seeing a patient with an apparent anti-D and anti-C and making an assumption they are not an RhIG candidate could have significant consequences if that patient has, in fact, instead, an anti-G. genotypes for G-negative: (in black) rr rr” r”r” anti-G can be associated with hemolytic disease of the fetus/newborn (HDFN), though it tends to be milder most important question for pregnant D-negative women: “Is anti-D present?” The presence of anti-G can be assumed if anti-D is not identified. proceeded immediately to the OR history and physical The distinction is much more important in prenatal workups and in managing a pregnant patient. . . the distinction makes NO difference. G is an antigen present whenever D and/or C is present Anti-G will react against D+, C +, and D+C+ RBCs Anti-G transfusion management: Almost all D-negative RBCs will be compatible Identifying anti-G is most important for: anti-G in prenatal patients IS an indication for RhIG, even though ab screens looks D+. Teasing out a patient’s antibody specificity is time-consuming, but is valuable for ensuring RhIG is used when indicated, and not unnecessarily Adsorptions and double adsorptions. . . What difference does it make if a patient has a single antibody (anti-G) or TWO antibodies (anti-D AND anti-C)? Can be induced either by pregnancy transfusion Most commonly results from exposure of an rr patient to blood from r’ (C) or sometimes R0 (D)haplotype. QUESTION: If the antibody really is anti-D, the patient does not need to receive Rh Immune Globulin (RhIG) to prevent the formation of the antibody, because it is too late already! (Be cautious, though, and be sure that the patient has not recently received RhIG before making that decision) If the antibody is NOT anti-D and is actually anti-G, however, RhIG is indicated to protect the mother from actually forming anti-D > 30 min after delivery patient could not tolerate more aggressive fundal massage umbilical cord was also quite thin and could not be aggressively pulled brisk vaginal bleeding started different from main group of Rh antigens (D, C, c, E, and e). G is only absent when a person’s red cells lack both D and C. rr most common 15% of U.S. Caucasian population rr'', r''r'' < than 1% combined the vast majority of G-negative people who could make anti-G are D-negative with the rr genotype. From the perspective of a patient who is about to be transfused. . . type and screen ab positive haplotypes leading to G-positivity (in red) ie D, C, or both TRANSFUSION MEDICINE: case presentation Melanie Estrella DO pgy-1 15mar2017 Biochemically, expression of the G antigen depends on presence of a common amino acid (serine 103) Ser103 is present on surface of both D and C antigens http://www.bbguy.org/2016/06/17/want-g-wiz/ What is the likelihood of forming anti G? Prior retained placenta requiring manual exrtraction - s/p PTSD. If need manual extraction this time need to go to OR with general anesthesia Rh neg s/p rhogam short cut: D-differentiation ***NOTE: . . . there are a very small number of D+C- people that lack G, as well as a very small number of D-C- people that have G. These are the exceptions rather than the rule, but either situation can definitely happen. The next step is to dissociate (“elute”) the bound antibodies from the test cells and use the eluate (containing anti-D and anti-G) to perform a second adsorption (the “double adsorption” I mentioned above) with red cells of a different phenotype, as shown in figure 5 below: 45F G3P1011 at 38w0d by IVF presenting from clinic for IOL U/S: baby IUGR in 5th%ile (RHD, RHCe, and RHCE) D is present without C D-negative patient never been knowingly exposed to Rh + blood presents with an antibody that looks like combination of anti-D anti-C (sometimes called “anti-CD”). ob hx With D-negative blood A patient with

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