Internal Medicine III Logbook 2011-2012 | Gout | Inflammatory Bowel Disease

College of Medicine, Al-Ahssa DEPARTMENT OF MEDICINE 6TH YEAR STUDENT

Course Coordinator: Dr. Abdulmaguid AL-Ballat
Student's name: Qasim Hussain Al-Haleimi Academic number: 207002113

Contents:
 Activities & Discussion  Summary of clinical cases Presented  Clinical clerkship: Cases & follow up  Assignment  Notes  Extra reading

ACTIVITIES & DISCUSSION

CLINICAL CASES PRESENTED

CLINICAL CLERKSHIP: CASES & FOLLOW UP

ASSIGNMENTS

NOTES

EXTRA-READING

Activities & Discussion
First Day: 19 – 11 – 2011 Saturday Introduction & Oreintation about the course Disscussion: Causes of sudden attack of dyspnea:   Tension pneumothorax Foreign Body inhalation

Types of Angina pectoris Unstable: 1. Angina at rest 2. Recent onset angina occurs in the last 2 months which is class 3 least 3. Accelerating angina in severity & duration 4. Post infarction angina Grades of Angina pectoris: NYHA or Canadian HA Review on How to read an ECG: Rate : 300/ Num of Big squares between 2 R waves if regular, If irregular Num of R waves between 15 Big squares * 20 If > 100 tachycardia If < 60 bardycardia Rhythm: regular or irregular Axis: Look to Lead I & III if the direction Both R waves Positive Normal Lead I Positive & Lead II Negative (Left Axis) Lead II Positive & Lead I Negative (Right Axis) Waves & Intervals P wave: Normally 2.5 in duration & 2.5 in amplitude. Broad Bifid P wave: Atrial Flutter Absence P wave & Presence of F wave either course or fine is Atrial Fibrillation P Wave is best seen In Lead II P wave can be seen after QRS incase of AV nodal rhythm with regular rhythm. P wave is Enlarged in case of Atrial hypertrophy.

P-R interval is a reflection of the conduction between atria & ventricles. Normally 3-5 small squares. Prolonged P-R interval occur in Heart Block with different degrees QRS wave represent ventricular contraction Normally Sharp Narrow not wide take 2 - 3 small squares. QRS should be looked for evidence of pathologic Q wave which represent previous MI. Pathologic Q wave is a Q wave of > 4mm usually present in the Inferior leads II , III , AVF. Q-T interval normally < 10.5 samll squares, Cases ware Q-T interval increase beyond 10.5 small squares is usually abnormal S-T interval is very important in cases of ischemia, Electrolytes abnormality, & Infarction. ---------------Date: 21 – 11 – 2011 Monday Only case discussion --------Date: 22 – 11- 2011 Tuesday Discussion:  Causes of syncope  ECG commenting Dr.Abdulmaguid Dr.Naushad

---------Date: 23 – 11 – 2011 Wednesday Case Discussion Management of a case of Bronchial Asthma Dr.Naushad

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Date: 26 – 11 – 2011 Saturday Case Discussion Rheumatoid arthritis

Dr.Naushad

Source Amarican college of Rheumatology In the new criteria set, classification as “definite RA” is based on the confirmed presence of synovitis in at least 1 joint, absence of an alternative diagnosis that better explains the synovitis, and achievement of a total score of 6 or greater (of a possible 10) from the individual scores in 4 domains: number and site of involved

joints (score range 0–5), serologic abnormality (score range 0–3), elevated acute-phase response (score range 0–1), and symptom duration (2 levels; range 0–1). This new classification system redefines the current paradigm of RA by focusing on features at earlier stages of disease that are associated with persistent and/or erosive disease, rather than defining the disease by its late-stage features. This will refocus attention on the important need for earlier diagnosis and institution of effective disease-suppressing therapy to prevent or minimize the occurrence of the undesirable sequelae that currently comprise the paradigm underlying the disease construct “rheumatoid arthritis.”

-------Date: 28 – 11 – 2011 Monday Case discussion SLE Dr.Naushad

---------Date: 29 – 11 – 2011 Tuesday Case discussion Heart failure & pulmonary edema Commonest Causes of HF: 1. Coronary artery disease 2. Hypertension 3. Valvular heart disease 4. Cardiomyopathy 5. Cor pulmonale ACE Inhibitors: Adverse Effect: • • • • • Dry cough Hypotension (1st dose effect) Worsening renal function Hyperkalemia Angioedema Dr.Abdulmaguid

Rash, neutropenia

Contraindications: • • • • • • ---Date: 30 – 11 – 2011 Wednesday Case discussion (Cardiomayopathy) IHD Dr.Abdulmaguid Pregnancy Renal insufficiency (creatinine > 3 mg/dl) Hyperkalemia (> 5,5 mmol/l) Severe hypotension Bilateral renal artery stenosis Angiodema

Diagnosis of Myocardial Infarction by 2 of 3:    --------Date: 02 – 12 – 2011 Saturday Case Discussion: Arthritis (Gouty arthritis) Gout is a type of inflammatory arthritis induced by the deposition of monosodium urate crystals in synovial fluid and other tissues. It is associated with hyperuricemia, which is defined as a serum urate level of 6.8 mg per deciliter (404 μmol per liter) or more , the limit of urate solubility at physiologic temperature and pH.1 Humans lack uricase and thus cannot convert urate to soluble allantoin as the end product of purine metabolism. Hyperuricemia that is caused by the overproduction of urate or, more commonly, by renal urate underexcretion is necessary but not sufficient to cause gout. Gout has two clinical phases. The first phase is characterized by intermittent acute attacks that spontaneously resolve, typically over a period of 7 to 10 days, with asymptomatic periods between attacks. With inadequately treated hyperuricemia, transition to the second phase can occur, manifested as chronic tophaceous gout, which often involves polyarticular attacks, symptoms between attacks, and crystal deposition (tophi) in soft tissues or joints Risk Factors Dr.Naushad Ischemic Chest Pain which is either typical or not. ECG changes of S-T segment elevation Cardiac Enzymes

The use of thiazide diuretics, cyclosporine, and low-dose aspirin (<1 g per day) can cause hyperuricemia, whereas high-dose aspirin (≥3 g per day) is uricosuric. Factors that are associated with hyperuricemia and gout include insulin resistance, the metabolic syndrome, obesity, renal insufficiency, hypertension, congestive heart failure, and organ transplantation. The diagnostic standard remains synovial fluid or tophus aspiration with identification of negatively birefringent monosodium urate crystals under polarizing microscopy A typical presentation that is strongly suggestive of the diagnosis includes rapid development of severe pain (i.e., within 24 hours), erythema, and swelling in a characteristic joint distribution — for example, in the first metatarsophalangeal joint (podagra).

DVT & Unilateral lower limb edema Interesting Case Summary: (Hiccups & Fever) An 80 year old Saudi male patient living in Al-Mazroiah married with 7 offspring The informant was his son admitted through ER Last night complaining of Hiccups & Fever this fever was gradual progressive continuous not responding to analgesics. Associated with intermittent Hiccups which was progressive starting at the morning at around 10 & relieved at the night with no association to food or allergy, This Condition was associated with diarrhea, that leads to dehydration & the patient was admitted for

management & investigation of the cause. The patient report the same history to occur before 6 months but the son record that there was no specific diagnosis as the patient complain improve. This hiccup was in my thought due to GI cause. As the patient did not report any symptoms other than Diarrhea in association with the hiccups. ---------Date: 04 – 12 – 2011 Monday Case discussion: 1. GBS (Guilian bare syndrome) 2. Decompansated Heart failure Summary (Shortcase): Sarah AL-Hazaa is a 50 year old Saudi female, housewife married with 7 offspring admitted yesterday complaining of Dyspnea which was progressive continuous started before sleep but become at rest associated with orthopnea, & PND there are symptoms suggesting neuropathy including lower limb numbness, coldness. There is a history of tinnitus in right ear. The patient is bedridden with difficulty in movement of the limb as the patient undergone disc prolapse operation before 20 years. She is a known case of HTN & DM (Since 20 years). She is a known case of CHF since 3 months. The patient has a history of operation to the left eye with a resultant blindness. The patient also has a history of hysterectomy (since 7 years). The patient is receiving medications regularly. Drugs: Antihypertensive, Antihyperlypidemia, & Antidiabetes ------Date: 07 – 12 – 2011 Wednesday Case discussion: Arrhythmias mainly AF Dr.Abdulmaguid Dr.Naushad

Management of AF: If unstable: DC Shock If stable: More than 48 hours start thrombolytic therapy Less no thrombolytic therapy B-Blockers or Ca-Channel Blocker Antiarrhythmic drugs can be used. Management of Ventricular Fibrillation: DC shock cardioversion ICD (Implantable Cardiovertor Defibrillator)

CRT (Cardiac Resynchronisation Therapy) ------Date: 10 – 12 – 2011 Saturday Case discussion: Arrhythmia AF Cardiac symptomatology Cardiac Examination JVP ------Date: 12 – 12 – 2011 Monday Case discussion: COPD Pulmonary hypertension in SCD patient Examination ------Date: 13 – 12 – 2011 Tuesday Disscusion: Pulmonary Embolism Indications for Venous Filter: 1. Refractory Pulmonary Embolism dispite adequate thrombolytic & Anticoagulant treatment. 2. Contraindications to Anticoagulant therapy 3. Extensive Massive Pulmonary Embolism Virchow Triad:    Venous Stasis : Immobility, CHF, Prior Venous thromboembolism Venous wall Injury: Autoimmune, Trauma, Surgery Hypercoagulable State: Dr.Rabah Dr. Amr Dr.Hesham Rasheed

Congenital:    Factor V leiden Mutation Protein C & S deficiency Antithrombin III deficiency

Aquaired:    -----Date: 17 – 12 – 2011 Saturday Disscusion : The Patient Has 6 Risk Factors for IHD: 1. Age: 75 2. HTN 3. DM 4. Male 5. Obesity 6. Smoking By Examination: Irregularly Irregular Pulse (AF) Ascites Lower Limb Edema Home work: Cardiac Effect of DM Cardiac Examination Review about sounds & murmurs. -------Date: 19 – 12 – 2011 Monday Disscusion: Causes of Lymphadnopathy Localized or Generalized Unilateral or Bilateral Characters of the Lymphnodes Associated with systemic symptoms & manifestations or not. Cardiac Complications of COPD: Dr.Amr Dr.Hesham Rasheed Estrogen Use (Oral Contraceptive) Pregnancy Hormonal changes Malignancy secreting estrogen like factors.

    --------

Corpulmonale which may lead to Right sided Heart Failure Ischemic Myocardial Infarction Pulmonary Embolism Arrhythmia & Arrest

Date : 20 – 12 – 2011 Tuesday Inflammatory Bowel Syndrome

Dr.Rabah

Definition: Inflammatory bowel disease (IBD) is an idiopathic disease, probably involving an immune reaction of the body to its own intestinal tract. The 2 major types of IBD are ulcerative colitis (UC) and Crohn disease (CD). As the name suggests, ulcerative colitis is limited to the colon. Crohn disease can involve any segment of the gastrointestinal (GI) tract from the mouth to the anus.

Date : 21 -12 – 2011 Wednesday Disscusion: CHF Goitre & AF. ---------Date: 24 – 12 – 2011 Saturday Disscusion: HTN DM & Renal Disease. ---------Date: 26 – 12 – 2011 Monday Disscusion: Obstructive renal injury Cervical Lymphoma Anemia --------Date: 27 – 12 – 2011 Tuesday Disscusion: Left Lung carcinoma

Dr.Nboliy

Dr.M.Salah

Dr.Naushad

Dr. Amr

Consolidation pneumonia with bronchiectasis Hepatocellular carcinoma, with marked hepatomegaly --------Date: 28 – 12 – 2011 Discussion: SCD Nephrotic syndrome --------Date: 31 – 12 – 2011 Saturday Dr.Hesham Rasheed Case of Heart Failure (Dilated Cardiomyopathy) Dr.Surendra

Cardiac Examintion ------Date: 2 – 1 – 2012 Monday Dr.M.Salah Case of CKD Reffered from AL-Jabber Hospital for Perminant Arteriovenous Fistula Discussion on all aspects of symptoms, Blood transfusion complications. ------Date: 3 – 1 – 2012 Tuesday Case of Plaural Effusion Case of COPD Mixed type Case of Goiter Case of COPD with respiratory Failure. --------Dr.Amr Darwish

Crohns disease
Epidemiology,R isk factors, & Etiology Family History higher, No sex predilection, Several gene mutations, Smoking is risk, NSAIDs are increasing the risk. No specific etiology 80 % small bowel involvement, usually in the distal ileum (Ilietis) 50% involvement of both the ileum and colon(Iliocolitis) 33% have perianal disease Transmural inflammation

Ulcerative Colitis
Family History, No sex predilection, Smoking is protective. Both have a risk of malignancy

Common Site & Endoscopic Picture

The rectum is always involved. continuous lesions of the mucosa and the submucosa. Endoscope:  Erythema  Edema/loss of the usual fine vascular pattern  Granularity of the mucosa  Friability/spontaneous bleeding  Pseudopolyps  Erosions  Ulcers Systemic symptoms are common in IBD and include fever, sweats, malaise, and arthralgias.

Clinical Features

Fatigue, prolonged diarrhea with abdominal pain (right lower quadrant crampy), weight loss Bouts of Diarrhea & conistipation. Systemic symptoms are common in IBD and include fever, sweats, malaise, and arthralgias. - Peripheral arthritis - Involve large joints ,migratory and transient. - Episcleritis . - Aphthous stomatitis. - Erythema nodosum. - Pyoderma gangrenosum Disorders independent to disease : - Ankylosing spondylitis. - Sacroiliitis. - Uveitis. - Primary sclerosing cholangitis. may precede IBD by many years - Liver disease (e.g., fatty liver, autoimmune hepatitis, pericholangitis, cirrhosis) occurs in 3 to 5% of patients. Malabsorption: B12, Folic acid deficiency Kidney stones

Extraintestinal Manifestation

- Peripheral arthritis - Involve large joints ,migratory and transient. - Episcleritis . - Aphthous stomatitis. - Erythema nodosum. - Pyoderma gangrenosum Disorders independent to disease : - Ankylosing spondylitis. - Sacroiliitis. - Uveitis. - Primary sclerosing cholangitis. may precede IBD by many years - Liver disease (e.g., fatty liver, autoimmune hepatitis, pericholangitis, cirrhosis) occurs in 3 to 5% of patients. Malabsorption: B12, Folic acid deficiency Kidney stones

Pathophysiolog y

chronic transmural inflammatory disease that usually affects the distal ileum and colon but may occur in any part of the GI tract . lymphedema and thickening of the bowel wall Mesenteric lymph nodes often enlarge. Abscesses & fistulas are common Non caseating Granulomatus lesions. The string sign (a narrow band of barium flowing through an inflamed or scarred area) Abdominal x-ray Ultrasound CT GI endoscopy Biopsy for Histopathology -Non-systemic glucocorticoids (eg, budesonide) Other agents can be used:as other corticosteroids agents, immunosuppressives, antibiotics, and biologic agents. Surgical Intervention is not curative but sometimes indicated.

Inflammation affects the mucosa and submucosa, there is a sharp border between normal and affected tissue. Toxic colitis (Transmural inflammation) Toxic megacolon Abscesses are uncommon.

Investigations

The stovepipe sign seen on barium enema (the colon becomes a rigid foreshortened tube that lacks its usual haustral markings) Abdominal x-ray Ultrasound Sigmoidoscopy Histopathology -Oral 5-aminosalicylates (eg, sulfasalazine, mesalamine) Other agents can be used: as corticosteroids, immunosuppressives, and biologic agents Surgical intervention for ulcerative colitis is curative for colonic disease and potential colonic malignancy.

Treatment

Both diseases have two stages: Active stage (Flare) Remission stage. Symptoms correspond well to the degree of inflammation present
D.Diagnosis:

Treatment: -Oral 5-aminosalicylates (eg, sulfasalazine, mesalamine)

-Antibiotics (eg, ciprofloxacin,metronidazole) -Conventional glucocorticoids (eg, prednisone) -Non-systemic glucocorticoids (eg, budesonide) -Immunomodulators (eg, azathioprine, 6-mercaptopurine, methotrexate) -Biologic therapies (eg, infliximab, adalimumab) Aminosalicylates and Intestinal Activity

Ulcerative colitis patients who require surgery are often offered an ileal pouch–anal anastomosis. At surgery, a total proctocolectomy is done, the distal small bowel is fashioned into a -shaped reservoir, and the ileal pouch is stapled to the anal verge.

Clinical Cases Summary
Date: 21 – 11 – 2011 Monday Case # 1 Abdul rahman Ibrahim Al-Mubarrak is an 84 year old Saudi male patient, admitted before 3days through ER complaining of shortness of breath, & awareness of heart beat 3 days prior to admission. This dyspnea was of acute onset progressive in course associated with mild exercise (Climbing the stairs) , generalized fatigue, but not associated with posture, or time (No PND, or Orthopnea) There is also chest pain , hemoptysis. The patient is a known case of HTN, DM, since 20 years, Adrenal Insufficiency (Addison’s disease) since 5 years. The patient is receiving these drugs (Sitagliptines , Metformin , Vitamine B12 , Prednisilone , Aspirin ) D. Diagnosis: - CHF - COPD - Pneumonia - Ischemic heart disease - Malignancy Diagnosis: Based on history & examination (CHF with superimposed respiratory infection) Investigations :      CBC , DLC ABG ECG Chest X-ray & High resolution CT Echocardiography (Dr.Naushad)

Case # 2 A 28 year old Saudi male patient, single, smoker, prisoner , known case of SCD since birth, is coming to the ER complaining of left leg pain, which was acute, progressive, dull aching ,associated with pallor & mild jaundice, not associated with skin erythema , tenderness , or prominent leg swelling or edema , the patient also report frequent hospitalization of the same condition as 1 every 2-3 months , the patient was diagnosed as SCD VOC D.Diagnosis: Osteomyelitis Gouty arthritis ----------------Date: 25 – 11 – 2011 Saturday (Dr.Naushad) Case # 1

A 52 year old Saudi female patient , married , non smoker , known case of SCD since birth , Psorisis , hypertension & Rhematism??? , coming to the ER complaining of fever for the past 3 days,

D.Diagnosis:

Case # 2 Acute renal Failure (Mostly due to infection), complicated by cellulitis & DIC A 52 year old Saudi male patient, married , non smoker, admitted through ER complaining of lower limb swelling & redness with associated upper limb swelling (Generalized edema) started after 3 days after doing opening of the VAS which was previously closed , this edema started first in the lower limb then it become progressive to the upper limb,associated with oliguria, which was progressive till anuria develop, but there is no associated abdominal pain, dyspnea, puffiness or swelling around the eye, chest pain, & after admission the patient develop DIC which necissate admission to ICU and urgent heamodialysis was done, systemic antibiotics were administered & the patient become stable. Diagnosis: Acute renal failure ----------Date: 28 – 11 – 2011 Monday (Dr.Naushad)

Case # 1 SLE, with renal, heamatological, & skin involvement , 28 years

Case # 2 SLE , with renal, brain , & vascular involvement, HTN , 52 years --------Date: 29 – 11 – 2011 Tuesday (Dr.Abdulmaguid) Case # 1 HTN,DM,HF 65 years old Bagher Abdullah Al-Mumatin is 65 year old Saudi male patient living in Al-ahssa (AL-Jubbail Village) retired married with 12 offspring 4boys, 8 girls admitted last Saturday & the informant was his son. A known case of DM (Since 35 years), HTN (since 10 years), Stroke with weakness of the left side (Since 4 years) He was complaining of loss of consciousness that takes 20 min & the patient was transferred by the ambulance to ALJaffer Hospital & a serial of investigations was done & diagnosed as hypoglycemia management was done. This attack was preseded with Dyspnea, PND, & Orthopnea, chest pain, & cough associated with lower limb edema that is relieved by using Duretics (In the hospital). No abdominal pain, no chest wheezes, no cyanosis. Afterthat he was transferred to KFHH for admission & investigation through cardiology care unit. There is a history of ICU admission for Stroke since 4 years, Cardiac investigations. Drugs: Antidiabetic medications, Lasix , Aspirin

Patient care is brought by his daughter. Diagnosis: Hypertensive Heart Failure -----Date: 30 – 11 – 2011 Wednesday (Dr.Abdulmaguid) Case # 1 Cardiomyopathy with generalized weakness & the patient look very thin A 33 year old, Saudi male, single, working as workman, smoker(1pack per day for 20 years) admitted before 5 days complaining of Abdominal pain for 1 month, Chest Pain & Shortness of breath for 2 days prior to admission. Abdominal pain was epigastric, stabbing,associated with nausea & vomiting of food content for 3 times & Blacktarry stool 1 every 3 days. Dyspnea was gradual onset progressive first associated with exercise & then become during rest associated with chest pain which was around 20 min & decreased by rest. History of cough for 1 day There is a history of dark colored urine & decrease in urine amount & frequency. No significant past history. Diagnosis: Cardiomyopathy D.Diagnosis: IHD HTN heart disease Valvular Heart disease -----Date: 02 – 12 – 2011 Saturday (Dr.Naushad) Case # 1 Gouty Arthritis Case # 2 DVT ------Date: 04 – 12 – 2011 Monday (Dr.Naushad) Case # 1 GBS Case # 2 Decompansated HF with Pulmonary Edema Summary (Shortcase): Sarah AL-Hazaa is a 50 year old Saudi female, housewife married with 7 offspring admitted yesterday complaining of Dyspnea which was progressive continuous started before sleep but become at rest associated with orthopnea, & PND there are symptoms suggesting neuropathy including lower limb numbness, coldness. There is a history of tinnitus in right ear. The patient is bedridden with difficulty in movement of the limb as the patient undergone disc prolapse operation before 20 years. She is a known case of HTN & DM (Since 20 years). She is a known case of CHF since 3 months. The patient has a history of operation to the left eye with a resultant blindness. The patient also has a history

of hysterectomy (since 7 years). The patient is receiving medications regularly. Drugs: Antihypertensive, Antihyperlypidemia, & Antidiabetes -------Date: 07 – 12 – 2011 Wednesday (Dr. Abdulmaguid) Case #1 Atrial fibrillation Summary: A 40 years old Sudanese male patient non smoker admitted before 2 days by referral complaining of Awareness of the heart beat since 5days. This complaint was paroxysmal in onset, associated with dyspnea grade 4, sweating, Chest pain, but there is no loss of consciousness or sycope, no fever, then he went to AL-Mashafi Hospital & they done ECG & they reffered him to KFHH for evaluation & treatment. There is a history of Malaria. There are no history of Thyroid diseases, IHD, Any cardiac diseases, No history of Psychological diseases, No history of medication, No history of any cardiac interventions. On Examinations: Pulse is irregularly Irregular, There are missed Beats. Investigations:    ECG Echocardiography Exercise testing.

Choice of Management: Electric: DC shock if unstable. Pharmacologic: Adenosine Verapamil or Diltiazem (Nifidepine is only indicated if HTN) Propafenone If chronic: Heparin or LMWH . If recurrent in Highly risk Patient: Radiofrequency or Electrical Ablation (Meaze Procedure) Causes of Atrial Fibrillation:     ------Hyperthyroidism Drugs: Sympathomimetics Any organic Heart Disease. Loan AF

Date: 10 – 12 – 2011 Saturday (Dr.Hesham) Case # 1 Atrial fibrillation & review cardiology case history taking. -----Date: 12 – 12 – 2011 Monday (Dr.Amr ) Case # 1 COPD Summary: Ali Taher AL-Bagali is a 59 year old Saudi male, living in Al-Hoffuf working as a Besht Seller, married with 5 offspring (3boys, & 2girls) mild smoker since 30 years , admitted before 1.5 month complaining of Loss of consciousness. He is a known case of COPD. This loss of consciousness was sudden in onset, not proceded by stronge activity, associated with cough which is productive with greenish sputum, dyspnea, but the patient denial any history of chest pain, chest wheezes. The patient is also seeking psychiatric health. Drugs the patient is taking: Bronchodilator (Ventolin, & Ibratrobium Promide), Inhaled Glucocorticoids. The patient is also have a family history of Psychiatric illness in his sister. Other body systems are symptomatologically free. Causes of Loss of Consciousness in COPD patient:    Respiratory Failure Pulmonary Embolism Arrhythmia

Examination Finding: The patient looks drowsy In respiratory distress with use of accessory respiratory muscles with intercostal retraction. JVP is not elevated No lower limb edema -------Date: 13 – 12 – 2011 Tuesday (Dr.Rabah) Case # 1 DVT -----Date: 17 – 12 – 2011 Saturday (Dr.Hesham) Cardiac Examination Abnormal Heart sounds -------Date: 19 – 12 – 2011 Monday (Dr.Amr) Cervical lymphadenopathy & arthralgia. ------Date: 20 – 12 – 2011 Tuesday (Dr.Rabah) Inflammatory Bowel Diseases.

------Date: 21 – 12 – 2011 Wednesday (Dr.Naboliy) AF & Hyperthyroidism (Mostly toxic multinodular goiter) DKA ------Date: 24 – 12 – 2011 Saturday (Dr.M.Salah) HTN Grade III ---------Date: 26 – 12 – 2011 Monday (Dr.Naushad) Lymphoma Obstructive renal injury Chronic Anemia for investigation ------Date: 27 – 12 – 2011 Tuesday Left upper lobe lung cancer ------Date: 28 – 12 – 2011 Wednesday (Dr.Surendra) Nephrotic syndrome the main disscusion SCD ------Most of the cases are not with me I try to take them from my colleagues but time is shortage (Dr.Amr)

Clinical Clerkship
Bed Case 506 A, & B

Case # 1 SCD VOC Personal History:

Date: 21 – 11 – 2011 Monday

Yousef Ahmad AL-Hmood is a 32 year old Saudi male patient living in AL-Hulailah working in The Electric Company as Offices cleaner, nonsmoker, married before 2 years with still no offspring, admitted before 2 days. Patient Complain: Back pain since 2days History of Present Illness: He is a known case of SCD since childhood. He was in his usual state of health until 2 days prior to admission as the patient start to develop upper back pain which was acute, stationary , stabbing (As described by the patient) increased with exercise & decreased by analgesic (Diclovinac), moderate in severity of grade 5 out of 10 radiated to the neck & the arms , associated with left upper abdominal tenderness & pain, & headache. There are no history of fever, Pallor, reddish discoloration of urine, jaundice, trauma to the back, abnormal unusual exercise, This condition was preceded by URTI Hospital Course: The patient was admitted through ER and underwent a serial of investigation but the result are still awaited. The patient was receiving IV fluid around 1.5 liter per day (3 * 500 9% Nacl saline) with analgesics on demand up to morphine & tramadol. Systemic Review: CNS: No blurring of vision , hemiparesis, sezuire , tremors , involuntary movements. RS: No chest pain , hemoptysis , cough , dyspnea , wheezes , cyanosis . CVS: No palpitation, lower limb edema, right upper abdominal pain, oliguria, orthopnea, PND. GI: No diarrhea, conistipation , melena , vomiting. GUS: No dysuria , polyuria. MS: No lower limb pain. Past History:       Previous hospitalization was before 1year with similar presentation of pain in the lower limbs History of Admission to ICU & transfusion of 2 RBCs Pack No DM or HTN No allergy Abdominal(Central) Scar of previous surgery in childhood ?? No history of major operation as Splenectomy

 

No history of cholecystectomy No investigations of clinical importance except for SCD

Drug History:    Analgesic (Ibuprofen) 1 tab per day but the patient is not compliant Folic acid 1 tab per day but the patient is not compliant No history of drug allergy

Family History: SCD is prevelant in the family No DM or HTN Father is smoker & died by age of 70 years with no known cause. Mother is SCA age 60 years 3 Brothers have SCD one died by age of 21 years. 1Sibling do not have SCD Social History: The patient is living in his family house, married before 2 years , does not finish intermediate school only elementary school. He is working as an offices cleaner with insufficient income but he recives reword from the Government due to his disease. Diagnosis or D.Diagnosis: A case of chronic hemolysis (SCD) with vaso-occulosive crisis(SCD VOC). D.Diagnosis: Traumatic pain Rheumatoid arthritis Leukemia Exercise Fatigue musculoskeletal pain Examination Finding: General: BP: 110/65 mmHg Temp: 36.5 degree C Pulse: 68 beats /min, regular, rhythmic, symmetrical, average volume, average force & pressure, no radiofemoral delay. RR: 18 cycles/min

There is mild degree Pallor No lower limb edema No clubbing Mild jaundice No cyanosis No tremors GI: No tenderness Soft lax abdomen with no distension No visible palsations No organomegally Liver span with in normal 8CM RS: Normal vesicular breathing bilateraly CVS: S1 + S2 no added sounds or murmers Neurological: Not done it but I believe the patient is normal.

Provisional Diagnosis: A case of chronic hemolysis (SCD) with vaso-occulosive crisis(SCD VOC).

Investigation:  CBC, DLC.  Biochemistry: LDH  Total bilirubin  Periphral Blood smear & microscopy  Hb electrophoresis diagnostic Treatment:   Analgesics up to morphine IV Fluids (Given 1.5 the maintenance)

Follow up: (Monday - Wednesday) Investigations (+ Results) Biochemistry: LDH : 364 Hi Ab Total Bilirubin CBC: MCV : decrease 79.9 (80-94) (11.5-15.5) (130-400) U/L (100-190)

: 29 Hi Ab

RDW : 19.1 Hi Ab Platelet : 412 Hi Ab

HGb : decrease 8.2 Low Ab RBC count : 2.94 milion

The patient clinically improved with no deterioration or new symptoms or signs The patient told that he will be discharged by the end of the day. --------Case # 2 Uncontrolled Hypertension Personal History: Shahid Firdows Abdullghani is a 52 year old Pakistani male patient , living in Al-thulathiah , married since 30 years with three offspring (2Girls , 1Boy) working as a bus driver since 30 years, non smoker, with no happits of medical importance & the informant was the patient himself, admitted before 2 days (23 – 11 – 2011 Thursday) Patient complain: Nasal bleeding since 6 hours History of Present illness: The patient was in his usual state of health until he start to develop epistaxis which was acute in onset, progressive around the 100 ml (Cup of tea) from left nostril, for 5-10 min. The patient is a known case of HTN since 6 months in Pakistan presented previously with the same complaint and diagnosed as HTN. There were no headache, fatigue, blurring of vision , chest pain , palpitation, abdominal pain , oliguria , lower limb edema. There were no symptoms suggesting encephalopathy as there is no headache , blurring of vision There were no symptoms suggesting thromboembolic manifestations as , no loss of consciousness, body weakness or paralysis, oliguria . There were no ecchymosis , or skin rash No history of Recurrent Rhinitis or sinusitis (URTI) BP monitored during admission was 230/150 mmHg Date: 26 – 11 – 2011 Saturday

Systemic review: unremarkable CNS: No drowsiness , and fatigue, headache, paralysis, blurring of vision, hemiparesis, chorea or involuntary movement, tremors RS: No dyspnea, wheezes, cough, hemoptysis. CVS: Unremarkable GI: No diarrhea, conistipation, melena, hematochezia, vomiting. GUS: No hematuria , dysuria, oliguria.

Hospital Course: The patient was diagnosed as Uncontrolled HTN for which admission was recommended to investigate & stabilize the BP. BP when admitted was 230/150 mmHg A serial of Blood investigation for which 3Blood samples were withdrawn but the results are still awaited The patient receive Diuretics to decrease the blood pressure Instructions:    General Measures: Diet containing low salt BP Monitoring

Investigations:  CBC MCV : 64.2 Low Ab (80-94) Platelet Normal 306000 Hgb : 13.5 normal WBC : 8.33 normal RBCs : 6.31 Normal        Electrolytes Na, K K: 4 normal , Na : 149 mg/dl Hi Ab (53-45) (135-145) , MCH : 21.5 Low Ab (27-31)

Creatinine & urinalysis PT, PTT, INR Awaited Lipid profile Awaited

Creatinine : 118 Hi Ab

ECG with in Normal US of the abdomen awaited

ENT consultation no abnormality

Treatment Given:       Given Duretics Indapamide (1.5 mg 2 times per day) Atenolol Tablet of capoten 25mg Tablet of lisinopril 10 mg Tablet of Aspirin 81mg

Past History: The patient is a known case of HTN since 6 month No operations No DM, IHD, TB No Previous hospitalization No Blood transfusion Drug History: Atenolol 100 mg since 3months Family History:      No family history of HTN, DM, IHD Father Died with no known cause Mother is still live His children are of good health with no diseases. His daughter has TB but she was cured as he said

Social History: Good socioeconomic status with average salary of 1000 SR, living with his family in their own house in (Islamabad). Diagnosis: A case of epistaxis for investigations mainly uncontrolled HTN admitted for Education (Control) & investigation.

Examination: General: The patient is conscious, oriented to time, place & person. Comfortable & stable with no complain. No special decubitus. No jaundice, Cyanosis, &skin rash. The patient appears obese. Pulse: 60 beat/min ,regular, rhythmic,weak, arterial wall not felt, palpable on all extremities, average pressure, average volume, no radiofemoral delay.

BP:

135/90 mmHg

RR: 16 cycles/min

Temp: 36.5 degree C

Head to toe examination: Normal hair distribution, no eye problem Fundoscopy is not done, no facial nerve abnormality, no Xanthelasma, no cyanosis, no neck swelling, no clubbing, no lower limb edema, no tremors. No carotid bruit ENT examination to be consulted. Abdominal: Inspection:Distended abdomen, with no umbilical shift or hernia, no scar,no tenderness, no dilated veins. Palpation: No organomegaly, no ascites Ascultation: no renal bruit, visible peristaltic sounds. Neurology: unremarkable Chest: Unremarkable no abnormal sounds or murmers bilateraly vesicular breathing. Provisional Diagnosis: uncontrolled HTN admitted for Education (Control) & investigation. Follow up: the patient has been discharged the next day. ------Case # 3 SCD VOC with Acute tonsillitis Personal: Kadhim Abdullah AL-Tawail , is a 23 year old Saudi male ,living in Al-Mubarraz Married before 3 months, working as computer operator assistance in Al-Amanah, with no special habbits of medical importance (Non smoker), admitted through ER 1day ago in the morning. Patient complain: Fever & Generalized Body Pain or discomfort, for 1day History of present illness: The patient is a known case of SCD, "Thalasemia" ??? since childhood. The patient was in his usual state of health until 1day ago as the patient complain of fever, which was acute in onset, progressive, continuous , with no redness, skin rashes, rigors, chills, or convulsions, this is not aggravated & decreased by empirical analgesic (Ibuprofen). This fever measured on admission 39 degree C. The patient takes a shower to decrease the fever but after that he started to develop generalized body pain mainly in the lower limbs , which was gradual in onset, progressive, not related to excersize or stress, stabbing, associated with headache. There is no symtptoms of hyperhemolysis as there is no increased fatigue, palpitation, pallor, increased jaundice. Past history: Previous hospitalization before 3 months with same complaint ICU admission after trauma but improvement occurs Cholecystectomy before 5 years No splenectomy Date : 29 – 11 – 2011 Tuesday

Femur shaft fracture before 3 years with intramedullary nail fixation. No DM, HTN. No blood transfusion except 2Packs in ICU after trauma. Drug history: Folic acid Hydroxyuria before 5 years Tramadol specially after the operation. Ca, & Vitamin D for the bones Family history: 1 sister is SCD & she is admitted to the hospital & she will done splenectomy Father & Mother are SCA trait Family is composed of 6 boys, & 6 Girls 1brother is DM Grandmother is DM Social history: The patient is an relatively good socioeconomic state, graduated from the college of technology, living with his family in his family house, non smoker, no frequent admissions, no frequent absence from work but as the patient said he is know scared because his work started recently & he scare of rejection because of absence due to his health state. Systemic review: Unremarkable CNS: Headache, no blurring of vision , no weakness in the limbs, no tremors, no vertigo, no loss of consciousness. RS: no dyspnea, chest wheezes, cough, hemoptysis, expectorations. CVS: no palpitations, GUS: no dysuria, painfull erection, histency, urgency, no incontinence , oliguria, polyuria. Diagnosis & D.Diagnosis: SCD VOC with acute tonsilitis Examination: Unremarkable Mild Jaundice Provisional Diagnosis: SCD VOC with acute tonsilitis Investigations:   Chest x-ray Urine analysis

Blood investigations

Treatment:      Tramadol & Morphine IV Fluids 1.5 the maintenance Antibiotics Hydroxyuria Panadole

Follow up: the Patient has been discharged the next day & Under Oral Antibiotic treatment. --------Case # 4 FFI (Mostly Hepatitis A) Short case: Date: 13 – 12 – 2011 Tuesday

Hanif Said AL-Hagg, is a 34 year old Bangladish, living in AL-Hoffuf working as a coffee Maker, mild smoker of 1Pack per day for 3 years. Married with 2 offspring, admitted Before 4 days complaining of Fever for 2 day duration.This fever was acute in onset, progressive in course, decreased by Usual analgesic but not relieved, & not aggravated by anything. Associated with headache, but not associated with abdominal Pain, chest pain , Rigors, Chills, or Convulsions. No associated skin rash. Associated with Jaundice that was gradual, yellowish in color associated with Dark colored burning urine, & greesy stool. Past history there is no history of Similar attack of Pain with headache, travel, Operation, Blood Transfusion. No family history of the same Illness. Diagnosis: Fever for Investigation mostly Hepatitis. Management: Investigations: CBC,DLC Liver serology BUN Urine Analysis Treatment : Analgesics & IV Fluids. Follow up: The patient has been discharged the next day. --------Case # 5 SCD VOC Personal: Mohammad Bagher AL-Khallof , is a 28 year old saudi male , single, living in AL-Hullailah working as Guard in the entrance of AL-Othaim Moal, & he is non smoker admitted before 3 days. Date: 17 – 12 – 2011 Saturday

Patient complain: Back Pain for 1 day History of present illness: The patient was in his usual state of health as he is a known case of SCD since childhood (7year old). Until one day prior to admission as he start to develop Back pain, which was acute in onset progressive in course with no specific character, radiated to the neck & shoulders, decreased by Analgesics (Profen) & aggravated by exercise. This was associated with headache, Shortness of breath, Generalized fatigue, but there is no fever, chest pain, nausea, or vomiting. The patient believe that this pain is due to SCD. Hospital Course: Blood investigations Analgesics up to Morphine (IV Paracetamol, & Tramadul, Pethidine) IV Fluids Normal saline 3 Packs (1.5 L) Past history: Hospitalization before 1 week for the same complain. Operation of Femur Fracture before 6 years due to Trauma No splenectomy, Cholecystectomy There is a history of Blood Transfusion 1 Time for the Operation Drug history: Ibuprofen 2 Tabs per day since 7 years. Folic acid Medication No drug compliance Family history: Family is known to have SCD 2 Sibling are SCD (2 Girls)

Social history: Good socioeconomic Status, Study till Intermediate school & After the trauma he does not continue Systemic review: Other Body Systems are symptomatologically free The patient have difficulty in movement due to Operation in his Right limb. Diagnosis & D.Diagnosis: SCD VOC Examination:

Mild Jaundice Vital signs are stable with no abnormality Other examination are unremarkable Provisional Diagnosis: SCD VOC Investigations: CBC Total Bilirubin MCV MCHC MCH RDW HCT 22.8 Hi Abnormal umol/L

63 Low AB 32.1 Low AB 20.2 Hi AB 21 Hi AB 31.5 Low AB

Others are normal Biochemistry Treatment: Analgesics:Morphine IV fluids Follow Up: The patient has been Discharged the next Day. ---------Case # 6 SCD Personal: Najeeb Ali Al-Bahari is 27 year old Saudi male, living in Al-Munazlah, working as a supermarket(Bandah) counter, Married with 1 offspring, mild smoker of 1 cegarit per day for 10 years, admitted a week back. Patient complaint: Generalized body pain since 1 day Chest pain & Dyspnea 3 hours History of present illness: The patient is a known case of SCD since childhood. He was in his usual state of health until three days prior to admission as he start to develop fever which was gradual progressive, with no specific character, no aggravated & relieved by usual analgesics. Two days later the patient develop Lower limb pain which was gradual, progressive, Compressing, increased by exercise, & coldness & decreased by rest & analgesics few hours later he start to develop central chest pain, which was acute, progressive, with no specific character, not related to food intake, or exercise Date: 24 – 12 – 2011 Saturday

associated with dyspnea (Grade II), that the patient seek medical emergency and was admitted to ICU for 5 days, with central venous catheter insertion & Blood transfusion 3Packs. Other body systems are symptomatologically free. Past history: Similar attack before 6 months 2-3 Times hospital admission due to SCD attack. Frequent Blood transfusion before 6 months Post traumatic Urinary Ureter connection before 2 years No history of cholecystectomy or Splenectomy No history of Allergy No history of special vaccinations for SCD Drug history: Folic acid 1 tab per day but the patient is not complaint Needs education (The patient is not satisfied) Family history: Father & Mother are SCA Trait 1 Sister is SCD Marriage counciling has been started. Social history: Living in there family house, with good socioeconomic status, but there was relatively high absence from school till the patient start to goes on knight school & later in secondary school he stop studying. Systemic review: Unremarkable Diagnosis & D.Diagnosis: SCD VOC (Acute chest syndrome) Examination: The patient is comfortable in bed underbelt,with CV Catheter inserted in the Right Internal juglar vein. Stable, no complaining or in pain. Vital signs are relatively stable with mild tachycardia. RR: 18 Breath / min , BP: 110 / 90 mmHg , Temp : 36.9 degree , Pulse: 90 beats / min with positive waterhammar pulse. There is mild jaundice , pallor, no skin rash, no clubbing, no cold extremities. Chest: Apical pulsations are clear on inspection in the fifth left intercostal space midclavicular line , no chest abnormalities on all examination S1 is prominent at the apex & the base Abdomen: soft, Lax, with Hepatomegally 1 finger breadth from the right costal margin, No splenomegally. Infraumbilical scar for the previous urinary surgery with other small scar for the laparoscope insertion.

Provisional Diagnosis: SCD VOC (Acute Chest Syndrome) Investigations: Urinalysis: No abnormality ER Biochemistry: PH: 7.318 Lo Ab Pco2 : 51.5 Hi Ab ECG: Sinus tachycardia (100) Slight Depressed S-T Wave on Lateral Leads V4-5 ER Lab: Direct Bilirubin: 10.1 Hi Ab LDH: 837 Hi Ab Total Bilirubin : 42.7 Hi Ab CBC: MCH: 32.4 HI AB RDW: 19.5 HI AB Platelet : 397000 Hi Ab HCT: 22.3 Lo Ab HGb: 7.9 Lo Ab Treatment: Analgesics up to morphine IV Fluids Diet for G6PD The patient has been discharged in the same day of the history. -------Case # 7 SCD with left hypochondrial Pain Personal: Fadhil Mohammad AL-Hamood is 23 year old Saudi male, living in Ascan AL-Kulabiah, Jobless (Previously working in Al-Seef Transformer Company ) ,Single, Non smoker, admitted last Saturday through referral from ALMoasat Dispensary. Patient complaint: Localized Left Abdominal Pain Since 1week Date : 26 – 12 – 2011 Monday

History of present illness: The patient is a known case of SCD since childhood. He was in his usual state of health until 10 days prior to admission as the patient start to develop lower limb pain, which was gradual, progressive compressing, increased with exercise & movement of the limbs & decreased but not releived with analgesics , few hours later the pain increase & he was transferred to the nearest hospital (PBJH) were He was severely pallor , & investigations reveals Severe anemia with Hb of 6 that reveals urgent Blood transfusion. The patient recive 3 Packs of Blood Until Hb become Above 9. Three days later he was discharged. One day later the patient start to have Left Hypochondrial Pain which is localized, gradual, stationary, not radiated, increased with lying at the bed & not decreased by anything. A week Later the patient seek medical Advice at AL-Moasat Hospital were serial of investigations were done including Ultrasound & he was reffered. This pain was not associated with food, Nausea & Vomiting, Cough, Trauma, or skin rash. Other Body systems are symptomatologically free. Past history: No similar attack No History of previous operations 4-5 times per year admission of Musculoskeletal Complications of SCD. History of frequent Blood transfusion (Hemochromatosis & Hemosiderosis to be considered). Drug history: Analgesics : Ibuprofen On demand Folic acid 1 tab per day but the patient is not compliant (Need education) Family history: Father & Mother are SCA Trait 2 Sisters are SCD 1 Brother is SCD 3 Brothers are normal Social history: Good socioeconomic status, living with his family in their own house, finishes only elementary school , he try to complete his education at night school but he fails 2 times then he stops. Systemic review: Unremarkable. Diagnosis & D.Diagnosis: SCA With post transfusion pain (May be sequestration crisis or Hematoma or Mass in the spleen. Summary: Examination: Only Tachycardia No added sounds

Relative restriction of chest expansion bilateral Spleen is relatively enlarged but not palpaple. Provisional Diagnosis: Left Hypochondrial Mass (Most likely Hematoma) Investigations: Ultrasound: It shows subcapsular hematoma with no palsation on examination Surgical Consultation is to be introduced Others: AL-Moassat Report: -Marked Thrombocytosis -Leukocytosis Hypochromic Microcytic anemia for Investigations In Hospital: Liver Enzymes are within normal ALP: 301 Hi Ab CBC: MCV : 68.9 Microcytosis HGb : 9.74 Lo Ab HCT : 32.6 Lo Ab RDW: 23 Hi Ab MCH : 20.6 Lo Ab MCHC: 29.9 Lo Ab Biochemistry: K: 5.5 Hi Ab Total Bilirubin : 13.4 normal ECG & Chest x-ray Ultrasound Treatment: CT of the Abdomen is scheduled Vascular surgery consultation Follow up: The patient has been discharged.

Assignments
Syncope: Syncope, a transient loss of consciousness and postural tone due to reduced cerebral blood flow, is associated with spontaneous recovery. It may occur suddenly, without warning, or may be preceded by symptoms of faintness (“presyncope”). These symptoms include lightheadedness, dizziness, a feeling of warmth, diaphoresis, nausea, and visual blurring occasionally proceeding to transient blindness. Pathophysiology :     Decrease venous return Bradycardia & Tachycardia Decrease Cardiac output Systemic Vasodilatation.

Causes of Syncope:  Neuraly Mediated: Vasovagal syncope: the most common usually associated with stressful conditions as hearing bad news, seeing bad sites. Reflex syncope : as carotid sinus syndrome Situational syncope: post tosiph , post micturition, post defecation.  Orthostatic (Pustural) hypotension: Due to drugs causing Vasodilatation : old ACEi (First dose hypotension) , Nitrates. Due to hypovolemia : as in dehydration, use of diuretics , hemorrhage(Trauma, Postpartum hemorrhage).  Cardiogenic (The least 11%): Obstruction of the Blood flow by: Thrombus Tumor (Atrial myxoma) Stenosis (Aortic stenosis) Embolus (Pulmonary embolism) Tachyarrythmia or Bradyarrythmia (Extremes)

--------D.Diagnosis of Chronic Dyspnea?? 1- Cardiac:

- Chronic LVF, MS 2- Chest: - Lungs: Obstructive and restrictive lung diseases - Pleura: Large pleural effusion - Chest wall: Severe deformities as kyphoscoliosis 3- Metabolic Causes: Ketoacidiosis, ASA poisoning. 4- Other causes: Anemia, Obesity. ------------

How to measure (Pulsus Paradoxicus , Waterhamar Pulse ,or Collapsing Pulse )?? Pulsus Paradoxicus: an inspiratory decline in systolic BP more than 10 mmHg Measured as usual but one reading with full expiration & another with full inspiration and stop of breathing. Or ask the patient to take breath for 15 seconds & measure pulse * 4, & another reading normal & compare. This occurs in:    Cardiac tamponade Constrictive pericarditis Obstructive pulmonary disease as(Bronchial asthma, & COPD)

WaterHamar Pulse: A pulse that is bounding and forceful, or, in other words, rapidly increasing and subsequently collapsing, as if it were the hitting of a water hammer that was causing the pulse. associated with increased stroke volume of the left ventricle and decrease in the peripheral resistance leading to the widened pulse pressure More than 50 or 60 mmHg Pulse Pressure = Systole – Diastole Common cause: Aortic regurge Other causes: 1. Physiological
 

Normally 40 + or - (20)

Fever Pregnancy

2. Cardiac lesions

     

Aortic regurgitation Patent ductus arteriosus Systolic hypertension Bradycardia Aortopulmonary window Rupture of sinus of Valsalva into heart chambers

3. Syndromes or High output states
       

Anemia Cor pulmonale Cirrhosis of liver Beriberi Thyrotoxicosis Arteriovenous fistula as in Hemodialysis Patient Paget's disease Chronic alcoholism

------------Chest x-ray finding in Heart Failure:      Cardiomegaly (Increased cardiothoracic ratio) Pulmonary congestion (Upper lobe diversion) Kerley’s B line Pleural effusion Interstitial & alveolar edema

------------Cardiac Effect of DM: Increase the Teratogenicity of heart in infant of DM mother (The resulting anomalies are varied and include transposition of the great arteries, mitral and pulmonary atresia, double outlet of the right ventricle, tetralogy of Fallot, and fetal cardiomyopathy) IHD due to increase atherogenesis Silent Ischemia (Asymptomatic) Hypertrophic & Dilated Cardiomyopathy (Increase LV mass & volume)

HTN & HF Microangiopathy --------Osteoporosis: Definition: It is a metabolic bone disease characterized by loss of bone density & mass in a fully grown bone. Etiology: several classifications according to etiology and localization in the skeleton. Osteoporosis is initially divided into localized and generalized categories. These 2 main categories are classified further into primary and secondary osteoporosis. Postmenopausal osteoporosis (PMO) is primarily due to estrogen deficiency; senile osteoporosis is primarily due to an aging skeleton and calcium deficiency. Primary: Juvenile and idiopathic osteoporosis. Idiopathic osteoporosis can be further subdivided into postmenopausal (type I) and age-associated or senile (type II) osteoporosis Secondary: occurs when an underlying disease, deficiency, or drug causes osteoporosis. Genetic (congenital) causes of osteoporosis include the following:
             

Cystic fibrosis Ehlers-Danlos syndrome Glycogen storage disease Gaucher disease Hemochromatosis Homocystinuria Hypophosphatasia Idiopathic hypercalciuria Marfan syndrome Menkes steely hair syndrome Osteogenesis imperfecta Porphyria Riley-Day syndrome Hypogonadal states (Androgen insensitivity,Anorexia nervosa/bulimia nervosa, Hyperprolactinemia, Panhypopituitarism, Premature menopause, Turner syndrome, Klinefelter syndrome) Endocrinal disorders (Acromegaly, Adrenal insufficiency, Cushing syndrome, Estrogen deficiency, Diabetes mellitus, Hyperparathyroidism, Hyperthyroidism, Hypogonadism, Pregnancy, Prolactinoma) Deficency states (Ca deficiency, Mg deficiency, Protein deficiency, Vit D deficiency, Bariatric surgery, Celiac disease, Gastrectomy, Malabsorption, Malnutrition, Parenteral nutrition, Primary biliary cirrhosis) Inflammatory diseases (IBD, Ankylosing spondylitis, R A, Systemic lupus erythematosus)

Hematologic & neoplastic (Hemochromatosis, Hemophilia, Leukemia, Lymphoma, Multiple myeloma, Sickle cell anemia, Systemic mastocytosis, Thalassemia, Metastatic disease) Drugs : 1. (Anticonvulsants - Phenytoin, barbiturates, carbamazepine (these agents are associated with treatmentinduced vitamin D deficiency) 2. Antipsychotic drugs 3. Antiretroviral drugs 4. Aromatase inhibitors - Exemestane, anastrozole 5. Chemotherapeutic/transplant drugs - Cyclosporine, tacrolimus, platinum compounds, cyclophosphamide, ifosfamide, methotrexate 6. Furosemide 7. Glucocorticoids and corticotropin - Prednisone (≥5 mg/d for ≥3 mo) 8. Heparin (long-term) 9. Hormonal/endocrine therapies - Gonadotropin-releasing hormone (GnRH) agonists, luteinizing hormonereleasing hormone (LHRH) analogs, depomedroxyprogesterone, excessive thyroid supplementation 10. Lithium 11. Methotrexate 12. Selective serotonin reuptake inhibitors 13. Thyroxine (excessive)

Missellenious : 1. Alcoholism 2. Amyloidosis 3. Chronic metabolic acidosis 4. Congestive heart failure 5. Depression 6. Emphysema 7. Chronic or end-stage renal disease 8. Chronic liver disease 9. HIV disease/AIDS 10. Idiopathic calciuria 11. Idiopathic scoliosis 12. Immobility 13. Multiple sclerosis

14. Ochronosis 15. Organ transplantation 16. Pregnancy/lactation 17. Sarcoidosis 18. Weightlessness

Risk factors:
          

Advanced age (50 years or older) Female sex White or Asian ethnicity Genetic factors, such as a family history of osteoporosis Thin build or small stature (eg, body weight less than 127 pounds) Amenorrhea Late menarche Early menopause Postmenopausal state Physical inactivity or immobilization Use of drugs - Anticonvulsants, systemic steroids, thyroid supplements, heparin, chemotherapeutic agents, insulin Alcohol and tobacco use Androgen or estrogen deficiency Calcium deficiency

  

Diagnosis: Most of the patient are detected by either screening or high clinical suspicion of due to presentation of complication such as fractures. DEXA criteria for osteoporosis, as defined by the World Health Organization, are spinal or hip bone mineral density (BMD) of 2.5 SDs or more below the mean for healthy, young women (T-score of −2.5 or below). Criteria for osteopenia are spinal or hip BMD between 1 and 2.5 or more SDs below the mean. Treatment: mainly by detecting the cause. First line effective treatment: fall prevention, adequate calcium intake of at least 1200 mg/day, and vitamin D intake of at least 700 to 800 IU/day. Bisphosphonate are also recommended

    

Alendronate, 70 mg/week, administered orally, for hip, vertebral, and nonvertebral fractures Ibandronate, 150 mg/month, administered orally, for vertebral fractures Risedronate, 35 mg/week, administered orally, for hip, vertebral, and nonvertebral fractures Ibandronate, 3 mg every 3 months for 4 doses, given intravenously to increase bone mineral density, although fracture endpoints were not evaluated Zoledronic acid, 5 mg/year for 3 doses, given intravenously for hip, vertebral, and nonvertebral fractures

Calcitonin can be used to prevent recurrent vertebral fractures. -----Causes of Atrial Fibrillation:     Hyperthyroidism Drugs: Sympathomimetics Any organic Heart Disease. Loan AF

Describe Different Types of Insulin & duration of action?? INSULIN PREPARATIONS EFFECT ONSET, PEAK, AND DURATION AFTER SUBCUTANEOUS ADMINISTRATION Class Rapid acting Short acting Preparation Onset of Effect Peak Effect (hr) Duration of Action (hr) 1–2 2–4 6–12 3–4 5–8 16–24

Lispro, aspart, or glulisine 10–15 min Regular (R) 30 min 2–4 hours

Intermediate acting NPH (N) or Lente Orange Long acting (‫ )بنفسجي‬Ultralente (U) Glargine Detemir Source :

4–6 hours 2–4 hours 1 hour

8–16 No peak No peak

∼24 >30 Up to 24

Goldman: Cecil Medicine, 23rd edChapter 247 – TYPE 1 DIABETES MELLITUS

Types of Insulin

1. Ultra-short acting insulins: • • • Insulin lispro, insulin aspart and insulin glulycine. They are human insulin analoges produced by recombinant technology. Following SC injection, they are rapidly absorbed with rapid onset of action (within 20 minutes), and have short duration of action (3-4 hours). They are given 15 minutes and do not produce hypoglycemia.

2. Short-acting insulins: • • Regular insulin has onset of action of 30-45 minutes and duration of action is about 6-8 hours. It is the only type of insulins that can be used intravenously in cases of emergency as in diabetic ketoacidosis (DKA), surgery, trauma, infection, stress.

3. Intermediate-acting insulins: • • NPH insulin (neutral protamine hagedron or isophane insulin) with protamine added as a retarding agent (insulin : protamine is 10 : 1 by weight). It has slow onset (1-2 hours) and long duration of action (18-24 hours).

4. Long-acting insulins: • • -------Celiac Disease Definition & Clinical Features?? Celiac disease (CD) is a multifactorial, autoimmune disorder that occurs in genetically susceptible individuals. [1] It is triggered by a well-identified environmental factor (gluten and related prolamins), and the autoantigen is also well known (ie, the ubiquitous enzyme tissue transglutaminase). The disease primarily affects the small intestine, where it progressively leads to flattening of the small intestinal mucosa (Celiac disease is an immune-mediated enteropathy triggered by the ingestion of gluten-containing grains (including wheat, rye, and barley) in genetically susceptible individuals) Clinical features: Malabsorption syndrome (chronic diarrhea, weight loss, abdominal distension) affecting children, as well as with a spectrum of symptoms potentially involving any organ system While in adults: Extraintestinal forms of celiac disease are much more frequent than classical pediatric forms of the disease. Because celiac disease often presents in an atypical or even silent manner, many cases remain undiagnosed and carry the risk of long-term complications, including osteoporosis, infertility, neurologic disorders, or cancer. Diagnosis of celiac disease depends on the use of serologic markers in conjunction with an intestinal biopsy Previous diagnosis: based on nonspecific tests, including fecal fat, D-xylose absorption, and serum carotene Now mainly by serologic markers: anti-gliadin IgA and IgG antibodies, anti-endomysium IgA antibodies, and for antitissue transglutaminase (tTG) IgA and IgG antibodies. Source: Medscape Insulin glargine is the first long-acting synthetic analog of human insulin. It has a slow onset (2-4 hours) and long duration (36 hours).

Notes

-Increased cardiothoracic ratio in chest x-ray film:     Congestive heart failure Pericardial effusion Multivalvular heart disease Cardiomyopathy

-Polyuria, & polydipsia:     Diabetes mellitus Diabetes insipidus (Central & nephrogenic type) ( lack of ADH or its action). UTIs Psychotic disorder (Psychotic related polydipsia)

D.Diagnosis of Epigastric pain:            Peptic ulcer Gastritis Stomach cancer Gastroesophageal reflux disease Pancreatitis Hepatic congestion Cholecystitis Biliary colic Inferior myocardial infarction Referred pain (pleurisy, pericarditis) Superior mesenteric artery syndrome

-Darkening of the nipple:   Pregnancy Race

Inflammation (Dermatomyocytis)

-Abdominal fullness:      Fetus (Pregnancy) Feces (Intestinal Obstruction) Flatus(Air or gases) Fat (Obesity) Fluid (Ascites)

Causes of Clubbing:  Cardiac : - Cyanotic congenital HD - Endocarditis  Pulmonary: - Bronchogenic carcinoma. - Suppurative lung syndromes (empyema, abscess, bronchiectasis, cystic fibrosis). - Fibrosing alveolitis.  GIT: - Crohn's disease). - Billiary cirrhosis of liver. - Malabsorption, e.g. celiac disease.  Rare causes: - Familial

Grading of clubbing:
Grade I: Obliteration of nail angle Grade II: increased nail convexity (parrot peak) Grade III: Nail soft tissue is swollen (Drum stick). Grade IV: Hypertrophic pulmonary osteo-arthropathy Subperiostal calcium deposition, Pain and tenderness may be present Joints mostly involved: knees, ankles, wrists, elbows, and metacarpophalangeal joints Usually symmetric. )may resemble rheumatoid arthritis) Plain X-ray is the mainstay of diagnosis

Causes of Lower Limb Edema: Generalized or Local, pitting or Non pitting

-Pitting edema:
1. Cardiac (CHF) 2. Hepatic: cirrhosis 3. Renal: nephrotic syndrome 4. Hypoproteinemia Protein energy Malnutrition (Kwashiorkor or Marasmic Kwashiorkor)

N.B: - In bed ridden patients: look at sacrum

- In children: Look at facial edema

-Non pitting edema:
1. Lymphatic obstruction(Filariasis) Unilateral or Bilateral 2. Pretibial myxedema (Hypothyroidism mainly in children) 3. Lymphedema(Common in female after breast cancer surgery with radiation) Turner syndrome 4. Lymphadenitis 5. DVT (Unilateral) 6. Cellulitis(Unilateral)

-Differential Diagnosis of cough:
1- Acute cough (Less than 2 weeks). 2-Chronic cough (More than 3 weeks).

Acute cough: -URTI (Upper Respiratory Tract Infections). -Bacterial Infections causing pneumonia. -Whooping cough in children & Croup. -Pulmonary embolus in severe cases leads to cough.

Chronic cough: -Bronchitis & Bronchiactasis. -In smoker patients COPD & Lung Cancer. -Drugs specially ACEinhibitors (like captopril,enalapril) & B-blockers. -Bronchial Asthma. -GERD (GastroEsophgeal Reflux Disease).

-Post nasal Drip syndrome. -Tuberculosis. -Psychogenic cough. -Congestive Heart failure & mitral stenosis.

Differential diagnosis of Melena(Black- tarry stool) 12-14 hours bleeding of 50-100cc of blood:
-Upper GI Bleeding 90%. -Lower GI Bleeding10%. Differential diagnosis of Hematocchesia(Blood per-rectum): -Lower GI Bleeding 90%. -Upper GI Bleeding10%.

Peptic ulcer due to: -NSAIDs. -Hb PYLORI causing (gastric ulcer, gastric cancer, MALToma , or gastritis). Esophageal varices. Gastric erosions. Esophagitis common causes: -Viral infection. -Candidiasis. -NSAIDs. -Steroids. -Immunocompromised. Esophageal adenocarcenoma. Gasteroesophageal reflux disease. Esophageal tearing.

Common causes of chronic gastritis:
-Autoimmune -Bacterial mainly Hb pylori. -Chemical as drugs mainly NSAIDs.

Common side effect of ACE inhibitors:
-Cough. -Arrythmia. -Hypotension in the first dose (mainly in old ACEi). -Hyperkalemia in patient with renal impairment as in renal failure. Contraindications for using ACE inhibitors: -Hyperkalemia. -Renal artery stenosis.

Causes of Red urination:
1-Pegmintation 2-Blood (Hematuria)

Pegmintation due to :
-Drug metabolites excretion refampine. -Iron hemosiderosis(Iron offerload). -Certain foods such as carrot

Blood(Hematuria): -Intial urination lower urinary tract disease in urinary bladder or lower. -Total urination it means kidney disease mostly glumeruler disease. -Terminal urination is synchronized with bladder contraction so urinary bladder disease.

-B12 deficiency leads to neurological manifestations while folic acid deficiency does not. -B12 deficiency will appear after 3-5 years while folic acid will appear with in 2 months.

WHO criteria to HB level to define anemia:  Adult male ˂13g/dL is anemic normal Range: 13-18g/dL  Adult female ˂12g/dL is anemic normal Range:12-16g/dL  In pregnant women ˂11g/dL is anemic

Main Corpascular Volume (MCV) Normal 80-100% Microcytic ˂80% common in iron deficiency anemia Macrocytic˃100%

Iron profile in iron deficiency anemia:     Serum iron ---decreased Ferrus-----decreased Total iron binding capacity------increased Firritin-------decreased

Daily requirement of iron is 20mg   10% from diatry product absorption 90% from blood distruction

Commonest cause of iron deficiency is bleeding(Mainly from the GIT)

Commonest cause of GI bleeding is:
  90% peptic ulcer disease Others: Erosion, & Esophagial varices.

Complications of Peptic ulcer: 1. Bleeding 2. Perforation 3. Penetration 4. Stricture & stenosis

Diagnostic studies for peptic ulcer caused by Hb.pylori:
 Non invasive:

1. Antibodies 2. Stool antigen 3. Uria breath test

Invasive

1. Urease enzyme 2. Culture 3. PCR

Differential Leukocyte count (Normal):      Neutrophils 45-75% Leukocyte 20-40% Basophil ˂1% Eosinophil 5% Monocyte 2-4%

Causes of raised liver enzymes????
All diseases that is associated with chronic liver problem is a cause. Any cause that leads to liver cirrhosis is a cause.               Viral hepatitis(A,B,C,D,E,G) [Viral serology] Viral atypical hepatitis (CMV, EBV, Herpes, Mumps, & TB) Reactive hepatitis Shocked liver Autoimmune hepatitis Wilsons disease (Ceruloplasmin level) Hemochromatosis (Iron profile) Hepatocellular carcinoma Drug Hepatotoxicity Primary biliary cirrhosis Biliary cholangitis Alcoholic liver disease Chronic rejection of liver transplant Infiltrative liver disease

-----Causes of coronary artery disease: Atheroscelerosis > 90% Arteritis:     SLE Rheumatoid arthritis Polyartritis nodosa Takayasu artritis

Ankylosing spondylitis

Embolism:      Infective endocarditis Thrombus in left atria or ventricle Tumor in left atria or ventricle Prosthetic valve thrombus Complication of cardiac catheterization

Coronary artery thickening:   Amyloidosis Hurler’s syndrome

Lumenal narrowing:   Aortic dissection Coronary spasm

Congenital:   Anomalous origin from pulmonary artery AV fistula

Causes of angina:  Impaired myocardial oxygen supply     Coronary artery disease Coronary artery spasm Congenital Severe anemia

 Increased myocardial oxygen demand   -------Indications for hemodialysis: 1. Uremia - azotemia with symptoms and/or signs 2. Severe Hyperkalemia 3. Volume Overload - usually with pulmonary edema Left ventricular hypertrophy (HTN , Aortic valve disease , Hypertrophic cardiomyopathy) Tachyarrythmias

-----------To localize the site of myocardial infarction by ECG looking for S-T segment, & T wave changes: Site of MI: 1. Anterior: V 1-6. 2. High lateral: Lead 1, aVL. 3. Extensive anterior: Lead I. aVL. V 1-6. 4. Anteroseptal: V 1-4. . 5. Inferior: Lead II, III. aVF. 6. Posterior: V1: tall R with ST depression and upright T. V7-8. 7. RV Infarction: ST rise in V3R, V4R. ---------Causes of Renal Failure??? Acute:

Chronic:

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Signs of Hypervolemia & Hypovolemia

---Causes of Hypokalemia:

1) Decreased net intake 2) Increased entry into cells 3) Increased GI losses 4) Increased urinary losses 5) Increased sweat losses 6) Increased other losses (dialysis)

Signs of Hypokalemia: • • • • Muscle weakness, loss of tendon reflexes Fatigue, apathy, confusion Cardiac arrhythmia, ECG changes: ST segment depression, broad T waves, U waves following T waves

Management: Repletion of K Treatment of the cause. --------LVF - History: - known cardiac disease Bronchial asthma - Asthmatic attacks - Chronic cough and expectoration - Sputum - frothy pink Tenacious white or purulent - Signs of emphysema - Expiratory rhonchi

- Physical examination

- Fine BBC Cardiomegally, S3 gallop, - murmurs

- Morphine - High concentration O2 - CXR

- Helpful - Useful

- May be fatal - May be dangerous if respiratory F. - Emphysema or other chest infectn

- Signs of pulm. oedema

- PCO2

- Usually low

- High

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Chest Pain

--Causes of Chronic Dyspnea?? Physiological: Obesity Late Pregnancy Pulmonary: Bronchial Asthma Pneumonia COPD Interstitial Lung diseases Pleural Effusion Pneumothorax Severe Chest Trauma Cardiac: Congestive Heart Failure

LVF with Pulmonary Edema Pericarditis Pericardial Effusion Abdominal: Tense Ascites Hepatosplenomegaly Systemic: SLE,RA, Vasculitis with interstitial Lung Disease. Hematological: Anemia ----------Signs of Hypocalcemia: CHVOSTEK’S SIGN Elicitation: Tapping on the face at a point just anterior to the ear and just below the zygomatic bone Postitive response: Twitching of the ipsilateral facial muscles, suggestive of neuromuscular excitability caused by hypocalcemia TROUSSEAU’S SIGN Elicitation: Inflating a sphygmomanometer cuff above systolic blood pressure for several minutes Postitive response: Muscular contraction including flexion of the wrist and metacarpophalangeal joints, hyperextension of the fingers, and flexion of the thumb on the palm, suggestive of neuromuscular excitability caused by hypocalcemia .

Extra Readings
Deep Venous Thrombosis(DVT)& Pulmonary Embolism(PE):
Venous thromboembolism includes both deep-vein thrombosis (DVT) and pulmonary thromboembolism (PE). DVT results from blood clot formation within large veins, usually in the legs. PE results from DVTs that have broken off and traveled to the pulmonary arterial circulation. DVT is approximately three times more common than PE. Although DVTs are typically related to thrombus formation in the legs and/or pelvis, indwelling venous catheters have increased the occurrence of upper extremity DVT. In the absence of PE, the major complication of DVT is postphlebitic syndrome, which causes chronic leg swelling and discomfort due to damage to the venous valves of the affected leg. PE is often fatal, usually due to progressive right ventricular failure. Some genetic risk factors, including factor V Leiden and the prothrombin G20210A mutation, have been identified, but they account for only a minority of venous thromboembolic disease. A variety of other risk factors have been identified, including immobilization during prolonged travel, obesity, smoking, surgery, trauma, oral contraceptives, and postmenopausal hormone replacement. Medical conditions that increase the risk of venous thromboembolism include cancer and antiphospholipid antibody syndrome. Clinical Evaluation: History:     progressive lower calf discomfort dyspnea Chest pain & hemoptysis Syncope

Physical Examination: Tachypnea and tachycardia are common in PE. Low-grade fever, neck vein distention, and a loud P2 on cardiac examination can be seen. Hypotension and cyanosis suggest massive PE. Physical examination with DVT may be notable only for mild calf tenderness. However, with massive DVT, marked thigh swelling and inguinal tenderness can be observed. Laboratory test: Normal D-dimer level (<500 μg/mL by ELISA) essentially rules out PE, although hospitalized pts often have elevated D-dimer levels due to other disease processes. Although hypoxemia and an increased alveolar-arterial O2 gradient may be observed in PE, arterial blood gases are rarely useful in diagnosing PE. Elevated serum troponin and brain natriuretic peptide levels are associated with increased risk of complications in PE. The ECG can show an S1Q3T3 sign in PE, but that finding is not frequently observed. Imaging studies: Venous ultrasonography can detect DVT by demonstrating loss of normal venous compressibility. When combined with Doppler imaging of venous flow, the detection of DVT by ultrasonography is excellent. For pts with nondiagnostic venous ultrasound studies, CT or MRI can be used to assess for DVT. Contrast phlebography is very rarely required. In PE, a normal chest x-ray (CXR) is common. Although not commonly observed, focal oligemia and peripheral wedge-shaped densities on CXR are well established findings in PE. Chest CT with IV contrast has become the primary diagnostic imaging test for PE. Ventilation/perfusion lung scanning is primarily used for subjects unable to tolerate IV contrast. Transthoracic echocardiography is valuable to assess for RV hypokinesis with moderate to large PE, but it is not typically useful for diagnosing the presence of a PE. With the advent of contrast chest CT scans for PE diagnosis, pulmonary angiography studies are rarely performed.

Differential Diagnosis:

Diagnosis:

Management: Anticoagulants: Although anticoagulants do not dissolve existing clots in DVT or PE directly, they limit further thrombus formation and allow fibrinolysis to occur. In order to provide effective anticoagulation rapidly, parenteral anticoagulation is used for the initial treatment of venous thromboembolism. Traditionally, unfractionated heparin (UFH) has been used, with a target activated partial thromboplastin time (aPTT) of 2–3 times the upper limit of the normal laboratory value. UFH is typically administered with a bolus of 5000–10,000 U followed by a continuous infusion of approximately 1000 U/h. Frequent dosage adjustments are often required to achieve and maintain a therapeutic aPTT with UFH. Heparin-induced thrombocytopenia can occur with UFH. However, the short-half life of UFH remains a significant advantage. Alternatives to UFH for acute anticoagulation include low-molecular- weight heparins (LMWHs) such as enoxaparin and tinzaparin. Laboratory monitoring is not required, but doses are adjusted for renal impairment or obesity. Fondaparinux, a pentasaccharide, is another parenteral alternative to UFH that does not require laboratory monitoring but does require dose adjustment for renal insufficiency. After initiating treatment with a parenteral agent, warfarin is typically used for long-term oral anticoagulation. Warfarin can be initiated soon after a parenteral agent is given; however, 5–7 days are typically required for

warfarin to achieve therapeutic anticoagulation. Warfarin is given to achieve a therapeutic international normalized ratio (INR) of the prothrombin time, which is typically an INR of 2–3. Pts vary widely in their required warfarin doses; dosing often begins at 5 mg/d, with adjustment based on the INR. The most troublesome adverse event from anticoagulation treatment is hemorrhage. For severe hemorrhage while undergoing treatment with UFH or LMWH, protamine can be given to reverse anticoagulation. Severe bleeding while anticoagulated with warfarin can be treated with fresh frozen plasma or cryoprecipitate; milder hemorrhage or markedly elevated INR values can be treated with vitamin K. Warfarin should be avoided in pregnant pts. The duration of anticoagulation for an initial DVT or PE is at least 3–6 months. Recurrent DVT or PE typically requires lifelong anticoagulation. Other Treatment Modalities Although anticoagulation is the mainstay of therapy for venous thromboembolism, additional therapeutic modalities also can be employed. Inferior vena cava filters can be used if thrombosis recurs despite adequate anticoagulation. Fibrinolytic therapy (often with tissue plasminogen activator) should be considered for massive PE, although the risk of hemorrhage is significant. Surgical embolectomy also can be considered for massive PE. If PE pts develop chronic thromboembolic pulmonary hypertension, surgical intervention (pulmonary thromboendarterectomy) can be performed. ----------

Sickle Cell disease:

History,Examination, Investigation, & Treatment or Management History: -Personal Information: name,age,gender,occupation,marital status,consinguinus marriage,day of admission,Residency,take the premarriage testing. Chief complaints: The two major problems (Crisis) that brought the SCA patient to the hospital are: 1-Hemolytic anemia. 2-Tissue infarction due to vaso-occlusion (Which is the most common). Usually the SCD patient come with one or two of these complaints: Long-term complains due to hemolysis: -Generalized fatigue. -Increased susceptibility to infections (chest infection as pneumonia ,meningitis,osteomyelitis). -Leg ulcers due to ischemia. -Gallstones so some patient are having cholecystectomy. -Aseptic necrosis of bones specially femoral head so patient may present with hip or pelvic pain. -Blindness due to retinal detachment.

-Chronic kidney disease due to vascular abnormalitiy. -Bossing of the skull and sometimes the sternum as a compensatory mechanism in infantile age to less than one year of age. Infarctions due to vaso-occlusion: -Bone pain is the most common problem patients come with. It defer in child as well as in adults. In child the most common bones affected are fingers & toes, while in adults legs,arms, and sometimes the back & the chest. -Spleen infarction or autosplenectomy and spleenomegaly. -Kidney disease presenting as hematuria which is more common in SCT leading to papillary necrosis of the renal calysis. -Mesentaric infarctions are not so common but may occur presented as acute abdomen. -Chest pain is almost common due to pulmonary infarctions which may be exacerbated by dehydration, chilling, & chest infection mainly streptococcus penumoniae. -CNS stroke or Transient ischemic attack (TIA) may occur in thrombosis. -Penile disease known as priapism (Painfull erection) due to blockage of corpora cavernosa. Other manifestations not specific includes: -Hepatomegaly. -Jaundice. -Delayed puberty. -Non-healing ulcers in the legs. History of the Presenting illness: detailed description of the patient complaints regarding: -Site, onset, duration, pattern, course, character, severity, radiation, associated symptoms, relieving factors, & exacerbating factors. Negative signs should be presented. Past medical & surgical history: -Any previous attack similar to this condition. -Hip replacement. -Cholecystectomy. -Chest infection. -Cardiac disease. -Infectious diseases(malaria,& schestosomiasis, hepatitis). -Endocrine disorders (Thyroid, or pituitary disease).

-Kidney disorders. - Blood transfusion. -Bone marrow transplantation. -Splenictomy. Drug History: -History of drugs that cause hemolysis: Extravascular Hemolysis -Alpha-methyldopa & levodopa -Diclofenac -Ibuprofen -Interferon alfa -Mefenamic acid -Penicillin(Carbenicillin,ampicillin,& methicillin) -Procainamide Intravascular Hemolysis: -Acetaminophen -Chlorpromazine -Fluorouracil -Hydrochlorothiazide -Hydralazine -Insulin -Isoniazid -Melphalan -Phenacetin -Probenacid -Quinidine & Quinine (treatment for malaria). -Rifampin -Streptomycin -Sulfonamides -Sulindac

-Tetracycline History of addicting analgesic drugs as morphine. History of folic acid tablet which increase RBCs production as compensatory mechanism. Family history: -Genertic disease in the family. -History of multifactorial disease. -Consinguinus marriage. -History of sudden infantile death. Social history: Living where, hows taking care of you, especially during the attack. How much your fond per month. Educational level of the patient & his/her parents. Smoking , or alcohol. Menstrual history: Regular, disturbed, normal amount of blood, painfull menses (Dysmenorrhea) , last period, stoppage of menses in elderly when (Amenorrhea) , pregnancy. Review of systems: General: -Posture of the patient usually is important indicating pain. -Hair distribution -Eye discolorations: Jaundice 80-90% of the SCA patients have at least a mild degree of jaundice. Pallorness. Red eye in conjunctivitis. -Skin turger as a mild degree of dehydration. -Generalized fatigability. -Vital signs: (RR, BP, P, & TEMP). -Look for cyanosis. -Carotid pulses,& JVP. -Localize the apex beat. -Look for clubbing. RS: -Chest shape.

-Trachea. -Breath sounds. -Detection of any adventitious sounds. CVS: -Palpation: Carotid, suprasternal , epigastric , aortic , pulmonary, tricuspid, & mitral areas. -Auscultation: S1,S2, splitting between aortic & pulmonary sounds with respiration. -Any additional murmer and localize it in systole or diastole. GI: -Ask for any GI symptoms as constipation,diarrhea,vomiting,hematemesis,melena,heartburn,dyspepsia,dysphagia. Inspection: -Look for the abdomen shape (Countor) ,localize the umbilicus, look for the oral cavity ouder ,hygiene, whitish discoloration of the cavity which suggest oral candidiasis, look below the tongue for cyanosis, look to the abdomen for hernia femoral, inguinal, diaphragmatic,& umbilical. Look for scars, dilated veins. Palpation: Superfecial palpation for swelling & tenderness. Deep plapation for organs liver,spleen,& kidneys.(Look for splenomegaly or hepatomegaly) Percussion: Liver span Ascultation: Intestinal prestalesis. Aortic bruit. Renal bruit. GUS: ask for urine frequency & color ,micturation pain, pripism(Painfull erection). MS: ask for screening exam GALS(Gait, Arms, Legs, & Spine) for inspection ,palpation , & movements specially legs & arms. CNS: Ask the patient to walk around the room for gait assessment, perform cranial nerve examination, motor & sensory system examination.

Investigations :(Lab,Imaging,&Biopsey) Laboratory:

-CBC, WBC, DLC, Reticulocyte count. -Liver function tests. -LDH. -Bilirubin assy. - Hemoglubin electrophoresis HbF should be less than 40%. -Urinalysis for urobilinogen mainly. -Sickling test. -ECG Imaging: -Chest x-ray for chest infection consolidations. -Abdominal Ultrasound for hepatomegaly, splenomegaly, biliary obstruction.

Treatment or Management: Treatment of the acute case by: -Hydration. -Oxygenation by ventilation. -Blood transfusion or exchange. -Antibiotic as needed. -Analgesia. -Histamine receptor antagonist for itching. Treatment as a chronic case: -Hydroxyurea. -Folic acid. -Penicillin as preventive measure. -Cholestyramine In children : -Bone marrow transplantation is effective. Under research: -Gene therapy. -Stem cells.

-Phytochemicals like Nicosan the same antisickling effect as hydroxyurea.

Vaccination for the Encapsolated organism mainly salmonella, Pneumococcal, Meningococcal, Hemophilus influanzae & chlamydial organism.

Major cause of death: -Acute chest syndrome. -TIA & Stroke. -Coronary syndrome.

Complications:

Overwhelming post-(auto)splenectomy infection (OPSI), which is due to functional asplenia, caused by encapsulated organisms such as Streptococcus pneumoniae and Haemophilus influenzae. Daily penicillin prophylaxis is the most commonly used treatment during childhood, with some haematologists (hematologists) continuing treatment indefinitely. Patients benefit today from routine vaccination for H. influenzae, S. pneumoniae, and Neisseria meningitidis. Stroke, which can result from a progressive narrowing of blood vessels, preventing oxygen from reaching the brain. Cerebral infarction occurs in children and cerebral hemorrhage in adults. Cholelithiasis (gallstones) and cholecystitis, which may result from excessive bilirubin production and precipitation due to prolonged haemolysis. Avascular necrosis (aseptic bone necrosis) of the hip and other major joints, which may occur as a result of ischemia. Decreased immune reactions due to hyposplenism (malfunctioning of the spleen). Priapism and infarction of the penis. Osteomyelitis (bacterial bone infection); the most common cause of osteomyelitis in sickle cell disease is Salmonella (especially the non-typical serotypes Salmonella typhimurium, Salmonella enteritidis, Salmonella choleraesuis and Salmonella paratyphi B), followed by Staphylococcus aureus and Gram-negative enteric bacilli perhaps because intravascular sickling of the bowel leads to patchy ischaemic infarction. Opioid tolerance, which can occur as a normal, physiologic response to the therapeutic use of opiates. Addiction to opiates occurs no more commonly among individuals with sickle-cell disease than among other individuals treated with opiates for other reasons. Acute papillary necrosis in the kidneys. Leg skin ulcers. In eyes, background retinopathy, proliferative retinopathy, vitreous haemorrhages and retinal detachments, resulting in blindness. Regular annual eye checks are recommended.

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During pregnancy, intrauterine growth retardation, spontaneous abortion, and pre-eclampsia. Chronic pain: Even in the absence of acute vaso-occlusive pain, many patients have chronic pain that is not reported. Pulmonary hypertension (increased pressure on the pulmonary artery), leading to strain on the right ventricle and a risk of heart failure; typical symptoms are shortness of breath, decreased exercise tolerance and episodes of syncope. Chronic renal failure due to Sickle cell nephropathy—manifests itself with hypertension (high blood pressure), proteinuria (protein loss in the urine), hematuria (haematuria) (loss of red blood cells in urine) and worsened anaemia. If it progresses to end-stage renal failure, it carries a poor prognosis.

----------SLE Systemic Lupus Erythematosus: Systemic lupus erythematosus (SLE) is a multisystem, potentially fatal autoimmune disease that can involve the skin, joints, muscles, heart, lung, kidneys, peripheral nerves, central nervous system (CNS), and blood. The severity is largely determined by which organs are involved, patients with CNS or renal involvement often having the most serious disease. The diagnosis of SLE is made if patients fulfill at least 4 of the 11 criteria designated by the American College of Rheumatology. Criteria for the classification of SLE (If any 4 or more of 11 criteria are met) 1. Malar rash 2. Discoid rash 3. Photosensitivity 4. Oral ulcers 5. Arthritis 6. Serositis 7. Renal diseas: >0.5 f/d proteinuria, or >3+ dipstick proteinuria, or cellular casts 8. Neurologic disease: seizures, or psychosis (without other cause) 9. Hematologic disorders:
o o o

a. Hemolytic anemia, or b. Leukopenia <400/uL, or c. Thrombocytopenia <100,000/uL

10. Immunologic abnormalities:
o o o o

a. Positive LE cell prep, or b. Antibody to native DNA, or c. Antibody to Sm, or d. False-positive serologic syphilis test

11. Positive ANA test.

Drugs associated with lupus like syndrome: Symptoms include fever, arthritis, and serositis but not renal or CNS disease and normally resolve in 6 to 8 weeks after the drug is stopped. In 90% of the cases an anti-histone antibody can be identified.

Definitive association: - chlorpromazine, hydralzine, isoniazid, methyldopa, procainamide, quinidine. Possible association: - acebutoloo, atenolol, captopril, carbamazepine, cimetidine, ethosuximide, hydrazines, labetalol, levodopa, lithium, mephynytoin, methimazole, metoprolol, nitrofurantoin, oxprenolol, penicillamine, phenelzine, phynytoin, pindolol, practolol, propranolol, prophylthiouracil, sulfasalazine, sulfonamides, trimethadione. Unlikely association: - allopurinol, chlorthalidone, gold salts, griseofulvin, methysergide, oral contraceptives, penicillin, phenylbutazone, reserpine, streptomycin, tetracyclines.

Constitutional Symptoms: are frequent, especially fatigue, which is reported by 80 to 100% of patients. Fever and weight loss occur in more than 60% of patients as well. Lymphadenopathy is a common manifestation of SLE. Skin Manifestations including the typical malar rash & the Discoid lupus erythematosus (DLE) lesions that are scarring and occur either alone or in association with SLE. Subacute cutaneous LE (SCLE) includes two types of lesions: psoriasiform and annular polycyclic. Renal Manifestations Renal disease is common in most patients with SLE and can be asymptomatic until there's advanced disease. The excretion of more than 500 mg of urinary protein /24 hours (or greater than 3+ proteinuria on dipstick testing), the presence of casts (including RBCs, hemoglobin, granular, tubular, or mixed), hematuria (more than 5 RBCs /hpf) or pyuria (more than 5 WBCs/hpf ), or an elevated serum creatinine level is evidence of renal disease and should prompt the clinician to a more thorough investigation of renal status and referral to a specialist. The World Health Organization (WHO) classification of lupus nephritis is the standard by which most lesions are classified and can prognosticate survival of the kidney.     Mesangial abnormalities (WHO class II) - in 40% of the patients. Focal glomerulonephritis (class IIIA and class IIIB) -in 20% of the patients. Diffuse proliferative glomerulonephritis (class IV) - in 40% of the patients. Predominant membranous lesion (class V) - in less than 10 % of the patients.

Class I and class II lesions require no treatment. Class III lesions can undergo transition to a more proliferative and diffuse process, necessitating treatment. The consequences of nephrotic syndrome, hypertension, hyperlipidemia, and hypercoagulability, seen with both class IV and class V lesions, can increase mortality in these patients. Class V (membranous) lesions usually have a slowly progressive course, and treatment varies, including steroids or immunosuppressives, neither of which have been shown to alter the course of the disease. Class IV (diffuse proliferative) lesions affect more than 50% of the glomeruli, with progression to renal failure in most cases.

Musculoskeletal Manifestations common, including acute arthritis, typically involving the small joints of the hands, wrists, and knees, is usually episodic and symmetrical in distribution. Avascular necrosis (AVN) is seen in 5% of SLE patients, affecting the hip most commonly but also the shoulder, knee, and ankle. Cardiac Manifestations Pericarditis is the most common cardiac Sx (precordial chest pain and a pericardial rub), 20 to 30% in most large series. Myocarditis presenting as dysrhythmias and/or cardiomegaly is a less common manifestation . Libman-Sacks endocarditis, with sterile verrucous vegetations on the mitral valve, is less common. Premature atherosclerosis is a major cause of morbidity and mortality in SLE.

Pulmonary Manifestations include pleuritis, pulmonary alveolar hemorrhage, pneumonitis, pulmonary infiltrates, chronic interstitial lung disease, shrinking lung syndrome, pulmonary hypertension, and pulmonary embolism. Acute pneumonitis frequently responds to corticosteroids (1 mg per kg per day). Pulmonary alveolar hemorrhage is a rare but serious manifestation and carries a high mortality. Very aggressive treatment is required for improved survival, and cytotoxic agents or plasmapheresis may be necessary. Patients with chronic interstitial lung disease can present with typical symptoms of restrictive lung disease, including nonproductive cough, dyspnea on exertion, and basilar rales on physical examination. Pulmonary hypertension may be a finding in many of the collagen-vascular diseases and occurs in 1 to 2% of SLE patients. Pulmonary hypertension can present insidiously with progressive exertional dyspnea, and early disease can be detected by an abnormal carbon monoxide diffusing capacity (DL CO) on pulmonary function testing. Pulmonary embolus is a serious potential complication of antiphospholipid (APL) antibody syndrome (discussed later) in patients with SLE. Pleuritic chest pain in an SLE patient cannot be assumed to be due to SLE serositis. In an SLE patient with a normal chest film, pulmonary embolus must be excluded. Gastrointestinal Manifestations Abdominal pain, anorexia, nausea, and vomiting are common gastrointestinal manifestations of SLE. Serositis is the most common underlying causative disorder and frequently responds to moderate doses of corticosteroids. The presenting manifestation of mesenteric vasculitis can be lower abdominal pain accompanied by frank or occult rectal bleeding, and perforation of the bowel can result. If the diagnosis of mesenteric vasculitis is suspected, intensive investigation should be undertaken, with appropriate treatment with high doses of steroids. Acute pancreatitis can occur in SLE patients, manifesting as abdominal pain, nausea, vomiting, and elevated serum amylase. Neuropsychiatric Manifestations Diffuse manifestations are the most common CNS presentation in NP-SLE patients (60% of cases).
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Headaches occur in 30 to 50% of patients. Frank psychosis is seen in 5 to 15% of patients. Major depression or dementia can also be a manifestation of the disease secondary to NP-SLE activity; a reactive depression secondary to a chronic devastating illness is also possible. In addition, dementia can be a sequela of multiple infarctions secondary to APL antibody syndrome (Anti Phospholipid Antibodies) or other vasculopathy. Seizures can be caused by a number of factors, including focal infarct or ischemia from vasculitis or APL antibody syndrome, embolic phenomenon or hemorrhage, or brain-reactive antibodies. Focal manifestations such as strokes occur in the minority of CNS SLE patients (10 to 35% of cases). These stroke syndromes can affect any area of the brain and are usually caused by thrombosis from vasculopathy or by emboli from cardiac valvular lesions.

Cranial neuropathies can be transient, resolving with corticosteroid therapy. They are frequently associated with APL antibody syndrome and are presumed to be of thrombotic origin. Transverse myelitis is an infrequent but devastating manifestation of NP-SLE and can frequently be the presenting manifestation of SLE. Characteristic findings include an elevated CSF protein (in 82% of cases), CSF pleocytosis (in 70%), and a low (less than 30 mg per dL) CSF glucose (in 50%). Owing to the poor prognosis with transverse myelitis, early diagnosis and aggressive therapy are important. Mononeuritis multiplex secondary to small vessel vasculitis can also be seen in SLE. Movement disorders such as chorea are rare.

The most common histologic finding in the brain of SLE patients is a vasculopathy, with associated microinfarcts. True vasculitis is rare. The evaluation of an SLE patient with CNS manifestations includes cerebrospinal fluid (CSF) evaluation for routine studies, antineuronal antibodies (seen in patients with diffuse manifestations), quantitative CSF immunoglobulins, and oligoclonal bands (elevations commonly seen in active CNS SLE disease). Magnetic resonance imaging (MRI) can sometimes demonstrate small, high-signal-intensity vascular lesions but cannot define active disease. Treatment of the diffuse manifestations may include administration of antiseizure drugs or antipsychotics but usually requires high-dose steroids (1 mg per kg per day) or pulse high-dose steroids (1 gram per day for 3 days). Refractory cases sometimes respond to intravenous cyclophosphamide, plasmapheresis, or a combination of these. Focal manifestations seen in association with APL antibodies are treated with anticoagulation, in addition to the aforementioned medications. Hematologic Manifestations Cytopenias, including anemia, leukopenia, lymphopenia, and thrombocytopenia, are frequent findings in SLE.
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Hemolysis in SLE is usually Coombs'-positive owing to the presence of antibodies directed against RBC antigens. Leukopenia (2500 to 4000 WBCs per mm3 ) in an SLE patient suggests active disease, although other causes of leukopenia such as infection or drugs must be excluded. Neither leukopenia nor lymphopenia (less than 1500 WBCs per mm3 ) predisposes to infection, because the bone marrow is usually normal. Thrombocytopenia (platelet counts of less than 100,000 per mm3 ) in an SLE patient is common but, like anemia, requires that other possible causes such as infection or drug effect be excluded. Most thrombocytopenic patients with SLE are asymptomatic, but in some patients, the platelet counts can drop quite low and predispose to bleeding, requiring aggressive management with highdose steroids, cytotoxic drugs, intravenous immune globulin, and very rarely, splenectomy. A subset of SLE patients with thrombocytopenia have associated APL antibody syndrome and are predisposed to thrombotic events.

Malignancy
Malignancy continues to increase in SLE patients with increasing use of alkylating agents. Over 100 cases of non-Hodgkin's lymphoma have been reported, and there is an increased frequency of gynecologic cancers. In one series, the mean time from onset of treatment to cancer was only 4.1 years. Frequent surveillance, including Papanicolaou smears and mammograms, is important.

Antiphospholipid Antibodies: (Pulmonary embolism & SLE) A variety of clotting abnormalities, including the presence of the lupus anticoagulant, manifested as a prolonged activated partial thromboplastin time (APTT) that does not normalize with mixing studies. Patients with the lupus anticoagulant, a false-positive result on VDRL testing, or a high titer of anticardiolipin antibodies fall under the umbrella term of "APL antibody-positive" and are predisposed to thrombotic events. The APL antibody syndrome

describes the association of these APL antibodies with arterial and venous thrombosis, recurrent fetal loss, and immune thrombocytopenia. Management of SLE patients with APL antibodies who have never had a thrombotic event is usually with low-dose aspirin therapy. Once patients have had a thromboembolic event, lifelong anticoagulation with warfarin is established, with an INR (International Normalized Ratio) of 3.0, to prevent recurrent events. Common Lab results:
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ANA 95-100%,Anti-native DNA 50%,Anti-Sm 20%, Hypocomplementemia 60% Rheum.Factor 20%, False-positive syphilis test 25% Anemia 60%,Leukopenia 45%,Thrombocytopenia 30% Proteinuria 30%, Hematuria 30% Direct Coombs-positive 30%, Anti-cardiolipin Ab 25%, Lupus anticoagulant 7%

Treatment: There is no cure for SLE. Complete sustained remissions are rare. Goal of Rx: to control acute, severe flares and to develop maintenance strategies in which symptoms are suppressed to an acceptable level, usually at the cost of some drug side effects. Approximately 25% of SLE patients have mild disease with no life-threatening manifestations, although pain and fatigue may be disabling. These patients should be managed without glucocorticoids. Arthralgias, arthritis, myalgias, fever, and mild serositis may improve on nonsteroidal anti-inflammatory drugs (NSAIDs) including salicylates. The dermatitides of SLE, fatigue, and lupus arthritis may respond to antimalarials. Doses of 400 mg hydroxychloroquine daily may improve skin lesions in a few weeks. Side effects are uncommon and include retinal toxicity, rash, myopathy, and neuropathy. Regular ophthalmologic examinations should be performed at least annually, since retinal toxicity is related to cumulative dose. Other therapies include sunscreens (an SPF rating 15 is recommended), topical or intralesional glucocorticoids, quinacrine, retinoids, and dapsone. Recent studies suggest that daily oral doses of dihydroepiandrosterone may lower disease activity in patients with mild SLE. Systemic glucocorticoids should be reserved for patients with disabling disease unresponsive to these conservative measures. Life-threatening, severely disabling manifestations of SLE that are responsive to immunosuppression should be treated with high doses of glucocorticoids (1 to 2 mg/kg per day). When disease is active, glucocorticoids should be given in divided doses every 8 to 12 h. Acutely ill lupus patients, including those with proliferative GN, can be treated with 3 to 5 days of 1000 mg intravenous "pulses" of methylprednisolone, followed by maintenance daily or alternate-day glucocorticoids. Disease flares are probably controlled more rapidly by this approach, but it is unclear whether long-term outcome is changed. The use of cytotoxic agents (azathioprine, chlorambucil, cyclophosphamide, methotrexate, mycophenolate mofetil) in SLE is probably beneficial in controlling active disease, reducing the rate of disease flares, and reducing steroid requirements. Patients with lupus nephritis have significantly less renal failure and better survival if treated with combinations of glucocorticoids plus intravenous cyclophosphamide; azathioprine as the second drug is less beneficial but is also effective in preventing renal failure.

Course FeedBack
The course is Very good in terms of information received in this short period but I recommend to expose the students to acute cases as for example one day per week to improve their skills in diagnosing & managing in ER , & also to know the common cases reported in the ER.

Faculty FeedBack: Dr.Mohammad Salah Very Good Explanation specially when the case is related to his speciality But There is no practical Case review in Bedside. Lectures need a little modification Calculations Should Be with examples to intensify that knowledge. Dr.Naboli Very Good in demonstration of the important clinical knowladge Lectures are good Case demonistration is relatively good. Very good endocrinologist Case discussion usually goes beyond the case Dr.Abdullmaguid: Very good lectures in all aspects Disscusion usually on the patient complaint Should impress more in the important knowledge that is expected from all students

Clinical cases review in my opinion should be marked so that all the students can participate in taking the cases, & remark the deficiency in the case & personal knowledge

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