Internal Medicine III Logbook 2011-2012

College of Medicine, Al-Ahssa

DEPARTMENT OF MEDICINE 6TH

YEAR STUDENT

Student's name: Qasim Hussain Al-Haleimi

Academic number: 207002113

Course Coordinator: Dr. Abdulmaguid AL-Ballat

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

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 Dr.Naushad

Only case discussion

---------

Date: 22 – 11- 2011 Tuesday Dr.Abdulmaguid

Discussion:

Causes of syncope

ECG commenting

----------

Date: 23 – 11 – 2011 Wednesday Dr.Naushad

Case Discussion

Management of a case of Bronchial Asthma

------

Date: 26 – 11 – 2011 Saturday Dr.Naushad

Case Discussion

Rheumatoid arthritis

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.”

--------


Case discussion

SLE

----------

Date: 29 – 11 – 2011 Tuesday Dr.Abdulmaguid

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

• Rash, neutropenia

Contraindications:

• Pregnancy

• Renal insufficiency (creatinine > 3 mg/dl)

• Hyperkalemia (> 5,5 mmol/l)

• Severe hypotension

• Bilateral renal artery stenosis

• Angiodema

----

Date: 30 – 11 – 2011 Wednesday Dr.Abdulmaguid

Case discussion (Cardiomayopathy)

IHD

Diagnosis of Myocardial Infarction by 2 of 3:

Ischemic Chest Pain which is either typical or not.

ECG changes of S-T segment elevation

Cardiac Enzymes

---------

Date: 02 – 12 – 2011 Saturday Dr.Naushad

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

http://www.nejm.org/doi/full/10.1056/NEJMcp1001124?ssource=spec_coll#ref1

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.

----------


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 Dr.Abdulmaguid

Case discussion:

Arrhythmias mainly AF

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 Dr.Hesham Rasheed

Case discussion:

Arrhythmia AF

Cardiac symptomatology

Cardiac Examination

JVP

-------

Date: 12 – 12 – 2011 Monday Dr. Amr

Case discussion:

COPD

Pulmonary hypertension in SCD patient

Examination

-------

Date: 13 – 12 – 2011 Tuesday Dr.Rabah

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:

Congenital:

Factor V leiden Mutation

Protein C & S deficiency

Antithrombin III deficiency

Aquaired:

Estrogen Use (Oral Contraceptive)

Pregnancy Hormonal changes

Malignancy secreting estrogen like factors.

------


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 Dr.Amr

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:

Corpulmonale which may lead to Right sided Heart Failure

Ischemic Myocardial Infarction

Pulmonary Embolism

Arrhythmia & Arrest

--------

Date : 20 – 12 – 2011 Tuesday Dr.Rabah

Inflammatory Bowel Syndrome

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 Dr.Nboliy

Disscusion:

CHF

Goitre & AF.

----------

Date: 24 – 12 – 2011 Saturday Dr.M.Salah

Disscusion:

HTN

DM

& Renal Disease.

----------


Disscusion:

Obstructive renal injury

Cervical Lymphoma

Anemia

---------

Date: 27 – 12 – 2011 Tuesday Dr. Amr

Disscusion:

Left Lung carcinoma

Consolidation pneumonia with bronchiectasis

Hepatocellular carcinoma, with marked hepatomegaly

---------

Date: 28 – 12 – 2011 Dr.Surendra

Discussion:

SCD

Nephrotic syndrome

---------


Case of Heart Failure (Dilated Cardiomyopathy)

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 Dr.Amr Darwish

Case of Plaural Effusion

Case of COPD Mixed type

Case of Goiter

Case of COPD with respiratory Failure.

---------

Crohns disease Ulcerative Colitis 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

Family History, No sex predilection,

Smoking is protective.

Both have a risk of malignancy

Common Site &

Endoscopic

Picture

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

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

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.

Systemic symptoms are common in

IBD and include fever, sweats,

malaise, and arthralgias.

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

- 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.

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 string sign (a narrow band of

barium flowing through an inflamed or

scarred area)

Abdominal x-ray

Ultrasound

CT

GI endoscopy

Biopsy for Histopathology

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

Treatment -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.

-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.

Both diseases have two stages:

Active stage (Flare)

Remission stage.

Symptoms correspond well to the degree of inflammation present

D.Diagnosis:

http://www.uptodate.com/contents/budesonide-drug-information?source=see_link

http://www.uptodate.com/contents/sulfasalazine-drug-information?source=see_link

http://www.uptodate.com/contents/mesalamine-drug-information?source=see_link

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

http://www.uptodate.com/contents/sulfasalazine-drug-information?source=see_link

http://www.uptodate.com/contents/mesalamine-drug-information?source=see_link

http://www.uptodate.com/contents/ciprofloxacin-drug-information?source=see_link

http://www.uptodate.com/contents/metronidazole-drug-information?source=see_link

http://www.uptodate.com/contents/prednisone-drug-information?source=see_link

http://www.uptodate.com/contents/budesonide-drug-information?source=see_link

http://www.uptodate.com/contents/azathioprine-drug-information?source=see_link

http://www.uptodate.com/contents/methotrexate-drug-information?source=see_link

http://www.uptodate.com/contents/infliximab-drug-information?source=see_link

http://www.uptodate.com/contents/adalimumab-drug-information?source=see_link

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 (Dr.Naushad)

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

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

-----------


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 AL-

Jaffer 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

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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

----------


Lymphoma

Obstructive renal injury

Chronic Anemia for investigation

-------

Date: 27 – 12 – 2011 Tuesday (Dr.Amr)

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

Clinical Clerkship

Bed Case 506 A, & B

Case # 1 SCD VOC Date: 21 – 11 – 2011 Monday

Personal History:

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


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 U/L (100-190)

Total Bilirubin : 29 Hi Ab

CBC:

MCV : decrease 79.9 (80-94)

RDW : 19.1 Hi Ab (11.5-15.5)

Platelet : 412 Hi Ab (130-400)

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 Date: 26 – 11 – 2011 Saturday

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

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) , MCH : 21.5 Low Ab (27-31)

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 (135-145)

Creatinine & urinalysis Creatinine : 118 Hi Ab (53-45)

PT, PTT, INR Awaited

Lipid profile Awaited

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 Date : 29 – 11 – 2011 Tuesday

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

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 Date: 17 – 12 – 2011 Saturday

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.

Patient complain: Back Pain for 1 day


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.


SCD VOC

Examination:

Mild Jaundice

Vital signs are stable with no abnormality

Other examination are unremarkable


SCD VOC

Investigations:

CBC

Total Bilirubin 22.8 Hi Abnormal umol/L

MCV 63 Low AB

MCHC 32.1 Low AB

MCH 20.2 Hi AB

RDW 21 Hi AB

HCT 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 Date: 24 – 12 – 2011 Saturday

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


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

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


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 Date : 26 – 12 – 2011 Monday

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 AL-

Moasat Dispensary.

Patient complaint:

Localized Left Abdominal Pain Since 1week


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.


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.


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 Normally 40 + or - (20)

Common cause:

Aortic regurge

Other causes:

1. Physiological

Fever

Pregnancy

2. Cardiac lesions

http://en.wikipedia.org/wiki/Pulse

http://en.wikipedia.org/wiki/Water_hammer

http://en.wikipedia.org/wiki/Stroke_volume

http://en.wikipedia.org/wiki/Left_ventricle

http://en.wikipedia.org/wiki/Peripheral_resistance

http://en.wikipedia.org/wiki/Pulse_pressure

http://en.wikipedia.org/wiki/Fever

http://en.wikipedia.org/wiki/Pregnancy

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)

http://en.wikipedia.org/wiki/Aortic_regurgitation

http://en.wikipedia.org/wiki/Patent_ductus_arteriosus

http://en.wikipedia.org/wiki/Systolic_hypertension

http://en.wikipedia.org/wiki/Bradycardia

http://en.wikipedia.org/wiki/Aortopulmonary_window

http://en.wikipedia.org/w/index.php?title=Rupture_of_sinus_of_Valsalva_into_heart_chambers&action=edit&redlink=1

http://en.wikipedia.org/wiki/Anemia

http://en.wikipedia.org/wiki/Cor_pulmonale

http://en.wikipedia.org/wiki/Cirrhosis_of_liver

http://en.wikipedia.org/wiki/Beriberi

http://en.wikipedia.org/wiki/Thyrotoxicosis

http://en.wikipedia.org/wiki/Arteriovenous_fistula

http://en.wikipedia.org/wiki/Paget%27s_disease

http://en.wikipedia.org/wiki/Chronic_alcoholism

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 treatment-

induced 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 hormone-

releasing 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 Preparation Onset of Effect Peak Effect (hr) Duration of Action (hr)

Rapid acting Lispro, aspart, or glulisine 10–15 min 1–2 3–4

Short acting Regular (R) 30 min 2–4 5–8

Intermediate acting

Orange

NPH (N) or Lente 2–4 hours 6–12 16–24

Long acting (بنفسجي)

Ultralente (U) 4–6 hours 8–16 ∼24

Glargine 2–4 hours No peak >30

Detemir 1 hour No peak Up to 24

Source :

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:

• 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).

--------

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 anti-

tissue transglutaminase (tTG) IgA and IgG antibodies. Source: Medscape

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


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

Left ventricular hypertrophy (HTN , Aortic valve disease , Hypertrophic cardiomyopathy)

Tachyarrythmias

--------

Indications for hemodialysis:

1. Uremia - azotemia with symptoms and/or signs

2. Severe Hyperkalemia

3. Volume Overload - usually with pulmonary edema

------------

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:

--------

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.

---------

Bronchial asthma LVF

- Asthmatic attacks

- Chronic cough

and expectoration

- known cardiac disease - History:

Tenacious white or

purulent

- frothy pink - Sputum

- Signs of

emphysema

- Expiratory

rhonchi

- Fine BBC

Cardiomegally,

S3 gallop,

- murmurs

- Physical

examination

- May be fatal

- May be dangerous

if respiratory F.

- Helpful

- Useful

- Morphine

- High

concentration O2

- Emphysema or

other chest infectn

- Signs of pulm. oedema - CXR

- High - Usually low - PCO2

-------------

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

http://www.fpnotebook.com/Pharm/Analgesic/Ibprfn.htm

http://www.fpnotebook.com/GI/Pharm/IntrfrnAlf.htm

http://www.fpnotebook.com/ID/Pharm/NtrlPncln.htm

http://www.fpnotebook.com/CV/Pharm/Prcnmd.htm

http://www.fpnotebook.com/Pharm/Analgesic/Actmnphn.htm

http://www.fpnotebook.com/CV/Pharm/ThzdDrtc.htm

http://www.fpnotebook.com/CV/Pharm/DrctActngVsdltr.htm

http://www.fpnotebook.com/Endo/Pharm/Insln.htm

http://www.fpnotebook.com/Lung/Pharm/Isnzd.htm

http://www.fpnotebook.com/CV/Pharm/Qndn.htm

http://www.fpnotebook.com/Lung/Pharm/Rfmpn.htm

http://www.fpnotebook.com/Lung/Pharm/Strptmycn.htm

http://www.fpnotebook.com/ID/Pharm/Slfnmd.htm

-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.

http://www.fpnotebook.com/ID/Pharm/Ttrcycln.htm

-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.

http://en.wikipedia.org/wiki/Overwhelming_post-splenectomy_infection

http://en.wikipedia.org/wiki/Streptococcus_pneumoniae

http://en.wikipedia.org/wiki/Haemophilus_influenzae

http://en.wikipedia.org/wiki/Penicillin

http://en.wikipedia.org/wiki/Cerebrovascular_accident

http://en.wikipedia.org/wiki/Human_brain

http://en.wikipedia.org/wiki/Cholelithiasis

http://en.wikipedia.org/wiki/Cholecystitis

http://en.wikipedia.org/wiki/Bilirubin

http://en.wikipedia.org/wiki/Haemolysis

http://en.wikipedia.org/wiki/Aseptic_bone_necrosis

http://en.wikipedia.org/wiki/Immune_system

http://en.wikipedia.org/wiki/Hyposplenism

http://en.wikipedia.org/wiki/Priapism

http://en.wikipedia.org/wiki/Infarction

http://en.wikipedia.org/wiki/Penis

http://en.wikipedia.org/wiki/Osteomyelitis

http://en.wikipedia.org/wiki/Salmonella

http://en.wikipedia.org/wiki/Staphylococcus_aureus

http://en.wikipedia.org/wiki/Staphylococcus_aureus

http://en.wikipedia.org/wiki/Opioid

http://en.wikipedia.org/wiki/Renal_papillary_necrosis

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 a. Hemolytic anemia, or

o b. Leukopenia <400/uL, or

o c. Thrombocytopenia <100,000/uL

10. Immunologic abnormalities:

o a. Positive LE cell prep, or

o b. Antibody to native DNA, or

o c. Antibody to Sm, or

o d. False-positive serologic syphilis test

http://en.wikipedia.org/wiki/Intrauterine_growth_retardation

http://en.wikipedia.org/wiki/Abortion

http://en.wikipedia.org/wiki/Pre-eclampsia

http://en.wikipedia.org/wiki/Pulmonary_hypertension

http://en.wikipedia.org/wiki/Pulmonary_artery

http://en.wikipedia.org/wiki/Right_ventricle

http://en.wikipedia.org/wiki/Right_ventricle

http://en.wikipedia.org/wiki/Heart_failure

http://en.wikipedia.org/wiki/Syncope_(medicine)

http://en.wikipedia.org/wiki/Renal_failure

http://en.wikipedia.org/wiki/Sickle_cell_nephropathy

http://en.wikipedia.org/wiki/Hypertension

http://en.wikipedia.org/wiki/Proteinuria

http://en.wikipedia.org/wiki/Hematuria

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).

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.

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 high-

dose 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:

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

Internal Medicine III Logbook 2011-2012

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Transcript of Internal Medicine III Logbook 2011-2012