internal medicine (ii) 2011 logbook

8/6/2019 Internal Medicine (II) 2011 Logbook

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College of Medicine, Al-Ahsa

DEPARTMENT OF MEDICINE

5TH

YEAR

Student's name: Qasim Hussain Al-Haleimi

Academic number: 207002113

Course Coordinator: Dr. Naushad



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Contents:

1- Cases , & Discussion

2-Extra reading (Sickle cell disease, Stroke, Hypoglycemia, Chest Pain, Abdominal Pain, FUO, Syncope,

Pancreatitis, DM, DVT&PE)

3-Differential Diagnosis

4-Assignments

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

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1-Cases & Discussion

Presented case

Case # 1 Sickle cell vaso - occlusive crisis Dr. Surendra Date: 27-03- 2011 AD

Personal data:

Mohammad Ali , Saudi male patient , 29 year old , live in Al-Omran , work as security . married , admitted

since 6 days .

Chief complaint:

The patient complained of pain in : leg , chest and shoulder.

Presenting History:

The patient well known SCD, the pain has acute onset and contracted character.its moderate progressive

pain start in chest then radiate to shoulder and leg . The pain is continuous and relived by vulturine

injection , and there is no specific participating factor. The pain is associated with : Nausea and loss of

appetite . No history of jaundice and no history of hepatic pain . No diarrhea.

Past History: Known patient of SCD since birth , admitted 2-3 time / year , Known patient of inflammatory

bowel disease since 11 year, Blood transfusion 3-4 times / year , No previous surgery , No DM , NO HTN ,

NO chronic disease .

Drug history:

Folic acid = 2 tablet

Family History :

His parent is alive , trait

His brother and sister are known case of SCD.



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Social history :

He is heavy smoker since 15 years , study till intermediate school , live with family .

Systemic Review:

No significant systemic review .

On examination:

The patient conscious, alert, sitting position, oriented to time, place and person, he is cooperative, he looks

ill , and yellowish skin , and normal hair distribution .

In head examination:

Pale conjunctiva, good hygienic mouth .

In neck examination:

Trachea is centralized, No jugular vein congestion, Non palpable lymph node, Normal thyroid and carotid

pulse

In hand examination:

Clubbing nail, pale palms

In lower limb examination:

No edema , No nail changes and the pulse was present

Vital signs:

( 37c oral temp , bp 120 / 75 , pulse 86 beat / min ,with regular rythem and moderate volume , equally in both

hands and normal arterial wall , RR= 20 breath / min . )

D.D :

1- vasoclusive crises . 2- G6PD . 3- Thalassemia .

Discussion points:

participated factor for SCD :

1- Extreme of Temp.

2- Height altitude

3- Stress

4- Hypoxia

5- Infection and smoking



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Complication of SCD :

Vasoclusive crisis

Hemolytic crisis : anemia , jaundice

A plastic crisis : Parvovirus B19 .

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

Case 1: Hepatitis Sunday 27-3-2011 Dr.Surendra

Personal Data :

Abdulaziz ziad is a 43 year old Indian male patient , driver, married with 2 children, living in Al-Jafer

village, non smoker. Chief Complaint :

The patient admitted through ER since 3 days complaint of right upper abdominal pain 1 day prior to his

admission .

History of present illness: The patient is not known to have any chronic medical illness. The patient was in his usual state of health till

1 day prior to his admission when he started to complaining of fever followed by localized right upper

abdominal pain. The pain was sudden in onset, continuous and progressive, dull aching, moderate in

severity aggravated by pressure and relieved by analgesics. The pain associated with vomiting , 3times per

day with food contents , not projectile, and no special taste or smell. No history of dysphagia, diarrhea,

constipation, hematemesis, hematochazia, jaundice, change in color of urine or stool, pruritus.

Past history :

No history of similar attack

No history of past medical or surgical illness.

No history of hospitalization

No history of trauma

No history of blood transfusion.

Drug History :

No history of drug use.

Family History:

His father is 65 year old with HTN and DM, while his mother is 55 year old with paraplegia .

He has 2 sisters and 2 bothers . He is the 3rd

one .

No history of similar condition in the family.

Social History : The patient study till secondary school, work as driver, married with 2 children, living alone in a room with

satisfied socioeconomic status, non-smoker, no history of alcohol consumption, and no history of recent

travel.



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Review of systems:

-CNS : there is a history of mild headache. No history of dizziness, syncope, visual disturbance, hearing

problems, memory and concentration changes. - Respiratory System : No history of chest pain, dyspnea, hemoptysis, cough, and wheezing.

-CVS : No chest pain, syncope, dyspnea, orthopnea, PND, palpitation, lower limb edema . -GIT: there is a history of vomiting. No history of heartburn, dysphagia, odynophagia, hematemesis,

diarrhea, constipation, change in stool color, melena, hematochezia, jaundice. -GUS: No history of flank pain, dysuria, hematuria, polyuria, oliguria, nocturia, urgency, increase

frequency.

-Musculoskeletal: the pain is aggravated by pressure.

Physical Examination:

-General appearance:

A middle age, male patient, well nourished, lying comfortably on bed without pain or respiratory distress ,

cooperative , conscious, alert, oriented to time , place , and persons, connected to i.v cannula, and no any

obvious abnormality.

-Vital Signs :

Pulse : 70 beat/min, regular ,no special character, average volume , radio-radial synchronize ,no radio-

femoral delay, arterial wall is not felt.

B/P : 120/70 mmHg .

R/R : 18 breath/min.

Temperature : 37 C orally

-General Examination : ( head to toe )

Hair : No loss of hair.

Eye : No jaundice, No pallor

Mouth: moderate hygiene with no central cyanosis, no ulcer.

Neck: no palpable lymph nodes, no goiter, intact carotid pulse , Jugular vein is not congested , and trachea

is slightly deviation to the right side.

Upper limp:

-Nails: no pallor, no clubbing.

-Palme: no pallor, no palmer erythema, no muscle wasting, no fine tremor, no flapping tremor.

-Dorsum: no muscle wasting.

-Arm: no muscle wasting, no bruising, no scratching mark .



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Chest examination: no spider naevi, no gynaecomastia, no chest deformity, no scars .

Abdominal: no scars , no abdominal distension , no dilated veins.

Lower limp: Posterior tibial artery is weak and dorsalis pedis pulsation is good . he has a varicose veins in

his left leg.

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

Case 2: Monday 28-3-2011 Dr.Ahmed melhem

Personal history :

Khaled Alsufian is a 26 year old, Saudi male patient , work as transporter in a company in Al-khobar, single,

living in Al-Hofuf , smoker.

Chief complaint :

The patient presented to ER since a week C/O upper right abdominal pain starting 3 days prior to hisadmission .

History of Present illness :

The patient was in his usual state of health till 3 days prior to his admission when he started to pass a black

stool followed by upper right abdominal pain radiates to lower back , left shoulder and left side of neck &

face. The pain was sudden in onset, intermittent and progressive, spasmodic in nature, severe interfere with

his daily activity and awake him from sleep, aggravated by walking and relieved by bending forward . It is

associated with vomiting just started with the pain onset about 3 times daily ,with food contents and yellow

in color, not projectile .Also there was constipation , dysurea with red discoloration of the urine , andanorexia . No history of fever or itching.

Past history :

- No history of past chronic disease .

- History of neurological surgery after RTA since 4 year in his L.arm without complications .

- History of same condition before 3 months but less in severity . relieved by analgesics and fluids in

ER.

- Anemia trait .

- No history of blood transfusion.

Drug history:

Negative drug history

Family history :

- Father died in his 62 year by heart attack .

- Mother alive ,50 year old , with HTN .

- 7 sisters and 2 brothers . he has a twin brother .- No family history of same condition.



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Social history :

- He finished the intermediate school, living in his family house with Satisfied socioeconomic state .

- There is a history of daily alcohol intake for 2 years . and quit the alcohol just before 4 months .No

history of illegal sexual intercourse .

Systemic Review :

-CNS : there is a history of headache and dizziness. No history of syncope, visual disturbance, hearing

problems, memory and concentration changes.

- Respiratory System : there is a history of dyspnea . No history of chest pain, hemoptysis, cough, and

wheezing.

-CVS : No chest pain, syncope, dyspnea, orthopnea, PND, palpitation, lower limb edema . -GIT: there is a history of vomiting. No history of heartburn, dysphagia, odynophagia, hematemesis,

diarrhea, constipation, change in stool color, melena, hematochezia, jaundice. -GUS: there is a history red urine. No history of flank pain, dysuria, polyuria, oliguria, nocturia, urgency,increase frequency.

-Musculoskeletal: Generalized weakness. ----------------------

Case # 5 Leukemia Dr. Surendra Date Sunday 03-04-2011 AD

Personal Data :

Mohammad shams Al-Dine is a 39 Y/O, Bangladesh male patient, work as grocer, married with one child,

living in Salwa, non-smoker.

Chief Complaint :

The patient referred from Hofuf National Clinic 1 day ago, complaining of fever and left upper abdominal

pain 13 days prior to his admission.

History of present illness:

The patient is not known to have any chronic medical illness. The patient was in his usual state of health till

13 days prior to his admission when he started to complaining of fever and left upper abdominal pain. The

fever was gradual in onset, intermittent in nature, associated with sweating but not associated with diurnal

variation, chills and rigor, and shivering. While the pain was sudden in onset, intermittent and progressive,

throbbing in nature, moderate in severity, no aggravating factor , and relive by treatment. The patient give a

history of significant weight loss (loss half of weight according to the patient), diarrhea, joint pain,

muscular pain, and generalized weakness. No history of headache palpitation, projectile vomiting, bleeding

from mouth, nose, rectum, or blood in urine.



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Past history:

The patient is not known to have any chronic medical illness. No history of similar attack. No history of

medical or surgical illnesses. No history of blood transfusion.

Drug history:

-ve drug history. No history of drug allergy.

Family history:

-ve family history

Social history:

The patient study till 5th

class of primary school, work as grocer, living alone in a room, non-smoker. He

was in Saudi Arabia since 6 years.

Systemic review:

CNS: no headache, no dizziness, no loss of consciousness, no loss of sensation.

CVS: no palpitation, no chest pain, no dyspnea , no orthopnea, no PND, no syncope.

GIT: there is a history of diarrhea and upper left abdominal pain. No dysphagia, no abdominal distention,

no projectile vomiting, no constipation.

RS: no cough and sputum, no haemoptysis, no dyspnea, no chest pain.

US: there is a history of red urine after treatment, no dysurea, no polyurea.

MSK: there is a history of joint and muscle pain, no neck rigidity.

Examination:

Positive finding:

Mild jaundice, palor, no hepatomegaly, no spleenomegaly, no lymphadinopathy.

Pulse= 84b/min, regular, …..



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DDx:

1-infection( TB, brucellosis, infective mononucleosis, malaria, enteric fever)

2-Malignancy (less likely to be malignancy because age < 50 year)

3-Unknown etiology.

Discussion Points:

-Other diseases with similar picture to leukemia

-Different character of Fever.

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

Case # 6 FUO Dr. Ahmad Melhem Date Monday 04-04-2011 AD

Personal data:

Adnan Al-mousa, is a 22 years old Saudi male patient living in Al-Foudol in Al-Ahssa , Married with one

offspring studying at the college of technology in AL-Ahssa. Admitted by referral from AL-Jaffer hospital

yesterday.

Chief complaint:

Fever since 16 days prior to admission.

Presenting History:

The patient was in his usual state of health till 16 days prior to admission when he start to feel fatigue,

malaise, headache, accompanied with generalized moderate fever (39.7) that start suddenly with intermittent

character that is progressive, associated with,rigors,sheifering, loss of appetite, nausea & vomiting that is

increasing in number with food content, this fever is not aggravated by any thing but decreased by

antipyretics, the patient was admitted in Al-Jaffer hospital for investigations & recently they discover that he

is DM. after 3 times of visit to Al-jaffer hospital the patient was schedualed as FUO case for investigation &

referred to King Fahad Hospital in AL-HUFFOF. The patient have a significant weight loss in the last

month which is not desireable due to patient excersize. The patient do not have sweating, no polyurea, no

polydypsea, no polyphagia, no joint pain.

Hospital Course:

After discovering that the patient is Diabetic those investigations were scheduled:

-CBC, DLC, ESR, Hb.

-Brucella antigen.

-ECG .

-Urine analysis (creatinine, calcium, potassium, sodium, & urea)



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-Fundoscopic examination of the retina.

-Chest x-ray.

The patient is under insulin & antipyretics treatment.

Past history:

-No previous similar attack

-Newly diagnosed as DM 10 days ago

-No history of chronic illnesses

-No history of transfusion

-Adenoidectomy 7 years ago

Drug History:

-Insulin

-Antipyretics

-No history of drug allergy

Family history:

-Father & Mother are known case of DM.

-No similar attack in the family

-No chronic disease run in the family

Social History:

-Mild to moderate smoker.

-Moderate socioeconomic status.

-Living with his family

-Studying in College of technology

-The patient had a history of exposure to diary products & sheep & cattle.

Systemic Review:



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CNS: Headache, vomiting, no confussion, no loss consciousness, no rigidity, no flaccidity of the muscles.

GI: Vomiting, & nausea, no diarrhea , no conistipation , no abdominal pain, no jaundice, there is

odynophagia

RS: no dyspnea, no chest pain , no cough, neck pain, no hemoptysis, no chest wheezes.

CVS: no palpitation, no edema, no chest pain .

MS: generalized fatigue, no localized redness or pain.

GUS: no urinary symptoms, no sexual problems.

Differential Diagnosis:

-Brucellosis

-Malariasis (No history of transfer to endemic areas)

-URTI (It is likely because the patient refer that he had sore throat)

-Pneumonia (Unlikely because the patient had no respiratory symptoms)

-Infective endocarditis

-Juvenile rheumatoid.

Examination: Unreliable

Diagnosis: Brucellosis.

Discussion:

-Causes of FUO

-Critirea for FUO

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

Case # 7 Syncope Dr.Abdulmajid Al-ballat Tuesday: 05-04-2011

Personal data :

Ali Al-Abbad , 20 y/o , S M patient , single , student in secondary school, liven al-hofuf, admitted to hospital

since 2 days though the ER .

Chief Complaint :

Patient presented to ER a complaint of recurrent sudden loss of consciousness 3 days before admission tohospital.



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Patient is well known G6PD deficiency patient , he was in his usual condition, he was walk in street without

any heavy physical stress until he had sudden loss of consciousness and muscle power for few seconds and

complete recovery without any fatigue or drowsiness , the condition`s frequency is 3 in first day 5 in second

and 2 in last day , there in no aggravating or reliving factor , not associated with stiff neck ,no muscle

contraction , no tongue betting , no chest pain , no fever , no nausea and vomiting , no cough , no heard any

very bad or good news , no sudden change in position , no blurred vision . In the hospital he undergoes

CBC, Chest X ray, Brain CT, ECG and EEG with normal result.

Past history :

He doesn`t have previous similar condition, he has past history for head trauma due to falling down when he

was playing football before 5 years and it associated with loss of vision for 4 hours and recover completely

with rest without went to hospital , there is no other chronic diseases or previous hospitalization , previous

blood transfusion of drug allergy .

Drug history :

There is no history for drug intake.

Family history :

His father is DM and HTN patient and 3 of his brothers G6PD deficiency patients.

Social history :

Patient in teens of age non smoker, lived with his family in private home with good income , student in first

year of secondary school , without any emotional stress .

Systemic review :

No significant systemic review was detected.

Disscusion point:

Syncope

Differentiate it with epilepsy???

Postural hypotension

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

Case # 8 Sunday 17-4-2011 Dr.Surendra

Personal Data :

Kamal Al-Bash is a 49 year old, Saudi male patient, retired from military, married with 11 offspring, living

in Al-Majroaia in Al-Hassa, Shesha smoker.

Chief Complaint :

The patient admitted through ER since 3 days complaint of bloody vomiting and bloody diarrhea followed

by loss of consciousness 1 hour prior to his admission.



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The patient is a known case of IHD, HTN, and stoke. The patient was in his usual state of health till 1 hour

prior to his admission when he started to loss of consciousness. The patient was in the bathroom and give a

history of bloody vomiting and melena a short time prior to the loss of consciousness. The vomiting was

sudden in onset, one time, projectile, large in amount, coffee-ground color, no special smell or taste. No

history of abdominal pain, anorexia, weight loss, heartburn, dysphagia, odynophagia, dyspepsia,

constipation, jaundice. No history of chest pain, palpitation, dyspnea, lower limb swelling, cough,

hemoptysis, fever. No history of epistaxis.

Past history :

The patient is a known case of IHD, HTN, and stoke 4 years ago.

No history of similar attack

No history of past operation.

No history of trauma

No history of blood transfusion.

Drug History :Amlan 5 gm + Teretan 60 mg + lipenthyl 200 mg + ASA 100mg + Tevaten 600mg once daily for 4 years

without complication. The patient compliance with treatment.

Family History:

His father is 70 year old dead from colon cancer, while his mother is 65 year old with HTN, DM, renal and

heart failure. The patient has 5 brother and 6 sister, 9 sons and 2 daughter. No history of similar condition in

the family. No history of other congenital diseases in the family.

Social History :The patient study till intermediate school, retired from military, married with 11 offspring, living in rented

apartment, smoke shesha 5 time/day for 32 years. No history of recent travel.

Review of systems:

-CNS : No history of headache, dizziness, visual disturbance, hearing problems. - Respiratory System : No history of chest pain, dyspnea, hemoptysis, cough, and wheezing.

-CVS : No chest pain, syncope, dyspnea, orthopnea, PND, palpitation, lower limb edema . -GIT: there is a history of hematemesis, and melena. No history of heartburn, dysphagia, odynophagia,

diarrhea, constipation, change in stool color, hematochezia, jaundice. -GUS: No history of flank pain, dysuria, hematuria, polyuria, oliguria, nocturia, urgency, increase

frequency.

-Musculoskeletal: No history joint pain, stiffness, swelling, restriction of movement. From history the diagnosis: upper GI bleeding



Old male patient, lying comfortable in bed, no pain, no respiratory distress, conscious, alert, oriented to

time, place and person, connected to iv line, drop upper eyelid (ptosis).-Vital sign:



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Pulse = 76 b/min, regular, no special character, average volume , radio-radial synchronize ,no radio-femoral

delay, arterial wall is not felt.

Temperature: .......

RR= 22 breath/min

Blood pressure = 110/80 mmHg

-General examination:

Hair : No loss of hair.

Eye : Jaundice, No pallor, ptosis

Mouth: bad hygiene (dental carries) with no central cyanosis, no ulcer.

Neck: no palpable lymph nodes, no goiter, intact carotid pulse , Jugular vein is not congested , and trachea

is slightly deviation to the right side.

Upper limp:

-Nails: pallor, no clubbing.

-Palme: pallor, no palmer erythema, no muscle wasting, no fine tremor, no flapping tremor.

-Dorsum: no muscle wasting.

-Arm: no muscle wasting, no bruising, no scratching mark .

Chest examination: no spider naevi, no gynaecomastia, no chest deformity, no scars .

Abdominal: no scars , no abdominal distension , no dilated veins.

Lower limp: Posterior tibial and dorsalis pedis artery pulsation is intact.

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

Case # 9 DVT Monday 18-4-2011 Dr.Ahmed melhem

Personal data:

Mohammed Hider, 37 Y/O, S M patient, married with 3 offspring, driver, lived in Al-Omran, admitted

before 3 days.

Chief Complaint :

Patient presented to ER complaining of left leg pain 2 days before admission to hospital.


Patient was in his usual condition until felt sudden pain in the left leg under the knee coniferous,

progressive reach maximum in 1 day, severe, not radiating, increase by movement without reliving factor,

not radiation not associated with chest pain, no fever, no shortness of breath, no nausea or vomiting, no

diarrhea, no urine change, no abdominal pain, no loss of sensation or loss of consciousness.

Past history:



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Patient has similar condition in the right leg before 1 year, and hospitalized for 20 days and treated by

medication only. There is no history for other occupation depends on long time setting, no history of blood

disease or liver diseases. There is no past history for HTN, DM IHD or hyperlipidemia. No previous history

for other hospitalization or blood transfusion, no history of drug allergy.

Drug history:

Patient takes warfarine 1tablets/day with good compliance since 1 year.

Family history:

His uncle affect by same illness, his father dead due to cardiac attack associated with HTN in age 60, his

mother affected by DM and HTN.

Social history:

Patient is non smoker, with accepted education with low income, lived in his private home, without

emotional stress.

Systemic review:

No significant systemic review is detected.

Examination:

The patient refuse.

Discussion points:

-DVT & Pulmonary Embolism : Diagnosis & Management

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

Case-10 Sunday 24-4-2011 Dr.Naushad Abid

Personal Data :

Fahad Abdulkrem Al-Gonam, is an 80 year old Saudi male patient, living in Al-Moalmen in Al-Hasa, work

as sheep keeper, married with 3 offspring, non-smoker Chief Complaint :

The patient admitted through ER today, complaining of bilateral lower chest pain 10 days prior to his

admission.


The patient is a known case of CHF, and renal failure. The patient was in his usual state of health till 10 days

prior to his admission when he started to complaining of bilateral lower chest pain radiated to the back. The

pain was sudden in onset, continuous and progressive, dull aching, severe that prevent the patient from

sleep, aggravated by movement and cough, no reliving factors. The pain is associated with fever, nausea,

vomiting 4 time/day, food content, not projectile, constipation for 8 days, loss of appetite, polyurea in a term

of 5 time/day, dysurea and hesitancy , no change in color, no urine incontinence.

Past history:

-No history of similar attach



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-HTN since 1 year

-Past surgery: the patient give a history of 11 surgery including cardiac, eye, orthopdic surgery

-Positive history of blood transfusion

Drug history:......

Family history:.....

Social history:......

Systemic review: .....

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

Monday 25-4-2011 Dr.Rabah

Case-10

Personal Data :

Ahmed Alnofeay is a Saudi male patient 26y/o , single , working in a hospital , living in al-hassa , known

case of SCD , non smoker

Admitted before one week through ER

Chief Complaint :

admitted due to pain in left shoulder and arm for 2 days


The patient diagnosed with SCD when he was 4 y/o , come for the first time by back pain , the frequency of admissions is 3 times /year , all admissions in ward , usually the P.F are cold exposure and decreased sleep ,

the patient is taking folic acid 1tab./day

The patient was in his usual state of health until he started to develop the pain , it was gradual in onset ,

progressive in course , not radiated , sever , dull in nature , aggravated by cold weather and physical activity

associated with sleep disturbance , no history of nausea ,vomiting , fever, anorexia, weight loss , sweating ,

diarrhea , constipation

Hospital course:

There was pain in first day but the condition in general relieved with morphine

Past history :

There was history of similar attack , many admissions for the same cause

There was no history of hospitalization for another cause

There was no history of surgical operations

There was no history of blood transfusion\

There was no history of allergy

Drug History :



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Folic acid 1tab./day , he use it from the time of diagnosis

Analgesics when needed

Family History:

The parents are relatives

His mother and father are carriers

2 of his brothers are carriers

Social History :

the patient is took a good education , he graduated from nursing college , non smoker , he is in a moderate

socioeconomic state , the SCD not affect his studying and his work

Review of systems:

C.N.S : NAD

R.S : NAD

C.V.S : NAD

GIT :NAD

GUS.NAD

MSS: NAD


-General impression :

26 y/o male patient lying down on the bed looks sick , conscious , oriented to time place and person , in

average height and weight , connected to I.V canula with yellowish discoloration of the skin

-Vital signs :

Pulse : 88 b/m

BP : 130/75

RR : 22 b/m

Temperature : 37.1 C

-General examination :

Positive finding :

1- Pallor conjunctiva 2- Yellowish discoloration of skin and sclera



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3- Pale hands

-Abdominal examination :

Palpable spleen

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

15 Tuesday 26-4-2011 Dr.Mohamed Rashad

Case-11

Personal data :Abdulateef Ganem is 45 year old Saudi male patient , married with 6 off springs . living in althulathia ,

works as a teacher . admitted throw OPC since 3 days .

Chief complaint :

He reverted to KFH OPC Complaining of Dizziness , polyurea , Weight loss since 2 weeks .

History of present illness :The patient was a known case of HTN since 8 years . he started to have a dizziness which is aggravated

by work and decreased by rest , and he noticed weight loss by losing about 11 in 2 weeks . also he

complained of poly depsia and poly urea which is about 5\day which increase in amount and nocturea ,

with no dysurea or changing in colour .He feels fatigued and tiredness in most of times . +ve polyphagia

,peripheral numbness . lately he noticed a deterioration of vision . there was no fever . He wanted to

teaching hospital in al khobar dx as diabetic then he reverted to KFH .

Past History :

-He is HTN since 8 years .-No anaemia .

-No History of blood transfusion .

-History of surgery in his left hand for lipoma .

-Endoscopy before 8 months , for suspected peptic ulcer .

-Cardiac cathetarization before 18 months to exclude HTN complications.

-Epilepsy .

Drug History :Tegretol 2*200mg\day .

Coversyl 10 mg \ day .

Adalat 2 daily .No allergy for specific drug .

Family History :Mother was hypertensive and died during delivery .

Father has , HTN , DM type 2 .

He has 9 brothers and sisters ,2 brothers and 1 sister has DM type 2 .

Social History :Satisfied socioeconomic state .

Not smoker

Not alcoholic



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Systemic Review:

No significant systemic review .



The patient is in his 40s laying comfortable on bed without pain or respiratory distress, cooperative ,conscious ,alert, oriented to time place persons . connected to IV canula in his R-hand .

-Vital signs :


femoral delay, arterial wall is not felt.

B/P : 120/80 mmHg .

R/R : 25 breath/min.

Temperature : 37 C axillary


Head and neck :-Eye : no jaundice ,no pallor .

-Mouth : white coated tounge , no central cyanosis , moderate hygiene state .

-Neck : Acanthosis nigrecans , L- submandebular L.N enlargement .

Upper Limbs :-No pallor , no peripheral cyanosis.

-No clubbing .

-Scar in R-hand on the rest joint for lipoma surgery .

Lower limbs :-Dryness , hyperpigmentaion in both foot .

-Below knee pitting oedema in both legs.

- Weak Palpable dorsalis pedis and posterior tebial artery.

-Diminution of sensation.

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

Wednesday 27-4-2011 Dr.Mohamed Salah

Case-12

Personal Data :

Hesham Ibraheem Albuhaimed , is a 32 year old, Saudi male patient , married , no offspring ,living in

Althulathia in Al-Hasa , governmental employ,admitted before three days . Chief Complaint :

He presented to ER complaining of Decrease in the amount of urine since 4 days .


The patient was in his usual state till he started to have an oligourea , to less than 200 cc \day with decrease

in frequency to less than 2times \ day , dysurea , orange urine color ,with weak stream , no urgency , No

abdominal or back pain , no fever .nausea and vomiting 1\day with small amount and normal food contents .



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+ve dizziness and headache .

Past history :

No hx of similar attack .

No hx of chronic illness .

No hx of blood transfusion .

No past surgeries .

Drug History :

No chronic drug use

No allergy for specific drug .

Family History:

Father HTN,DM type 2 76 year old alive

Mother HTN ,DM type 2 56 year old alive

5 brothers

No hx of similar attack .

Social History :

Satisfied socioeconomic state .

Not smoker .



The patient is in his 40s laying comfortable on bed, cooperative , conscious ,alert oriented to time place

persons . connected to IV canula in his R-hand .

-Vital Signs :


femoral delay, arterial wall is not felt.BP : 140/90 mmHg .

RR : 18 breath/min.

Temperature : 36 C axillary


Head and neck :

- Eye : no jaundice ,no pallor .

- Mouth : white coated tounge , no central cyanosis , moderate hygiene state .

- Neck : Acanthosis nigrecans , L- sub mandebular L.N enlargement .

Upper Limbs :- No pallor , no peripheral cyanosis , normal temp .

- No clubbing .

Lower limbs:

Palbable dorsalis pedis and posterior tebial .

No edema .

Discussion points:

DM diagnostic criteria

Causes of polyuria & polydipsia other than diabetes



21

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

---

Extra reading

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 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 & thechest.



22

-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:



23

-History of drugs that cause hemolysis:

Extravascular Hemolysis

-Alpha-methyldopa & levodopa

-Diclofenac

-Ibuprofen

-Interferon alfa

-Mefenamic acid

-Penicillin(Carbenicillin,ampicillin,& methicillin)

-Procainamide

Intravascular Hemolysis:

-Acetaminophen

-Chlorpromazine

-Fluorouracil

-Hydrochlorothiazide

-Hydralazine

-Insulin

-Isoniazid

-Melphalan

-Phenacetin

-Probenacid

-Quinidine & Quinine (treatment for malaria).

-Rifampin

-Streptomycin

-Sulfonamides

-Sulindac

-Tetracycline

History of addicting analgesic drugs as morphine.

History of folic acid tablet which increase RBCs production as compensatory mechanism.

Family history:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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



25

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.



26

-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.



27

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 Staphylococcusaureus 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/Opioid

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

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

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



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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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



28

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.

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

Stroke:

Sudden onset of a neurologic deficit from a vascular mechanism

-85% are ischemic.

-15% are primary hemorrhages.

Stroke should be differentiated with TIA:

An ischemic deficit that resolves rapidly is termed as transient ischemic attack (TIA).

24 h is a commonly used boundary between TIA and stroke.

Stroke is the leading cause of neurologic disability in adults.

200,000 deaths annually in the United States.

Pathophysiology:

Ischemic stroke is most often due to embolic occlusion of large cerebral vessels; source of emboli may be

heart, aortic arch, or other arterial lesions such as the carotid arteries. Small, deep ischemic lesions are most

often related to intrinsic small-vessel disease (lacunar strokes). Low-flow strokes are seen with severe

proximal stenosis and inadequate collaterals challenged by systemic hypotensive episodes.

Hemorrhages most frequently result from rupture of aneurysms or small vessels within brain tissue.

Variability in stroke recovery is influenced by collateral vessels, blood pressure, and the specific site and

mechanism of vessel occlusion; if blood flow is restored prior to significant cell death, the pt may experience

only transient symptoms, i.e., a TIA.

Clinical features:

Ischemic stroke: Abrupt and dramatic onset of focal neurologic symptoms is typical of ischemic stroke.common ex:

Transient monocular blindness (amaurosis fugax) is a particular form of TIA due to retinal ischemia; pts describe a

shade descending over the visual field .

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/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

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

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


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

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

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

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



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

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

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

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

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



29

Intracranial hemorrhage: Vomiting and drowsiness occur in some cases, and headache in about one-half. Signs and

symptoms are often not confined to a single vascular territory. Etiologies are diverse but hypertension-related is the

most common. Common locations:

• Putamen: Contralateral hemiparesis.

• Thalamus: Hemiparesis with prominent sensory deficit.

• Pons: Quadriplegic, ―pinpoint‖ pupils, impaired horizontal eye movements.

• Cerebellum: Headache, vomiting, gait ataxia.

Management:

Stroke needs to be distinguished from potential mimics, including seizure, migraine, tumor, and metabolic

derangements. After initial stabilization, an emergency noncontrast head CT scan is necessary to differentiate

ischemic from hemorrhagic stroke. With large ischemic strok es, CT abnormalities are usually evident within the first

few hours, but small infarcts can be difficult to visualize by CT. CT or MR angiography (CTA/MRA) and perfusion

may help reveal vascular occlusions and tissue at risk for infarction. Diffusion-weighted MRI has a high sensitivity for

identifying ischemic stroke even minutes after onset.

Acute ischemic stroke:

Treatments designed to reverse or lessen tissue infarction include: (1) medical support, (2) thrombolysis and

endovascular techniques, (3) antiplatelet agents, (4) anticoagulation, and (5) neuroprotection.

(1) medical support: Immediate goal is to optimize perfusion in ischemic state, Blood pressure should never be

lowered precipitously (exacerbates the underlying ischemia), Intravascular volume should be maintained with isotonic

fluids, Osmotic therapy with mannitol may be necessary to control edema.

(2) thrombolysis and endovascular techniques: Ischemic deficits of <3 h duration, with no hemorrhage by CT criteria,

may benefit from thrombolytic therap y with IV recombinant tissue plasminogen activator see the figure



30

(3) antiplatelet agents: Aspirin (up to 325 mg/d) is safe and has a small but definite benefit in acute stroke.

(4) anticoagulation: Trials do not support the use of heparin or other anticoagulants for pts with acute stroke

although some physicians continue to use this treatment in specific situations such as TIA in the setting of atrial fibrillation.

(5) neuroprotection: Hypothermia is effective in coma following cardiac arrest but has not been adequately studied in

pts with stroke. Other neuroprotective agents have shown no benefit in human trials despite promising animal data.

Acute intracranial hemorrhage:

Noncontrast head CT will confirm diagnosis. Rapidly identify and correct any coagulopathy. prognosis is determined

by volume and location of hematoma. Stuporous or comatose patients generally are treated presumptively for elevated

ICP. Neurosurgical consultation should be sought for possible urgent evacuation of cerebellar hematoma; in other

locations, data do not support surgical intervention. Treatment for edema and mass effect with osmotic agents may be

necessary; glucocorticoids not helpful.

Although this management is not specific for the cause evaluation of the patient is important to know the cause of

stroke for prevention of reccurence & decreasing the risk factors. See the figure for causes of ischemic stroke.



31

See the figure for risk factors of stroke



32

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



33

-----------

Hypoglycemia:

Glucose is an obligate metabolic fuel for the brain. Hypoglycemia should be considered in any patient

with:

confusion

altered level of consciousness

seizures.

The laboratory diagnosis of hypoglycemia is usually defined as a plasma glucose level <2.5 – 2.8 mmol/L

(<45 – 50 mg/dL)



34

Absolute level for symptoms of hypoglycemia is case or patient dependent so, Whipple’s triad should be

present:

(1) Symptoms consistent with hypoglycemia

(2) A low plasma glucose concentration measured by precise method (not a glucose monitor)

(3) Relief of symptoms after the plasma glucose level is raised.

Etiology:

Hypoglycemia occurs most commonly as a result of treating patients with diabetes mellitus.

Additional factors include:

1. Drugs: insulin, insulin secretagogues (especially chlorpropamide, repaglinide, nateglinide), alcohol,

high doses of salicylates, sulfonamides, pentamidine, quinine, quinolones

2 . Critical illness: hepatic, renal, or cardiac failure; sepsis; prolonged starvation

3 . Hormone deficiencies: adrenal insufficiency, hypopituitarism

4. Insulinoma: pancreatic β cell tumor, β cell hyperplasia (a.k.a. nesidioblastosis; congenital or after

gastric or bariatric surgery)

5. Others: Non- β cell tumors (large mesenchymal or epithelial tumors producing IGF-II, other non-

pancreatic tumors), insulin or insulin receptor antibodies, inherited enzymatic defects

Clinical features:

See the previous slide named hypoglycemia…

Diagnosis:

Urgent treatment is often necessary in patients with suspected hypoglycemia. Nevertheless, blood

should be drawn at the time of symptoms, whenever possible before the administration of glucose, to allow

documentation of the glucose level. If the glucose level is low and the cause of hypoglycemia is unknown,

additional assays should be performed on blood obtained at the time of a low plasma glucose.



35

These should include insulin, C-peptide, sulfonylurea levels, cortisol, and ethanol.

Interpretation of fasting test results is shown:



36

Management:

Acute therapy of hypoglycemia requires administration of oral glucose or 25 g of a 50% solution IV

followed by a constant infusion of 5 or 10% dextrose if parenteral therapy is necessary. Hypoglycemia

from sulfonylureas is often prolonged , requiring treatment and monitoring for 24 h or more. Subcutaneous

or intramuscular glucagon can be used in diabetics. Prevention of recurrent hypoglycemia requires

treatment of the underlying cause of hypoglycemia, including discontinuation or dose reduction of

offending drugs, treatment of critical illnesses, replacement of hormonal deficiencies, and surgery of

insulinomas or other tumors. Treatment of other forms of hypoglycemia is dietary, with avoidance of fasting

and ingestion of frequent small meals.

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

Chest Pain:

There is little correlation between the severity of chest pain and the seriousness of its cause but the range of

causes that cause chest discomfort are shown in the table:



37

Serious causes:

It is useful to characterize the chest pain as (1) new, acute, and ongoing; (2) recurrent, episodic; and (3)

persistent, sometimes for days.

Myocardial Ischemia: Angina Pectoris Substernal pressure, squeezing, constriction, with radiation typicallyto left arm; usually on exertion, especially after meals or with emotional arousal. Characteristically relieved

by rest and nitroglycerin.

Acute Myocardial Infarction: Similar to angina but usually more severe, of longer duration (≥30 min), and

not immediately relieved by rest or nitroglycerin. S3 and S4 common.

Pulmonary Embolism: May be substernal or lateral, pleuritic in nature, and associated with hemoptysis,

tachycardia, and hypoxemia.

Aortic Dissection: Very severe, in center of chest, a sharp ―ripping‖ quality, radiates to back, not affected by

changes in position. May be associated with weak or absent peripheral pulses.

Mediastinal Emphysema Sharp, intense, localized to substernal region; often associated with audible

crepitus.

Acute Pericarditis : Usually steady, crushing, substernal; often has pleuritic component aggravated by

cough, deep inspiration, supine position, and relieved by sitting upright; one-, two-, or three-component

pericardial friction rub often audible.

Pleurisy Due to inflammation; less commonly tumor and pneumothorax.Usually unilateral, knifelike,

superficial, aggravated by cough and respiration.



38

Less serious causes:

Costochondral Pain In anterior chest, usually sharply localized, may be brief and darting or a persistent dull

ache. Can be reproduced by pressure on costochondral and/or chondrosternal junctions. In Tietze’ssyndrome (costochondritis), joints are swollen, red, and tender.



39

Chest Wall Pain Due to strain of muscles or ligaments from excessive exercise or rib fracture from trauma;

accompanied by local tenderness.

Esophageal Pain Deep thoracic discomfort; may be accompanied by dysphagia and regurgitation.

Emotional Disorders Prolonged ache or dartlike, brief, flashing pain; associated with fatigue, emotional

strain.

Other causes:

(1) Cervical disk; (2) osteoarthritis of cervical or thoracic spine; (3) abdominal disorders: peptic ulcer, hiatus

hernia, pancreatitis, biliary colic; (4) tracheo-bronchitis, pneumonia; (5) diseases of the breast

(inflammation, tumor); (6) intercostal neuritis (herpes zoster).

Approuch to a patient with chest pain:

A meticulous history of the behavior of pain, what precipitates it and what relieves it, aids diagnosis of

recurrent chest pain. Next figure presents clues to diagnosis and workup of acute, life-threatening chest pain.

An ECG is key to the initial evaluation to rapidly distinguish patients with acute ST elevation MI, who

typically warrant immediate reperfusion therapies.

Abdominal Pain:

Numerous causes, ranging from acute, life-threatening emergencies to chronic functional disease and

disorders of several organ systems, can generate abdominal pain. Evaluation of acute pain requires rapid

assessment of likely causes and early initiation of appropriate therapy. List of common causes of abdominalpain is shown:



40

Approuch to a patient with abdominal pain:

HISTORY:

History is of critical diagnostic importance. Physical exam may be unrevealing or misleading, and laboratory and

radiologic exams delayed or unhelpful.

CHARACTERISTIC FEATURES OF ABDOMINAL PAIN

Duration and Pattern: clues to nature and severity, although acute abdominal crisis may occasionally present

insidiously or on a background of chronic pain.

Type and location provide a rough guide to nature of disease. Visceralpain (due to distention of a hollow viscus)

localizes poorly and is often perceived in the midline. Intestinal pain tends to be crampy; when originating proximal



41

to the ileocecal valve, it usually localizes above and around the umbilicus. Pain of colonic origin is perceived in the

hypogastrium and lower quadrants. Pain from biliary or ureteral obstruction often causes pts towrithe in

discomfort. Somatic pain (due to peritoneal inflammation) is usually sharper and more precisely localized to the

diseased region (e.g., acute appendicitis; capsular distention of liver, kidney, or spleen), exacerbated bymovement,

causing pts to remain still . Pattern of radiation may be helpful: right shoulder (hepatobiliary origin), left shoulder

(splenic), midback (pan-creatic), flank (proximal urinary tract), groin (genital or distal urinary tract).

Factors That Precipitate or Relieve Pain:

Ask about its relationship to eating (e.g., upper GI, biliary, pancreatic, ischemic bowel disease), defecation

(colorectal), urination (genitourinary or colorectal), respiratory (pleuropulmonary, hepatobiliary), position

(pancreatic, gastroesophageal reflux, musculoskeletal), menstrual cycle/menarche (tuboovarian, endometrial,

including endometriosis), exertion (coronary/intestinal ischemia, musculoskeletal), medication or specific foods

(motility disorders, food intolerance, gastroesophageal reflux, porphyria, adrenal insufficiency, ketoacidosis, toxins),

and stress (motility disorders, nonulcer dyspepsia, irritable bowel syndrome).

Associated Symptoms

Look for fevers/chills (infection, inflammatory disease, infarction), weight loss (tumor, inflammatory disease,

malabsorption, ischemia), nausea/vomiting (o bstruction, infection, inflammatory disease, metabolic disease),

dysphagia/odynophagia (esophageal), early satiety (gastric), hematemesis (esophageal, gastric, duodenal), constipation

(colorectal, perianal, genitourinary), jaundice (hepatobiliary, hemolytic), diarrhea (inflammatory disease, infection,

malabsorption, secretory tumors, ischemia, genitourinary), dysuria/hematuria/vaginal or penile discharge

(genitourinary), hematochezia (colorectal or, rarely, urinary), skin/joint/eye disorders (inflammatory disease, bacterial

or viral infection).

Predisposing Factors

Inquire about family history (inflammatory disease, tumors, pancreatitis), hypertension and atherosclerotic disease

(ischemia), diabetes mellitus (motility disorders, ketoacidosis), connective tissue disease (motility disorders, serositis),

depression (motility disorders, tumors), smoking (ischemia), recent smoking cessation (inflammatory disease), ethanol

use (motility disorders, hepatobiliary, pancreatic, gastritis, peptic ulcer disease).

PHYSICAL EXAMINATION:

Evaluate abdomen for prior trauma or surgery, current trauma; abdominal distention, fluid, or air; direct, rebound,

and referred tenderness; liver and spleen size; masses, bruits, altered bowel sounds, hernias , arterial masses. Rectal

examination assesses presence and location of tenderness, masses, blood (gross or occult). Pelvic examination in

women is essential. General examination: evaluate for evidence of hemodynamic instability, acid-base disturbances,

nutritional deficiency, coagulopathy, arterial occlusive disease, stigmata of liver disease, cardiac dysfunction,

lymphadenopathy, and skin lesions.



42

ROUTINE LABORATORY AND RADIOLOGIC STUDIES

Choices depend on clinical setting (esp. severity of pain, rapidity of onset) and may include complete blood count,

serum electrolytes, coagulation parameters, serum glucose, and biochemical tests of liver, kidney, and pancreatic

function; chest x-ray to determine the presence of diseases involving heart, lung, mediastinum, and pleura;

electrocardiogram is helpful to exclude referred pain from cardiac disease; plain abdominal radiographs to evaluate

bowel displacement, intestinal distention, fluid and gas pattern, free peritoneal air, liver size, and abdominalcalcifications (e.g., gallstones, renal stones, chronic pancreatitis).

SPECIAL STUDIES

These include abdominal ultrasonography (to visualize biliary ducts, gallbladder, liver, pancreas, and kidneys); CT to

identify masses, abscesses, evidence of inflammation (bowel wall thickening, mesenteric ―stranding,‖

lymphadenopathy), aortic aneurysm; barium contrast radiographs (barium swallow, upper GI series, small-bowel

follow-through, barium enema); upper GI endoscopy, sigmoidoscopy, or colonoscopy; cholangiography (endoscopic,

percutaneous, or via MRI), angiography (direct or via CT or MRI), and radionuclide scanning. In selected cases,

percutaneous biopsy, laparoscopy, and exploratory laparotomy may be required.

Note that in acute catastrophic abdominal pain associated with trauma FAST & CT is done to consider serious

bleeding tendency.



43

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

FUO

Definitions: Temperature: Normal body temperature is maintained (≤37.2°C/ 98.9°F in the morning and

≤37.7°C/99.9°F in the evening) because the hypothalamic thermoregulatory center balances excess heat production

from metabolic activity in muscle and liver with heat dissipation from the skin and lungs.

Fever: an elevation of normal body temperature in conjunction with an increase in the hypothalamic set point.Infectious causes are common.

Fever Of Unknown Origin (FUO):

Fever of unknown origin (FUO) was defined by Petersdorf and Beeson in 1961 as (1) temperatures of >38.3°C

(>101°F) on several occasions; (2) a duration of fever of >3 weeks; and (3) failure to reach a diagnosis despite 1

week of inpatient investigation. While this classification has stood for more than 30 years, Durack and Street have

proposed a new system for classification of FUO: (1) classic FUO; (2) nosocomial FUO; (3) neutropenic FUO; and

(4) FUO associated with HIV infection.

1. Classic FUO: three outpt visits or 3 days in the hospital without elucidation of a cause of fever; or 1 week of unproductive intelligent and invasive ambulatory investigation, temperatures >38.3°C (>101°F) on several occasions,

and duration of fever for >3 weeks

2. Nosocomial FUO: at least 3 days of investigation and 2 days of culture incubation failing to elucidate a cause of

fever in a hospitalized pt with temperatures >38.3°C (>101°F) on several occasions and no infection on admission

3. Neutropenic FUO: at least 3 days of investigation and 2 days of culture incubation failing to elucidate a cause of

fever in a pt with temperatures >38.3°C (>101°F) on several occasions whose neutrophil count is <500/μL or is

expected to fall to that level within 1 – 2 days

4. HIV-associated FUO: failure of appropriate investigation to reveal a cause of fever in an HIV-infected pt withtemperatures >38.3°C (>101°F) on several occasions over a period of >4 weeks for outpts and >3 days for hospitalized

pts

Hyperpyrexia: temperatures >41.5°C (>106.7°F) that can occur with severe infections but more commonly occur

with CNS hemorrhages.

Etiology: Most fevers are associated with self-limited infections (usually viral) and have causes that are easily

identified.

Classic FUO: As the duration of fever increases, the likelihood of an infectious etiology decreases. Next

shows the percentage of different etiologies of Classic FUO in adults:

Other causes to consider:

1. Infection – e.g., extrapulmonary tuberculosis; EBV, CMV, or HIV infection; occult abscesses; endocarditis; fungal

disease



44

2. Neoplasm – e.g., lymphoma and hematologic malignancies, hepatoma, renal cell carcinoma

3. Miscellaneous noninfectious inflammatory diseases

a. Systemic rheumatologic disease or vasculitis –e.g., Still’s disease, lupus erythematosus

b. Granulomatous disease – e.g., granulomatous hepatitis, sarcoidosis, Crohn’s disease

c. Miscellaneous diseases – e.g., pulmonary embolism, hereditary fever syndromes, drug fever, factitious fevers

Comments on the diagram: In a series of 347 patients referred to the National Institutes of Health from 1961 to 1977,

only 6% had an infection. A significant proportion (9%) had factitious fevers— i.e., fevers due either to falseelevations of temperature or to self-induced disease. A substantial number of these factitious cases were in young

women in the health professions. It is worth noting that 8% of the patients with prolonged fevers (some of whom had

completely normal liver function studies) had granulomatous hepatitis, and 6% had adult Still’s disease. After

prolonged investigation, 19% of cases still had no specific diagnosis. A total of 27% of patients had no actual fever

during inpatient observation or had an exaggerated circadian temperature rhythm without chills, elevated pulse, or

other abnormalities.

Nosocomial FUO

Infectious – e.g., infected foreign bodies or catheters, Clostridium difficile colitis, sinusitis

Noninfectious – e.g., drug fever, pulmonary embolism

Neutropenic FUO: Neutropenic pts are susceptible to focal bacterial and fungal infections, bacteremic

infections, perianal infections, and catheter-associated infections. More than 50 – 60% of pts with febrile

neutropenia are infected, and 20% are bacteremic.

HIV-associated FUO: More than 80% of pts are infected, but drug fever and lymphoma are also possible

etiologies.

More than 200 etiologies can be considered for classic FUO but the most important:



45

Pathogenesis :The hypothalamic set point increases. The pt feels cold as a result of the peripheral vasoconstriction

and shivering that are needed to raise body temperature to a new set point. Peripheral vasodilation and sweating

commence when the set point is lowered again by resolution or treatment of the fever.

Fever caused by:

• Exogenous pyrogens (e.g., lipopolysaccharide endotoxin)

• Endogenous pyrogens [e.g., interleukin (IL) 1, tumor necrosis factor] induced by exogenous pyrogens

• Prostaglandin E2 (in CNS, raises hypothalamic set point; in peripheral tissues, causes myalgias and arthralgias)



46

Approuch to a patient with FUO:

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. Presyncopal symptoms vary in duration and may

increase in severity until loss of consciousness occurs, or they may resolve prior to loss of consciousness if the

cerebral ischemia is corrected. The differentiation of syncope from seizure is an important, sometimes difficult,

diagnostic problem.

Pathophysiology:

Under normal circumstances systemic blood pressure is regulated by a complex process that includes themusculature, venous valves, autonomic nervous system, and renin-aldosterone-angiotensin system. Knowledge of

these processes is important to understanding the pathophysiology of syncope. Approximately three-fourths of the



47

systemic blood volume is contained in the venous bed, and any interference in venous return may lead to a reduction

in cardiac output . Cerebral blood flow can be maintained if cardiac output and systemic arterial vasoconstriction

compensate, but when these adjustments fail, hypotension with resultant cerebral underperfusion to less than half of

normal results in syncope. Normally, the pooling of blood in the lower parts of the body is prevented by (1) pressor

reflexes that induce constriction of peripheral arterioles and venules, (2) reflex acceleration of the heart by means

of aortic and carotid reflexes, and (3) improvement of venous return to the heart by activity of the muscles of the

limbs. Tilting a normal person upright on a tilt table causes some blood to accumulate in the lower limbs and

diminishes cardiac output slightly; this may be followed by a slight transitory fall in systolic blood pressure. However,in a patient with defective vasomotor reflexes, upright tilt may produce an abrupt and sustained fall in blood pressure,

precipitating a faint.

Causes:

Transiently decreased cerebral blood flow is usually due to one of three general mechanisms: disorders of

vascular tone or blood volume, cardiovascular disorders including obstructive lesions and cardiac

arrhythmias, or cerebrovascular disease. Not infrequently,however, the cause of syncope is multifactorial.

Neurocardiogenic (Vasovagal and Vasodepressor) Syncope The common faint, experienced by

normal persons, accounts for approximately half of all episodes of syncope. It is frequently recurrent and may be provoked by hot or crowded environment, alcohol, fatigue, pain, hunger, prolonged

standing, or stressful situations.

Postural (Orthostatic) Hypotension Sudden rising from a recumbent position or standing quietly are

precipitating circumstances. Cause of syncope in 30% of elderly; polypharmacy with

antihypertensive or antidepressant drugs often a contributor; physical deconditioning may also play

a role. Also occurs with autonomic nervous system disorders, either peripheral (diabetes, nutritional,

or amyloid polyneuropathy) or central (multiple system atrophy, Parkinson’s disease). Some cases

are idiopathic.



48

Approach to the patient with syncope:



49

The cause of syncope may be apparent only at the time of the event , leaving few, if any, clues when the pt is seen by

the physician. First consider serious underlying etiologies; among these are massive internal hemorrhage or

myocardial infarction, which may be painless, and cardiac arrhythmias. In elderly persons, a sudden faint withoutobvious cause should raise the question of complete heart block or a tachyarrhythmia. Loss of consciousness in

particular situations, such as during venipuncture or micturition, suggests a benign abnormality of vascular tone. The

position of the pt at the time of the syncopal episode is important; syncope in the supine position is unlikely to be

vasovagal and suggests an arrhythmia or a seizure. Medications must be considered, including nonprescription drugs

or health store supplements,with particular attention to recent changes. Symptoms of impotence, bowel and bladder

difficulties, disturbed sweating, or an abnormal neurologic exam, suggest a primary neurogenic cause.


Anxiety Attacks Frequently resembles presyncope although the symptoms are not accompanied by facial pallor and

are not relieved by recumbency. Attacks can often be reproduced by hyperventilation and have associated symptomsof panic attacks such as a feeling of impending doom, air hunger, palpitations, and tingling of the fingers and perioral

region.

Seizures The differential diagnosis is often between syncope and a generalized seizure. Syncope is more likely if the

event was provoked by acute pain or anxiety or occurred immediately after arising from a lying or sitting position.

Seizures are typically not related to posture. Pts with syncope often describe a stereotyped transition from

consciousness to unconsciousness that develops over a few seconds. Seizures occur either very abruptly without a

transition or are preceded by premonitory symptoms such as an epigastric rising sensation, perception of odd odors, or

racing thoughts. Pallor is seen during syncope; cyanosis is usually seen during a seizure. The duration of

unconsciousness is usually very brief (i.e., seconds) in syncope and more prolonged (i.e., >5 min) in a seizure. Injury

from falling and incontinence are common in seizure, rare in syncope. Headache and drowsiness, which with mental

confusion are the usual sequelae of a seizure, do not follow a syncopal attack.



50

Hypoglycemia Severe hypoglycemia is usually due to a serious disease. The glucose level at the time of a spell is

diagnostic.

Hysterical Fainting The attack is usually unattended by an outward display of anxiety. Lack of change in pulse and

blood pressure or color of the skin distinguishes it from a vasodepressor faint.

Management:

Therapy is determined by the underlying cause. Pts with vasovagal syncope should be instructed to avoid

situations or stimuli that provoke attacks. Episodes associated with intravascular volume depletion may be prevented

by salt and fluid preloading prior to provocative events.

Drug therapy may be necessary for resistant vasovagal syncope. β-Adrenergic antagonists (metoprolol 25 – 50 mg

twice daily; atenolol 25 – 50 m/d; or nadolol 10 – 20 mg twice daily; all starting doses).

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

Pancreatitis:

Acute Pancreatitis:

The pathologic spectrum of acute pancreatitis varies from interstitial pancreatitis, which is usually a mild

and self-limited disorder, to necrotizing pancreatitis, in which the degree of pancreatic necrosis correlates

with the severity of the attack and its systemic manifestations.

Etiology: most common causes are Gallstone (30-60%) & alcohol (15-30%) others:



51

Clinical Features : Can vary from mild abdominal pain to shock . Common symptoms:

(1) Steady, boring midepigastric pain radiating to the back that is frequently increased in the supine position.

(2) Nausea, vomiting.

Physical exam:

1) Low-grade fever, tachycardia, hypotension.



52

2) erythematous skin nodules due to subcutaneous fat necrosis; (3) basilar rales, pleural effusion (often on

the left)

3) abdominal tenderness and rigidity, diminished bowel sounds, palpable upper abdominal mass

4) Cullen’s sign: blue discoloration in the periumbilical area due to hemoperitoneum

5) Turner’s sign: blue-red-purple or green- brown discoloration of the flanks due to tissue catabolism of

hemoglobin.

Laboratory

1. Serum amylase: Large elevations (>3 × normal) virtually assure the diagnosis if salivary gland disease and

intestinal perforation/infarction are excluded. However, normal serum amylase does not exclude the diagnosis of acute

pancreatitis, and the degree of elevation does not predict severity of pancreatitis. Amylase levels typically return to

normal in 48 – 72 h.

2. Urinary amylase – creatinine clearance ratio: no more sensitive or specific than blood amylase levels.

3. Serum lipase level : increases in parallel with amylase level and measurement of both tests increases the diagnostic

yield.

4. Other tests: Hypocalcemia occurs in ~25% of patients. Leukocytosis (15,000 –20,000/μL) occurs frequently.

Hypertriglyceridemia occurs in 15 – 20% of cases and can cause a spuriously normal serum amylase level.

Hyperglycemia is common. Serum bilirubin, alkaline phosphatase, and aspartate aminotransferase can be transiently

elevated. Hypoalbuminemia and marked elevations of serum lactic dehydrogenase (LDH) are associated with an

increased mortality rate. Hypoxemia is present in 25% of patients. Arterial pH < 7.32 may spuriously elevate serum

amylase.

Imaging

1. Abdominal radiographs are abnormal in 30 – 50% of patients but are not specific for pancreatitis. Common

findings include total or partial ileus (―sentinel loop‖) and the ―colon cut-off sign,‖ which results from isolated

distention of the transverse colon. Useful for excluding diagnoses such as intestinal perforation with free air.

2. Ultrasound often fails to visualize the pancreas because of overlying intestinal gas but may detect gallstones,

pseudocysts, mass lesions, or edema or enlargement of the pancreas.

3. CT can confirm diagnosis of pancreatitis (edematous pancreas) and is useful for predicting and identifying

late complications. Contrast-enhanced dynamic CT is indicated for clinical deterioration, the presence of risk

factors that adversely affect survival or other features of serious illness.



53

Differential Diagnosis: Intestinal perforation (especially peptic ulcer), cholecystitis, acute intestinal obstruction,

mesenteric ischemia, renal colic, myocardial ischemia, aortic dissection, connective tissue disorders, pneumonia, and

diabetic ketoacidosis.

Complications It is important to identify patients who are at risk of poor outcome. Fulminant pancreatitis requires

aggressive fluid support and meticulous management . Mortality is largely due to infection.

Systemic: Shock, GI bleeding, common duct obstruction, ileus, splenic infarction or rupture, DIC,

subcutaneous fat necrosis, ARDS, pleural effusion, acute renal failure, sudden blindness.

Local

1 . Sterile or infected pancreatic necrosis — necrosis may become secondarily infected in 40 – 60% of patients,

typically within 1 – 2 weeks after the onset of pancreatitis. Most frequent organisms: gram-negative bacteria of

alimentary origin, but intraabdominal Candida infection increasing in frequency . Necrosis can be visualized

by contrast-enhanced dynamic CT , with infection diagnosed by CT-guided needle aspiration. Laparotomy

with removal of necrotic material and adequate drainage should be considered for patients with sterile acute

necrotic pancreatitis, if patient continues to deteriorate despite conventional therapy. Infected pancreatic

necrosis requires aggressive surgical debridement and antibiotics.

2 . Pancreatic pseudocysts develop over 1 – 4 weeks in 15% of patients. Abdominal pain is the usual complaint,and a tender upper abdominal mass may be present. Can be detected by abdominal ultrasound or CT . In

patients who are stable and uncomplicated , treatment is supportive; pseudocysts that are >5cm in diameter and

persist for >6 weeks should be considered for drainage. In patients with an expanding pseudocyst or one

complicated by hemorrhage, rupture, or abscess, surgery should be performed.

3. Pancreatic abscess — ill-defined liquid collection of pus that evolves over 4 – 6 weeks. Can be treated

surgically or in selected cases by percutaneous drainage.

4. Pancreatic ascites and pleural effusions are usually due to disruption of the main pancreatic duct.

Treatment involves nasogastric suction and parenteral alimentation for 2 – 3 weeks. If medical management

fails, pancreatography followed by surgery should be performed .



54

Chronic Pancreatitis:

Chronic pancreatitis may occur as recurrent episodes of acute inflammation superimposed upon a previously injured

pancreas or as chronic damage with pain and malabsorption.

Etiology: Chronic alcoholism is most frequent cause of pancreatic exocrine insufficiency in U.S. adults; in 25% of

adults, etiology is unknown. Other causes:



55

Symptoms and Signs Pain is cardinal symptom. Weight loss, steatorrhea, and other signs and symptoms of

malabsorption common.

Physical exam often unremarkable.

Laboratory No specific laboratory test for chronic pancreatitis. Serum amylase and lipase levels are often normal.

Serum bilirubin and alkaline phosphatase may be elevated. Steatorrhea (fecal fat concentration ≥ 9.5%) late in the

course. The bentiromide test, a simple, effective test of pancreatic exocrine function, may be helpful. D-Xylose

urinary excretion test is usually normal. Impaired glucose tolerance is present in >50% of pts. Secretin stimulation test

is a relatively sensitive test for pancreatic exocrine deficiency.

Imaging: Plain films of the abdomen reveal pancreatic calcifications in 30 – 60%. Ultrasound and CT scans may show

dilation of the pancreatic duct. ERCP and endoscopic ultrasound (EUS) provide information about the mainpancreatic and smaller ducts.

Differential Diagnosis: Important to distinguish from pancreatic carcinoma; may require radiographically guided

biopsy.

Complications Vitamin B12 malabsorption in 40% of alcohol-induced and all cystic fibrosis cases. Impaired glucose

tolerance. Nondiabetic retinopathy due to vitamin A and/or zinc deficiency. GI bleeding, icterus, effusions,

subcutaneous fat necrosis, and bone pain occasionally occur. Increased risk for pancreatic carcinoma. Narcotic

addiction common.

Recommendation for treatment:

Aiming to control pain and malabsorption. Intermittent attacks treated like acute pancreatitis. Alcohol and large, fatty

meals must be avoided. Narcotics for severe pain, but subsequent addiction is common. Patients unable to maintain



56

adequate hydration should be hospitalized, while those with milder symptoms can be managed on an ambulatory

basis. Surgery may control pain if there is a ductal stricture. Subtotal pancreatectomy may also control pain but at the

cost of exocrine insufficiency and diabetes. Malabsorption is managed with a low-fat diet and pancreatic enzyme

replacement. Because pancreatic enzymes are inactivated by acid, agents that reduce acid production (e.g.,

omeprazole or sodium bicarbonate) may improve their efficacy (but should not be given with enteric-coated

preparations). Insulin may be necessary to control serum glucose.

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

Diabetes mellitus:

Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia.

Several distinct types of DM exist and are caused by a complex interaction of genetics and environmental factors.

Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion,

decreased glucose utilization, and increased glucose production. In the United States, DM is the leading cause of end-

stage renal disease (ESRD), nontraumatic lower extremity amputations, and adult blindness. It also predisposes to

cardiovascular diseases. With an increasing incidence worldwide, DM will be a leading cause of morbidity and

mortality for the foreseeable future.

Etiology:

DM is classified on the basis of the pathogenic process that leads to hyperglycemia, in to two broad categories type 1

and type 2. Both types of diabetes are preceded by a phase of abnormal glucose homeostasis as the pathogenic

processes progresses. Type 1 diabetes is the result of complete or near-total insulin deficiency. Type 2 DM is a

heterogeneous group of disorders characterized by variable degrees of insulin resistance, impaired insulin

secretion, and increased glucose production. Type 2 DM is preceded by a period of abnormal glucose homeostasis

classified as impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). Other etiologies for DM include

specific genetic defects in insulin secretion or action, metabolic abnormalities that impair insulin secretion,

mitochondrial abnormalities, and a host of conditions that impair glucose tolerance. DM can result from pancreatic

exocrine disease when the majority of pancreatic islets are destroyed. Hormones that antagonize insulin action canalso lead to DM. Maturity onset diabetes of the young (MODY) is a subtype of DM characterized by autosomal

dominant inheritance, early onset of hyperglycemia (usually <25 years), and impairment in insulin secretion.

Mutations in the insulin receptor cause a group of rare disorders characterized by severe insulin resistance.

GESTATIONAL DIABETES MELLITUS (GDM)

Glucose intolerance may develop during pregnancy. Insulin resistance is related to the metabolic changes of late

pregnancy, and the increased insulin requirements may lead to IGT.



57

Epidemiology:



58

The worldwide prevalence of DM has risen dramatically over the past two decades, from an estimated 30 million

cases in 1985 to 177 million in 2000. Based on current trends, >360 million individuals will have diabetes by the year

2030 . Although the prevalence of both type 1 and type 2 DM is increasing worldwide, the prevalence of type 2 DM

is rising much more rapidly because of increasing obesity and reduced activity levels as countries become more

industrialized. This is true in most countries, and 6 of the top 10 countries with the highest rates are in Asia.

Diagnosis:

The National Diabetes Data Group and World Health Organization have issued diagnostic criteria for DM:

Glucose tolerance is classified into three categories based on the FPG: (1) FPG < 5.6 mmol/L (100 mg/dL) is

considered normal; (2) FPG = 5.6 – 6.9 mmol/L (100 –125 mg/dL) is defined as IFG; and (3) FPG *7.0 mmol/L (126



59

mg/dL) warrants the diagnosis of DM . Based on the OGTT , IGT is defined as plasma glucose levels between 7.8

and 11.1 mmol/L (140 and 199 mg/dL) and diabetes is defined as a glucose > 11.1 mmol/L (200 mg/dL) 2 h after a

75-g oral glucose load . Individuals with IFG and/or IGT, recently designated pre-diabetes by the American Diabetes

Association (ADA), are at substantial risk for developing type 2 DM (25 – 40% risk over the next 5 years) and have an

increased risk of cardiovascular disease.

A random plasma glucose concentration *11.1 mmol/L (200 mg/dL) accompanied by classic symptoms of

DM (polyuria, polydipsia, weight loss) is sufficient for the diagnosis of DM.

Screening:

FPG as a screening test for type 2 DM is recommended

The ADA recommends screening all individuals >45 years every 3 years and screening individuals at an

earlier age if they are overweight [body mass index (BMI) > 25 km/m2] and have one additional risk factor

for diabetes

Clinical Features:

Common presenting symptoms of DM include polyuria, polydipsia, weight loss, fatigue, weakness, blurred vision,

frequent superficial infections, and poor wound healing. A complete medical history should be obtained with special

emphasis on weight, exercise, smoking, ethanol use, family history of DM, and risk factors for cardiovascular disease.

In a patient with established DM, assessment of prior diabetes care, HbA1c levels, self-monitoring blood glucose

results, frequency of hypoglycemia, and pt’s knowledge about DM should be obtained. Special attention should be

given on physical exam to retinal exam, orthostatic bp, foot exam (including vibratory sensation and monofilament

testing), peripheral pulses, and insulin injection sites. Acute complications of DM that may be seen on presentation

include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state

Complications:



60

Management:

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



61

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

Syncope


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 pt s 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.



62


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 isused 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.



63

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.

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

-----


-Increased cardiothoracic ratio in chest x-ray film:

Cardiomegaly

Pericardial effusion

Multivalvular heart disease

-Polyuria, & polydipsia:

Diabetes mellitus

Diabetes insipidus (Central & nephrogenic type) ( lack of ADH or its action).

UTIs

Psychotic disorder (Psychotic related polydipsia)

-Epigastric pain:



64

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

Feces

Flatus(Air or gases)

Fat (Obesity)

Fluid

-Clubbing:

Cardiac : - Cyanotic congenital HD

- Endocarditis

Pulmonary: - Bronchogenic carcinoma.

- Suppurative lung syndromes

(empyema, abscess, bronchiectasis, cystic fibrosis).

- Fibrosing alveolitis.



65

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

-Pitting edema:

1. Cardiac (CHF)

2. Hepatic: cirrhosis

3. Renal: nephrotic syndrome

4. Hypoproteinemia

N.B: - In bed ridden patients: look at sacrum - In children: Look at facial edema

- Non pitting edema:

1. Lymphatic obstruction(Filariasis)

2. Pretibial myxedema (Hypothyroidism mainly in children)

3. Lymphedema(Common in female after breast cancer surgery with radiation)

4. Lymphadenitis

- Differential Diagnosis of cough:

1- Acute cough (Less than 3 weeks).

2-Chronic cough (More than 3 weeks).



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Acute cough:

-URTI (Upper Respiratory Tract Infections).

-Bacterial Infections causing pneumonia.

-Whooping cough in children.

-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%:

Notes:

Peptic ulcer due to:

-NSAIDs.

-Hb PYLORI causing (gastric ulcer, gastric cancer, MALToma , or gastritis).

Esophageal varices.

Gastric erosions.



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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.

-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).



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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)



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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:

Neutrophils 45-75%

Leukocyte 20-40%

Basophil ˂1%

Eosinophil 5%

Monocyte 2-4%

Charcot's triad :

biliary colic

Intermittent jaundice

swinging pyrexia - fever and chills



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1g/L = 5.6 mmol/L

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

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Assignment

Causes of suprasternal pulsations:

Physiological:

High riding aortic arch

After exertion or exercise

In hyperdynamic state

Pathological:

Aneurysm of the aorta

Dissecting aneurysm

Atherosclerosis, either in carotid or aorta.

Hypertension

Retrosternal goiter

Causes of Polyuria, Polydipsia, with normal glycemic control:

-Diabetes insipidus

-Diuretics

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

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



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



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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



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internal medicine (ii) 2011 logbook

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