جامعة بابل | University of Babylon



Problem solving

اعداد فرع الطب الباطني

ا د علاء حسين حيدر الحلي

رئيس الفرع

2014-2015

The main Objectives in these cases :

There are typically four distinct steps objective to the systematic solving of clinical problems:

1. Making the diagnosis

2. Assessing the severity of the disease (stage)

3. Rendering a treatment based on the stage of the disease 4. Following the patient’s response to the treatment

Also in the objective of analysis of cases we should :

1. Understand the natural history of the problem.

2. Know the types of differential diagnosis & causes of the problem

3. Be familiar with the complications .

4. Be familiar with indications for management and for prophylactic medications

5 . Understand the patho physiology of the problem

Problem 1

Diabetic ketoacidosis

Objectives : 1 . To know the common acute complication in diabetes

2 . To learn pathophysiology & proper management

3 . To know the management and complication of this condition

Case history

A 19-year-old man is brought to the emergency department (ED) with diffuse abdominal pain, vomiting, and altered level of consciousness. The patient’s symptoms began several days ago, when he complained of acute URT infection His symptoms at that time included profound fatigue, nausea, mild abdominal discomfort and some urinary frequency. Today he was found in bed moaning but otherwise unresponsive. His past medical history is unremarkable, and he is currently taking no medications. O/E , the patient appears pale and ill. His temperature is 36.0°C (96.8°F), pulse rate is 140 beats per minute, blood pressure is 80/40 mm Hg, and the respiratory rate is 40 breaths per minute. His head and neck examination shows dry mucous membranes and sunken eyes; there is an unusual odor to his breath. The lungs are clear bilaterally with increased rate and depth of respiration. The cardiac examination reveals tachycardia, no murmurs ,rubs, or gallops. The abdomen is diffusely tender to palpation, with hypoactive bowel sounds and involuntary guarding. The rectal examination is normal. Skin is cool and dry with decreased turgor. On neurologic examination, the patient

in discomfort and localizes pain but does not speak coherently. Laboratory studies: pcv 25% the leukocyte count is 16,000 cells/uL, and the hemoglobin and hematocrit levels are normal. Electrolytes reveal a sodium of 124 mEq/L, potassium 3.4 mEq/L, chloride 98 mEq/L, and bicarbonate 6 mEq/L. B.urea and creatinine are mildly elevated. The serum glucose is 740 mg/dL (41.1 mmol/L). The serum amylase, bilirubin, AST, ALT, and alkaline phosphatase are within normal limits. A 12-lead ECG shows sinus tachycardia. His CXR is normal.

1.What's your provisional diagnosis?

2 . Explain the underlying pathophysiological mechanisms for development of this condition.

3.What are the risk factors which can produce such complication?

4.What are the complications of such condition?

5.What are the outlines of management?

6.How can you explain his low PCV?

7.How can you explain his abdominal pain?

8. After you star your management plan .you reduced his RBS within 1 hour to 200 mg/d. the patient develop headache .confusion. what's your explanation?

9.How can you correct this new complication?

10.few hours later your patient became well…what are the advises you would like to give him on discharge?

11 . Explain the underlying pathophysiological mechanisms for development of this condition.

Problem 2

Stroke

Objectives

1. Recognize the clinical findings of an acute stroke.

2. Understand the diagnostic and therapeutic approach to suspected stroke patients.

3. Know the most common mechanisms for ischemic stroke: carotid stenosis, cardio embolism, and small-vessel disease.

4. Understand the evaluation of a stroke patient with the goal of secondary prevention.

Case History

A 59-year-old man with a history of hypertension presents to the emergency department(ED)in MTH with right-sided paralysis and aphasia. The patient’s wife states he was in his normal state of health until one hour ago, when she heard a thud in the bathroom and walked in to find him collapsed on the floor. She immediately called emergency medical services, who transported the patient to your ED. His fingerstick blood sugar was 108 mg/dL. On arrival in the ED, the patient is placed on monitors and an IV is established. His temperature is 36.8 oC (98.2°F), blood pressure is 170/95 mm Hg, heart rate is 86 beats per minute, and respiratory rate is 20 breaths per minute. The patient has a noticeable left-gaze preference and is verbally unresponsive, although he follows simple commands such as raising his left thumb. He has a normal neurologic examination on the left, but on the right has a facial droop, no motor activity, decreased deep tendon reflexes (DTRs), and no sensation to light-touch.

1 . What is the most likely diagnosis?

2.What are the risk factors for this condition

3 . How do you explain decrease tendon reflexes?

4 . Is cardiac examination valid and why?

5 . What is the most appropriate next step?

6 . What is the best therapy? Discuss the types of treatments of this patient

7 . What is the anatomical localization of the lesion ? and how could you assess the prognosis ?

8 . Mention the important factors in the social life of this patient

Problem 3

Childhood Arthritis & its sequel

Case history

A 33-year-old unmarried man was admitted to MTH with a three months history of increasing oedema . In childhood he suffered a severe and deforming arthritis , requiring numerous hospital admissions . For 5 days he had noticed a reduction in his urinary output . He had been taking prednisolone 7.5 mg daily for the last 10 years . O/E he looked unwell and was grossly oedematous with pitting oedema in the ankles , legs & thighs with marked sacral oedema . His upper limbs were thin and he appeared wasted despite oedema . JVP not raised BP 120/60 lying and 90/50 standing . His feet were cold . Pulse 80 regular . Dullness at both lung bases . There was wide spread & advanced deforming arthritis with sublaxation of the joints of both hands . Feet , ankles , elbows and knees were also affected , but to lesser extent . Although tender and painful on movement , the joints were not hot or inflamed . The abdomen distended with ascitis . The spleen just palpable & liver was 2 cm BCM :

Investigations

Hb 7.9 gm/dl , ESR 100 mm / First Hour, WBC 8.4 X 10ʼ MCV81fl

K 4.3 mmol/L , Na 133mmol/L , HCO3 22 mmol/L, Chloride 95mmol/L

Urea 14mmol/L , Creatinine 80 µmol/L, Ca+2 1.9mmol/L,P 1.1mmol/L

Total Protein 55g/L , albumin 17g/L , LFT Normal

Urine Protein ++++ ; Blood +

1 . What is the differential diagnosis of this problem ?

2 . Consider the important investigations & what important tests that should be done in regards to proteinuria ?

3 . what treatment you consider in this patient ?

4 . What are the consequences of this condition & their management ?

Problem 4

Inflammatory bowel disease

Objective

1. Understand the initial evaluation and management of IBD.

2. Know the indications for management.

3. Be able to evaluate patients with chronic diarrhea and understand pathophysiologic mechanisms.

4. Understand the diagnosis, management, and complications of Crohn's diseases .

Case history

A 34-year-old pharmacologist presented with a history of diarrhea and abdominal pain . For some years he had noticed some looseness of the bowels , but he became acutely ill six weeks before presentation , where he was opening his bowels up to six times a day ; at times the stool contained mucus and occasionally blood , there is a colicky abdominal pain in the mid abdomen associated with mild distension . The patient has anorexia and mild weight loss about 4Kg . As he has mild fever , his GP doctor prescribed a five day course of amoxicillin but with no benefit . He has no recent travel abroad . O/E the patient appeared pale and ill , Tempt. 37.4°C , abdomen is diffusely tender , mildly distended , there is some fullness at the right lower abdomen . PR examination demonstrate perianal skin tags , painful anal fissure with positive blood . Sigmoidoscopy revealed hyperaemic rectal mucosa with loss of vascular pattern . Screening test results

Blood picture : Hb 11 g/dl , ESR 66 mm/First Hr, WBC 10000 , MCV 60fl , Platelets 520X 10’/ L ,K 3.6 mm/L , Na 140 mm/L , Chloride 101 mmol/L , HCO3 28 mmol/L , Blood urea 4.4mmol/L , Creatinine 87ᵤmol /L, Calcium 2.26 mmol/L , serum Phosphate 0.75 mmol/L Total protein 66 g/L , Albumin 28g/ L , LFT normal Urine examination is normal , Faecal calprotectin positive

1 . What is the differential diagnosis ?

2 . What further investigations would you consider ?

3 . How could you manage this patient , discussing the role of biologic therapy ?

4 . Mention four renal complications in this patient

5 . In future the patient might need surgical treatment , would you like to mention the indication in each differential diagnosis .

Problem 5

Acute appendicitis as acute presentation of Crohn's disease

You are working in the emergency department (ED) of a 15-bed rural hospital without U/S or CT scan capabilities, and a 25-year-old, previously healthy, woman presents for evaluation of abdominal pain. The patient describes her pain as having been present for the past 3 days. The pain is described as constant, exacerbated by movements, and associated with subjective fevers and chills. She denies any recent changes in bowel habits, urinary symptoms, or menses. Her last menstrual period was 6 days ago. The physical examination reveals temperature of 38.4°C (101.1°F),pulse rate of 110 beats per minute, blood pressure of 110/70 mm Hg, and respiratory rate of 18 breaths per minute. Her skin is nonicteric. Cardiopulmonary examination is unremarkable. The abdomen is mildly distended and tender in both right and left lower quadrants. Involuntary guarding and localized rebound tenderness are noted in the right lower quadrant. The pelvic examination reveals no cervical discharge; cervical motion tenderness and right adnexal tenderness are present. The rectal examination reveals no masses or tenderness.

Laboratory studies reveal:

white blood cell count (WBC) of 14,000 cells/mm3, a normal hemoglobin, and a normal hematocrit. The urinalysis reveals 3 to 5 WBC/high-power field (HPF), few bacteria, and trace ketones.

1 . What are the most likely diagnoses?

2 . How can you confirm the diagnosis?

3 . You send your patient to a surgeon and the surgeon on laprotomy he found oedematous small intestine and red oedematous caecum he tried not do further surgery and he manage to close the abdomen . Why ?

Problem 6

Bleeding esophageal varices

Objectives

1. Learn the differences in presentations and outcomes between upper and lower GI bleeding.

2. Understand the priorities, evaluations, and management of patients with GI hemorrhage.

3. Know the causes of UGITB.

4. Learn the complications of chronic hepatitis, such as cirrhosis and portal Hypertension & ALD .

5. Understand the pathophysiology of oedema & of ascites.

6. Know how to prevent further bleeding .

Case history

You are a house officer working in the emergency unit of MTH when a man presents at 5 am with moderately sever vomiting blood ( hematemesis ) . At first glance to the patient you noticed that the patient is confused with impaired mental status with yellowish skin and sclera . O/E you do indeed noticed some facial plethora , florid spider angiomata on the face and upper chest , in addition bilateral Dupuytren's contracture in both hands , fullness at both parotid regions and gynecomastia , his abdomen is distended and there is bilateral pedal oedema . BP 95/55 mmHg , PR 110BPM , Tempt 38°C also wasting of the proximal limbs muscles seen but there is no focal neurological signs . Urgent investigations show : Hb 11g/dl , WBC count 25X 10’/L , MCV 107fl , B. urea 7.9mmol/L , Bilirubin 420micromol/L , AST 125U/L , ALT 102 U/L , bile pigment +ve in his urine.Serum K 3.2 mmol/L , Serum Na 132 mmol/L.

1 . What is the first steps in the management of this patient ?

2 . According to clinical presentation of this patient what do you think the aetiology of his UGIT bleeding & jaundice ? And what further important investigations you order ?

3 . Why the patient has low serum potassium ?

4 . What is the pathophysiology of his pedal oedema and abdominal distension ?

5 . Give three explanations for high temperature in this patient

6 . Mention how you could prevent further upper GIT bleeding in this patient in future

Problem 7

CNS infection

Objectives

1. Understand the diagnostic and therapeutic approach to bacterial meningitis including when to obtain neuroimaging, when to perform a lumbar puncture, and what empiric therapies to initiate.

2. Recognize the clinical presentation of acute bacterial meningitis.

Case history

An otherwise healthy 19-year-old man is brought to the emergency department(ED) by his roommate who states that he has “not been acting right” for the past 24 hours. Per the roommate, the patient had complained of a headache 2 days prior to arrival, and has been progressively somnolent and confused since then. The patient has no past medical history and does not take any medications. His roommate states that the patient is a college student who does not use any illegal drugs and. Review of systems is positive for headache and altered mental status as stated above as well as a tactile fever for the past 2 days. Additional review of systems is unobtainable as the patient is unable to answer any questions. On physical examination the patient is noted to be febrile

to 38.5°C (101°F) orally, with a heart rate of 120 beats per minute, blood pressure of 114/69, and a respiratory rate of 20 breaths per minute. His oxygen saturation is 98% on room air. The head and neck examination are significant for dry mucous membranes and nuchal rigidity. His cardiopulmonary examination is within normal limits with the exception of tachycardia. The abdomen is soft and nontender. His skin is noted to be warm and well perfused without any rash. The neurologic examination is significant for an altered mental status with a Glasgow coma score (GCS) of 10 (eyes open to voice, patient moans to painful stimuli [2], and localizes painful stimuli . The motor examination is symmetric, and the patient appears to be sensate in all extremities. His reflexes are 2+ bilaterally throughout the upper and lower extremities with down going toes. Laboratory studies reveal:

a leukocytosis of 24,000/mm3 with a left shift, and are otherwise unremarkable. A CT scan is completed which shows no mass, shift, bleed, or edema.

1 . What is the most likely diagnosis?

2 . What is the next diagnostic study of choice?

3 . What is the most appropriate treatment of this condition?

4 . How could we prevent this condition ?

Problem 8

Poisoning

Objectives

1. Recognize the clinical manifestations of Paracetamol intoxication.

2. Know the treatment for acute Paracetamol intoxication.

Case history

An 18-year-old woman is brought by her mother to the emergency department (ED)about 30 minutes after she took “a bunch” of Paracetamol . The patient states she was upset with her brother who grounded her after she came home late from a party with her female friends ; she swallowed half a bottle of extra-strength Paracetamol in order to “make them feel sorry.” She is tearful, says she was “stupid,” and denies any true desire to hurt herself or anyone else. She has no other complaints and denies any past attempts to hurt herself. On examination, her blood pressure is 105/60 mm Hg, heart rate is 100 beats per minute, and respiratory rate is 24 breaths per minute (crying).

Her pupils are equal and reactive bilaterally. Her sclera is clear, and her mucous membranes are moist. The lungs are clear and the heart sounds are regular. The abdominal examination is benign with normal bowel sounds. She is awake and alert without any focal neurologic deficits.

1 . What is the most appropriate next step?

2 . What are the potential complications of this ingestion?

3 . What is the mechanism of acetaminophen toxicity?

4 . She was discharged home after 24 hour stay but unfortunately she returned 3 days later with jaundice , abdominal discomfort and confusion , what happen to her and how you are going to manage her ?

5 . If the patient develops life threatening liver failure how could you manage her ?

Problem 9

Sickle cell crises

Objectives

1. Recognize the clinical signs and symptoms of sickle cell crisis and its associated complications.

2. Understand the diagnosis and treatment of acute chest syndrome.

3. Understand the treatment of pain crises in patients with sickle cell disease.

A 30-year-old woman with a history of sickle cell disease presents to the emergency department (ED) complaining of chest pain for 2 days. She states that the pain is right sided, worse with inspiration, and is more severe than her usual “crisis pain.” She has subjective fevers, mild shortness of breath, and a productive cough. She denies vomiting, hemoptysis, or lower extremity swelling. Her last pain crisis was 3 months ago. She usually takes acetaminophen and hydrocodone for pain control during her crises, however, neither have been able to provide sufficient relief during this episode. On physical examination, her temperature is 38.3 (C (101(F), blood pressure is 130 /70 mm Hg, heart rate is 98 beats per minute, respiratory rate is 22 breaths per minute, and oxygen saturation is 94% on room air. Lung examination reveals crackles in the right lower lung field. She does not have any jugular venous distension, calf tenderness, or lower extremity edema.

1 . What is the most concerning issue regarding this patient?

2 . What is the initial management?

3 . Enumerate five other type of crisis in this condition ?

4 . Is there any long term treatment for this condition ?

5 . How would you approach the question of genetic counseling for someone with sickle disease ?

6 . What is Hb SC disease ?

7 . Mention the characteristic bone changes in this patient's X-ray

Problem 10

Cold Fingers in connective tissue diseases

Case history

A secretary aged 50 complained that her fingertips had become so painful that she could no longer type . Since childhood her fingers had blanched on exposure to cold and she described the the typical color changes of Raynaud's phenome non. During the year prior to presentation her fingers had remained persistently cold & purplish in colour and had become swollen . Painful ulcers had developed on tips of several fingers . She had history of heart burn attributed to occasional difficulty in swallowing . Heart burn relived by using excess pillows .

O/E appeared well . The skin of her hands cyanosed and swollen. There was pulp atrophy and terminal pitting ulceration of several fingers . The skin of the dorsum of the hands is also thickened . Her facial appearance was normal as was the remainder of physical examination . BP 130/75 mmHg .

Investigations :

ESR 30 mm/1st hr CBP MCV normal Renal LFT, Electrolytes normal Total Protein 78g/L , Albumin 40 g/L , Ca & P normal

Urine analysis normal

1 . What is the differential diagnosis ? Give 3 D Dx.

2 . What further investigations do you consider to reach a diagnosis ?

3 . How would you manage this patient ?

4 . What form of liver disease this patient might develop in future ?

5 . During the course of follow up of the patient , he present with nausea , vomiting , abdominal discomfort and marked abdominal distension . What is this complication ?

Problem 11

Headache due to CNS disorders

Objectives

1. Learn to differentiate emergent, urgent, and less urgent causes of headache.

2. Understand the treatment of various types of headache.

Case history

A 50-year-old woman presents with a severe headache of abrupt onset of 10 hours duration. The pain is diffuse, throbbing, and worsened when she went outside into the sunlight. She denies any recent fever, neck pain, numbness, weakness, vomiting, and any change in vision. She was concerned because she has never had a headache as strong as this before. Her past medical and family histories are unremarkable. She does not take any medications, does not smoke,

On examination, her temperature is 36.9°C (98.4°F), blood pressure 140/70 mm Hg, heart rate 88 beats per minute, and respiratory rate of 16 breaths per minute. She is not in any acute distress but appears to be mildly uncomfortable. Her pupils are equal and reactive bilaterally. There is no evidence of papilledema on fundoscopic examination. Movement of her neck causes her some increased discomfort. Her neurological examination is normal, including cranial nerves, strength, light touch sensation, deep-tendon reflexes, and finger-to-nose.

The computed tomography (CT) scan of her head is normal.

1 . What is the most likely diagnosis?

2 . What is the next diagnostic step?

3 . What are the three possible causes of this condition ?

4 . This lady during follow up you discover to have bilaterally enlarged kidneys and you decided to refer her to a neurosurgeon Why ?

Problem 12

Upper vs Lower UTI infection

Objectives

1. Recognize the clinical signs and symptoms of UT Is.

2. Understand the diagnosis and treatment of UTIs.

3. Understand the spectrum of UTIs and their variable treatment.

Case history

A 24-year-old woman presents to the emergency department (ED) with complaints of flank pain and fever for the last 1 to 2 days. She describes feeling pain with urination over the previous week. She is currently feeling febrile and nauseated, but has not vomited. The pain in her right flank is a dull, constant, non-radiating ache that she rates as 5/10 for pain. She took 600 mg of ibuprofen last night to help her sleep, but this morning the pain persisted so she came into the ED for evaluation. She reports that she is sexually active and her last menstrual period was 1 week ago. She denies any vaginal discharge or abdominal pain. Her vital signs include a temperature of 38.3°C (101°F), heart rate of 112 beats per minute, respiratory rate of 15 breaths per minute, and blood pressure of 119/68 mm Hg. Her examination is significant for tenderness to palpation on her right costovertebral angle .

1 . What is the most likely diagnosis?

2 . What is the best treatment?

3 . mention the important risk factors for development of this condition

4 . Mention the appropriate investigation of this patient in order to prevent future recurrence of this condition

Problem 13

Anemia

Background

As in any other clinical scenario, the investigation of this patient hinges on an accurate history and examination. In terms of causes of anemia, the most common by far is iron deficiency and the likelihood of this as an explanation should be fairly clear by paying close attention to diet history, enquiring for gastrointestinal symptoms and obtaining gynecological history in females. A lot of information can be gleaned from the full blood count result, the key parameter being red blood cell (RBC) size. In terms of etiology, the classification of anemia (Figure 1.1) is best approached based around the MCV. Clearly in uncomplicated iron deficiency, patients will have a microcytic hypochromic blood

film, and it is debatable whether such patients need referral to a specialist hematology clinic. The common causes of iron deficiency are related to occult gastrointestinal blood loss or menorrhagia and the appropriate management of such cases lies with the appropriate specialty. However, this case presents one of the commonest diagnostic dilemmas – the patient with a normocytic anemia in whom hematinic levels are normal and there is no morphological evidence of bone marrow failure or hemolysis. It is a common problem, the presence of which increases with age. Often patients are asymptomatic, the condition being discovered by ‘routine’ laboratory tests. Although all causes of microcytic and

macrocytic anemia can on occasion present with a normocytic anemia, often in this situation one is dealing with a decreased production of normal-sized RBCs, as occurs in the anemia of chronic disease (ACD) but also in aplastic anemia. A similar appearance can occur in an uncompensated increase in plasma volume, for example in pregnancy or

fluid overload. Anemia of chronic disease is thought to be the most common form of normocytic anemia and probably the second most common form of anemia worldwide after iron-deficiency anemia. It is often a disease of exclusion and the pathogenesis is usually multifactorial and thought to be related to hypo activity of the bone marrow with relative inadequate production of erythropoietin (EPO) or a poor response to EPO.

There is probably also reduced RBC survival. The clinical history and examination will often identify the underlying chronic disorder, which includes a wide range of inflammatory

conditions including arthritis, infections and malignant disease. Iron studies usually reveal a decreased serum iron level but with a decreased transferrin level (rather than a raised level as seen in iron deficiency) and a normal or elevated serum ferritin.

[pic]

GiFAbs, growth inhibitory factor antibodies; Hb, hemoglobin; thal, thalassemia; WCC, white cell count.

Treatment

Treatment of this condition is troublesome. The adage usually is that attention be given to the underlying disorder. In the very specific area of ACD associated with renal disease, which is more appropriately classified as a separate cause of a normocytic anemia, there is a relative underproduction of EPO and EPO therapy can transform the quality of life of these individuals. However, there are several reports in the literature of the effectiveness of EPO in ACD not associated with renal disease, with some reports suggesting that routine iron supplementation may enhance the response.

Conclusion

The possible causes of anemia in a middle-aged lady are many but iron deficiency remains the most important one to exclude and appropriately investigate (particularly for occult gastrointestinal neoplasm) if this is suspected, despite the presence of any coincidental inflammatory disorder. Anemia of chronic disease is often a diagnosis of exclusion,

but it is a very frequent clinical problem with no clear-cut way forward in terms of management other than addressing the underlying clinical problem. However, the likelihood of pharmacological intervention in the future (other than with EPO therapy) may be greater with the developing understanding of the mechanisms involved.

Objectives

1.To know the types of anemia

2. To know the clinical approach to managing this patient

Case history

A 55-year-old woman is referred to the hematology outpatient department by her General Practitioner. She consulted him because of symptoms of profound fatigue and dyspnea on exertion and a routine full blood count had revealed her to be anemic. Hemoglobin was 8.3 g/dl, mean cell volume (MCV) 82 fl, white cell count 5.6 (neutrophils 3.5, lymphocytes 2.1) × 109/l and platelets 287 × 109/l. Her doctor could not establish a clear-cut cause for this lady’s anemia and has sought further advice.

1.What important points you need to ask in the history

2. How can physical examination help you to know the cause

3.How would you investigate

Problem 14

Bleeding tendency

Background

A thorough, detailed history of the bleeding is vital in the assessment of patients with potential hemostatic defects, and it will impact on the extent of investigation. The duration of bleeding/bruising is important when considering whether the patient is likely to have a congenital or acquired hemostatic disorder. Bleeding since childhood, such as menorrhagia since menarche, would usually suggest a congenital disorder; however,

mild congenital disorders of coagulation may present in adult life. A family history of abnormal bleeding clearly would also support the presence of a congenital defect. It is useful to establish the details of bruising, in particular whether it is spontaneous, occurs after minimal trauma or after surgery, and its extent. Tonsillectomy and dental extraction in particular pose significant hemostatic challenges

and if these have not been associated with significant bleeding, a congenital disorder of hemostasis is much less likely.

Bleeding or bruising on multiple occasions and from different sites merits more extensive investigation as this suggests a systemic haemostatic defect. Repeatedly bleeding from one site, such as epistaxis from the same nostril, suggests a structural abnormality. Mucocutaneous bleeding (epistaxis, bruising, menorrhagia, gastrointestinal bleeding)

as in this case suggests a disorder of platelet function.

Coagulation factor deficiencies are more likely to be associated with haemarthrosis, muscle hematoma and post-operative bleeding.

Although menorrhagia is a common gynecological symptom, a specific cause is identified in less than 50% of affected women. Studies have shown that bleeding disorders are found in a substantial proportion of women with menorrhagia and a normal pelvis examination. Inherited bleeding disorders have been diagnosed in 17% of such patients,

with von Willebrand’s disease being the most common abnormality.

Systemic illness, in particular uremia and liver disease, may cause abnormalities of hemostasis (Table 2.1).

Table 2.1 Causes of platelet disorders

[pic]

A detailed drug history is clearly relevant; aspirin and non-steroidal anti-inflammatory

agents are common culprits causing platelet function defects, but many drugs are

implicated (Table 2.2).

Table 2.2 Drugs and other agents known to interfere with platelet function

[pic]

Clinical examination should focus on any bleeding, bruising or evidence of underlying systemic illness, particularly liver disease or a primary hematological disorder.

This lady has significant menorrhagia and marked bruising. She is not taking any medication and has no family history of abnormal bleeding, although her mother died in her thirties.

Investigation strategy

The patient’s history is suggestive of a platelet disorder or von Willebrand’s disease. VonWillebrand factor (VWF) is a plasma protein that mediates platelet adhesion to the subendothelium, mediates platelet aggregation and serves as a transport protein for factor VIII.

When vessel wall damage occurs, platelets undergo many responses including adhesion, release reactions, aggregation, exposure of a procoagulant surface, formation of micro particles and clot retraction. These changes lead to rapid formation of a hemostatic plug at the site of damage, which prevents blood loss. Defects in any of these functions

and/or platelet number usually cause impaired hemostasis and increased risk of bleeding.

Baseline investigations should include a full blood count to look for thrombocytopenia and a blood film. The blood film is important to look for evidence of a primary hematological disorder such as myelodysplasia, to assess platelet morphology and to show any abnormalities suggestive of hepatic or renal dysfunction.

A basic coagulation screen should be performed; this should include measurements of the prothrombin time, activated partial thromboplastin time and fibrinogen.

If her history was not particularly suggestive of a bleeding tendency, then the above investigations are probably sufficient.

However, her history is convincing despite these initial tests being normal, hence she requires further investigation. The next step would be to screen her for von Willebrand’s disease and assess her platelet function using a platelet function analyser (PFA-100® system).

Depending on the results she may require further assessment of her platelet function by performing platelet aggregometry, platelet glycoprotein analysis and platelet nucleotide analysis (Figure 2.1).

Figure 2.1 Investigation of easy bruising. DIC, disseminated intravascular coagulation; PFA, platelet function analyser.

[pic]

Conclusion

Investigation of the patient with easy bruising or abnormal bleeding requires a structured approach working through diagnostic tests in a logical, stepwise order.

Emphasis on the importance of taking a detailed and thorough bleeding history cannot

be stressed more. It is important to continue to investigate the patient despite normal initial investigations if the history is highly suggestive of a hemostatic defect. The PFA is superior to the bleeding time and is a promising screening tool for investigation of platelet disorders, although it is not 100% sensitive for all platelet disorders. Additional

clinical applications for the PFA are under development.

Objectives

1.To know the mechanism responsible for adequate hemostasis

2. to know the approach for patient with bleeding tendency

Case History

A 28-year-old woman is referred by her General Practitioner as she is complaining of easy bruising and menorrhagia.

What further information ( regarding history and physical examination) would you like?

2.What are the important factors for adequate hemostasis?

3.How can you differentiate clinically between bleeding due to defect in platelets or coagulator factor defect?

3. How do you investigate this patient ?

Problem 15

Pyrexia of unknown origin

Objectives

1.To know the definition of P.U.O

2. To know the possible causes

3. Know the approach to patient with P.U.O

Case history

A 32-year-old man is readmitted to a tertiary care hospital because of persistent fever. The story is complicated. He was admitted to the same hospital 3 months ago with an evening rise of temperature of 2 months’ duration. His temperature had risen to a maximum of 38.9°C and was associated with night sweats. He had lost 5 kg of body weight during the previous 2 months, but had no other symptoms except mild anorexia. He said that there were no cats and dogs in the family. There were no positive findings on physical examination. Extensive investigations were carried out .The patient was treated empirically with a four-drug regimen of antituberculosis chemotherapy. Not only did the fever persist, but he also developed clinical jaundice after 6 weeks of anti-TB chemotherapy. The jaundice, however, disappeared after stopping the drugs. A detailed history taken on this admission does not reveal any additional information.

1.What would your differential diagnosis include before examining

the patient?

2.Physical examination reveals that the patient is pale but not icteric. His axillary temperature is 38.1°C and he is sweating profusely; he appears chronically ill and thin. The liver edge is palpable 1 cm below the right costal border and is mildly tender; the spleen is also palpable 1.5 cm below the left costal margin. There are no peripheral lymph nodes. A grade 2/6 ejection systolic murmur is heard best at the lower left sternal border. The remainder of the examination is normal.

2.Has examination narrowed down your differential diagnosis?

Further investigations. Chest radiography and transoesophageal echocardiography are normal. Abdominal ultrasonography reveals mild splenomegaly with a small rounded hypoechoic lesion (19 mm) within the spleen. The liver is also enlarged with multiple rounded hypoechoic lesions of varying sizes involving both lobes. There are also multiple paraaortic,pre-aortic, precaval, retrocaval, mesenteric and peri-pancreatic lymph nodes .A rounded hypoechoic space-occupying lesion near the uncinate process of the head of the pancreas raises the possibility of a primary malignant tumour in the pancreas. A small amount of fluid is also seen in the pelvis. A contrast-enhanced computed tomogram (CT) of the abdomen and pelvis confirms the ultrasound findings, with peripheral enhancement of the lesions in the liver and spleen. A CT of the chest is normal.

3.Has the diagnosis been clinched?

An ultrasound-guided FNAC from a retroperitoneal lymph node reveals predominantly small lymphocytes admixed with binucleate Reed–Sternberg cells, which have enlarged vesicular nuclei and prominent nucleoli . Therefore, the cytomorphological features in this patient are those of Hodgkin’s lymphoma and imaging investigations indicate stage IV B disease.

4.How will you treat this patient?

This patient requires combination chemotherapy with 6–8 cycles of either ChIVPP (chlorambucil, vinblastine, procarbazine and prednisolone) or ABVD (Adriamycin, bleomycin, vinblastine and daunorubicin). The latter regimen is more potent, but is also more expensive. The patient should be informed about the side-effects of this chemotherapy. The stage of the disease, along with the presence or absence of systemic symptoms, influences the response to treatment. In the UK, a young man such as this, with extensive disease at presentation and treated with an ABVD regimen, would have a >80% 5-year survival. The treatment response should be evaluated by clinical criteria, as well as by repeat CT examination. Positron emission tomography (PET), if available, is the most sensitive means of documenting

Problem 16

Malaria

Objectives

1.To give a differential diagnosis of fever of short duration.

2.To know what are the physical signs of help.

3.To know how to investigate.

4. To know how to treat

Case history

A 30-year-old farmer is brought to an Emergency Department in Delhi on a hot July afternoon with a high-grade fever and altered conscious level. He was found in a disoriented state by co-workers in the field. His wife reports that he is normally very fit and well, but that he has had a very high temperature for the past 8 days and was febrile when he went out to work this morning. She gives no history of severe headache, loss of consciousness or seizures.

1.What would your differential diagnosis include before examining

the patient?

Examination

The patient’s rectal temperature is recorded to be 40°C and his skin is hot and dry. His Glasgow Coma Scale (GCS) is 7, but there is no meningism and no focal neurological signs. Pulse rate is 120/min and blood pressure is 94/52 mmHg. The spleen is palpable 2 cm below the costal margin. The rest of the examination is normal.

The patient’s clothes are removed, his entire body is sprayed with water in front of a fan and ice packs are applied. After a venous blood sample is taken, intravenous fluids are started. With this treatment, the patient’s temperature normalises in 45 min, but there is only mild improvement in his conscious level (GCS 10).

2.Has examination narrowed down your differential diagnosis?

Investigations

Blood cultures and a Widal test are negative. Magnetic resonance imagining (MRI) of the brain and cerebrospinal fluid (CSF) examination are normal. CSF testing

for Japanese B encephalitis virus is negative. Thick and thin peripheral blood smears show high levels (>5% infected red blood cells) of ring forms of Plasmodium falciparum.

3.Does this narrow down your differential

diagnosis?

4.How will you treat this patient?

Problem 17

Chronic Obstructive Pulmonary

Disease (COPD)

Background

Chronic obstructive pulmonary disease is estimated to affect three million people in the UK but is often not diagnosed until the patient is >50 years old. The principal cause is smoking. COPD is characterized by airflow obstruction that is not fully reversible and is usually progressive in the long term. Intermittent exacerbations cause rapid worsening of symptoms beyond normal day-to-day variation. COPD is defined as airflow obstruction with a reduction in the post-bronchodilator FEV1/FVC ratio to less than 0.7. Surprisingly, disability in COPD is often poorly reflected by the FEV1. If the FEV1 is ≥80% a diagnosis of COPD should only be made in the presence of respiratory symptoms (e.g. breathlessness, cough, reduced exercise tolerance, exacerbations) and formal lung function testing. As in this patient, airflow obstruction is irreversible following bronchodilator and steroid therapy (i.e. ................
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