Name: Dr. Williams E.

Adeyeye
EKSUTH, Ado-Ekiti

Cerebrovascular Disease

Introduction

It is one of the neurological emergencies because " time is neurone". The ischaemic or infarctive
is the commonest (80-90%) while haemorrhagic constitutes 10- 20%.

History

 Biodata
 Age
>50years in males
>60years in females
<40 - 45 years in both sex (stroke in the young)
 Sex M: F is 2:1
NB; ask whether the patient is right handed or left?
 Presenting complaint is usually sudden/gradual onset of
 Inability to use/weakness of one side of the body(R/L)
 Facial weakness of one side
 Inability to talk/speak
 History of presenting complaints
 Course
 symptoms lasting more than 24Hrs - If less than 24 hours then its a Transient
ischaemic attack.
 ? Onset, duration, progression of symptoms and the last activity before the symptoms:
 Sudden onset of symptoms in the absence of activity (ischaemic which could be
thrombotic or embolic)
Gradual and progressive weakness (likely thrombotic).
Weakness maximum at onset but improves with time (likely embolic)
Sudden onset of symptoms at peak of activity (likely haemorrhagic)
? Headache, dizziness, slurring of speech, visual disturbances nausea and vomiting
? Urine or fecal incontinence
?history of similar attack in the past
?who noticed the illness and the time it lasted
?any loss of consciousness or convulsions

Risk factors:
DM, HTN, obesity, smoking, alcoholism, history of past TIA, use of OCPs, family
history of stroke
R/O other differentials
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 I. History of head trauma - intracranial bleeds
II. Febrile followed by slow onset of presenting symptoms(r/o encephalitis, brain
abscess)
III. Any history of preceding convulsion(r/o Todd’s paralysis)
IV. History of last feed(r/o hypoglycemia)
V. R/O focal migraine
VI. Known Hbss? especially in stroke in the young
VII. Insidious onset of symptoms - brain tumours
VIII. Insidious onset of symptoms in a patient suspected to have tuberculosis -
Tuberculoma
Complications
-History of sores on the waist or lower extremities (bedsores)
-Leg swelling with associated pain (DVT)
-Pain on micturition (UTI)
-Features of raised intracranial pressure (ICP) such as headache, blurring of vision
(herniation) and projectile vomiting
-History of depression
-Features of hyperglycemia i.e. polyuria and polydipsia
-Features of hypoglycaemia
-Features of pneumonia such as cough fever (orthostatic pneumonia)
Care
What was done to the patient from the onset of symptoms at home, in transit and
while on admission in the hospital?
 Past medical and surgical history
a. Inquire about past hospital admission and reason, any cardiovascular surgery or
vascular catheterization?
 Family/social history
-Inquire about family history of risk factors
-Ask about physical inactivity/sedentary lifestyle.
-Ask about social habit of cigarette smoking, drug abuse, alcohol or other intoxicants
ingestion
 Systemic review

Examination

General physical examination

comment on the general appearance of the patient, take note of the posture, pressure
areas, running IV fluid, NG tube, urethral catheter and urine bag,
Neurological examination
1. higher centre functions: GCS, speech, judgement, memory etc.

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 2. motor “BTPR”(always compare findings in the opposite side): features are usually
that of upper motor neuron lesion except for the first week of stroke where they
may have indeterminate features due to spinal shock.
3. sensory examination
4. cerebellar examination
 Systemic examination. Particular attention to CVS (for etiology) and Respiratory system
(for complications).
Investigations
 To confirm diagnosis
-Brain CT scan: it differentiates ischemic from hemorrhagic stroke. In ischaemic
stroke erliest CT scan changes are visible within a few hours after the event but may
be delayed for a few days or more. (Read CT features of stroke)
-magnetic resonance imaging (MRI)
- Random blood sugar(r/o hypoglycemic coma and also hypoglycaemia is a
complication and poor prognostic factor of stroke)
-Electrocardiography
 Others
a) Full blood count, platelets, and ESR
b) Chest X-ray
c) Lumbar puncture
d) Lipid profile
e) Urea electrolyte and creatinine
Management

 ABC of resuscitation: maintain airway, ensure patient is breathing and give I.V fluid
(normal saline)
 Urgent RBS Must be done: hypoglycaemia is a differential and both hypeglycaemia
and hypoglycaemia are poor prognostic factors. Commence soluble insulin when
RBS > 14mmol/l even if the patient is not diabetic.
 If patient is unconscious pass NGT and catheter. Patient should remain NPO for 1st
48 hrs.
 Careful monitoring of blood pressure: Control blood pressure only if;
a- Persistent absolute systolic b.p > 220mmHg
b- Persistent absolute diastolic b.p > 120mmHg
c- Stroke co-existing with any of the hypertensive emergencies (e.g hypertensive
encephalopathy, acute left ventricular failure. acute MI, dissecting aortic aneurysm,
ARF, malignant hypertension etc.
d- When the Mean arterial b.p > 145mmHg. [MABP= Diastolic B.P + 1/3 (pulse
pressure). Pulse pressure= Systolic B.p - Diastolic B.p]
NB: REDUCE B.P CAUTIOUSLY PREFERABLY THROUGH ORAL OR NGT
 If there are features of raised ICP :

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 -Nurse at 300 head up tilt
-Avoid noxious stimuli
-Give 20% mannitol at 0.5 to 1g/kg over 30 mins and repeat every 8 hrs for 24 hrs
- frusemide I.V 40mg daily or b.d for 5 days.
- intubation and hyperventilation
 Control temperature if pyrexic : Fever is a poor prognostic factor.
 If there are signs of aspiration pneumonia, give IV antibiotics.
 Use of thrombolytics in ischemic stokes- however benefit obtained if given within 3
hrs of onset of stroke otherwise its not beneficial. e.g of thrombolytics- streptokinase,
recombinant tissue plasminogen activator.
 Antiplatelet agents after hemorrhagic stroke was ruled out- aspirin 300mg start oral or
PR then 75 mg maintenance.
 DVT prophylaxis: Refer to paraplegia
 Early physiotherapy.
NOTE: Haemorrhagic stroke should be managed in an ICU. Ptatient should be
planned for neurosurgical review and possible interventions.

Secondary Prevention
a- Bp control
 Routine antihypertensive therapy should be introduced 2 weeks following stroke
 If BP remains elevated – target blood pressure are:Diabetics:<130 / <80mmHg,
Non Diabetics <140/85mmHg
 Suggested therapy is: ACE INHIBITOR(Ramipril, Perindopril) PLUS Thiazide
Diuretic (Bendrofluazide, Indapamide). Combination therapy is the most effective
 Lifestyle advice should be given (to lose weight, reduce alcohol consumption,
avoid adding salt to food and increase exercise). Patients should be educated about
hypertension, the need for life long treatment & regular monitoring of their blood
pressure. They should be informed of their BP readings & given a diary to record
future measurements.

b-Lipid lowering
 Lipid lowering treatment with a Statin has been shown to be beneficial to ALL
patients with ischaemic stroke.
 ALL patients following ischaemic stroke or TIA should be commenced on a high
dose if: TOTAL CHOLESTEROL is > 3.5mmol/L, unless known to be intoleran of
statins. Suggested therapy is: SIMAVASTATIN 40mg or PRAVASTATIN 40mg
(especially if on Warfarin – no drug interactions)
 Liver function tests & CK should be checked after 4-6 weeks of treatment
 Additional dietary advice should be given on a lipid-lowering diet.

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NB: Causes of stroke in the young

1. Mitral valve prolapse

2. Patent foramen ovale
3. Sickle cell anemia
4. Fibromuscular displasia
5. Migraine
6. Cocaine / oral contraceptives
7. Congenital AV malformation
8. Antiphospholipid syndrome
9. Atrial fibrillation

Example of Clerking:
STROKE CLERKING:
PRESENTING COMPLIANTS

 Inability to move left upper limb X14 hours

 Inability to move left lower limb X14 hours

HISTORY OF PRESENTING COMPLAINTS

She was in her usual state of health until 14 hours prior to presentation when she had a fall. Fall was
said to have occurred a little while after waking up and going to the kitchen.

On falling, she hit her head on a table and had a transient moment of loss of consciousness. There was
no history of projectile vomiting, seizures or sudden severe headache. No history of photophobia, neck
pain, neck stiffness, fever or travel to the north. No history of monocular or binocular blindness. She is
not on any contraceptive or any estrogen containing medication

There is a positive history of slurring of speech and deviation of mouth to the right. Her last meal was
eba, taken about 8hours prior to onset of symptoms. There was a positive history of polydipsia (she
drinks up to 10 sachets of purewater a day) but no history of polyuria or polyphagia.

At onset of symptoms, she was taken to a private facility in Ado-Ekiti where she was given intravenous
fluids and medication (names unknown). When relatives saw that there was no improvement, she was
brought to this facility for expert management.

CHRONIC KIDNEY DISEASE (CKD)

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 Introduction:

CKD is a Kidney damage for ≥3 months and/or a ↓ GFR <60ml/min/1.73m2 for ≥3 months
with or without kidney damage.
Kidney damage refers to structural or functional abnormalities of the kidney (from
abnormal urinalysis, imaging studies or histology). With time many patients with CKD
progress to ESRD.
End-stage renal disease (ESRD) = decreasing GFR < 15ml/min/1.73m 2 accompanied by signs
and symptoms of kidney failure that necessitate RRT.

History

Presenting complain

 Uremic symptoms
 Anorexia, nausea, vomiting, diarrhea, hiccup, pruritus
 Fatigue, lethargy (anemia)
 Change in behavior, increase daytime somnolence (encephalopathy)
 Epistaxis, bleeding gums, hematemesis, malena (platelet dysfunction)
 Kidney symptoms
 Polyuria
 Nocturia
 Oliguria

History of presenting complain

Course: duration of illness >3 months

Cause:

 Hypertension: pt is a known hypertensive; for how long; is pt on medications; regular?, if not

why; is patient on follow up?, is it regular?
 Diabetes: is patient a known diabetic or with symptoms of polyuria, polyphagia, & polydipsia;
clerk as HTN above
 CGN: previous hx of sore throat or skin lesion
 Drug induce: hx of prolong intake of traditional concoction, NSAIDs, or antibiotics (specify)
 HIVAN: known RVD; hx of symptoms; hx of risk factors
 Family hx of kidney disease: polycystic kidney disease, reflux nephropathy
 Heavy metal nephropathy: long term use of mercury containing soap (e.g. Tura) or cream (e.g.
Hg containing skin lightening creams)
 Sickle cell nephropathy: known HbSS; hx of symptoms

R/O differentials

 CCF: body swelling, dyspnea, fatigue

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  CLD: hx of jaundice, steatorrhea, & risk factors
 Nephrotic syndrome: hx of body swelling, frothiness of urine
 Diabetic mellitus: polyuria, polydipsia, polyphagia, numbness

Complications

 Anemia: easy fatigability, dyspnea

 Coagulopathy: easy bruising, bleeding from orifices
 Encephalopathy: confusion, drowsiness, coma
 Neuropathy: numbness, parasthesia
 Endocrinopathy: menstrual irregularity, ↓libido
 GIT: features of acute pancreatitis, PUD
 Renal osteodystrophy: fracture
 Gout: painful toe

Care

 Drugs taken; any hx of dialysis?, how frequent, has pt had an A-V shunt, any complication?
 Outcome of care

Social hx:

 Is there any interference of life by symptoms or by treatment e.g. dialysis

Examination

Pertinent findings are those of anasarca with facial puffiness, altered sensorium, asterixes, raised blood
pressure, respiratory distress, sensory polyneuropathy, pericardial friction rub.

Investigations

To confirm diagnosis

 Urinalysis: proteinuria, hematuria, and glycosuria

 Urine M/C/S: RBC cast, WBC cast, CGN cast (waxy, broad), granular cast, eosinopyluria
 U/E/Cr: ↑Urea, ↑Cr, ↑K, ↓Ca, ↓HCO3, ↑Uric acid, ↔ or ↓Na, ↑PO4.
24hr urine clearance/ spot mid-stream urine analysis is done for estimation of GFR
o Creatinine clearance= (140-age)x lean body weight (kg) (x 0.85 in female)
In mL/min plasma Cr (mg/dL) x 72
 USS: shrunken kidneys (<9cm). Normal is 14cm. NB: kidneys are of normal size in polycystic
kidney disease, carcinoma, HIVAN, amyloidosis, sarcoidosis.

ANAEMIA

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Introduction: Anemia is defined as a hemoglobin concentration less than the lower limit of
normal for the patient’s age and sex. It is not a diagnosis but a clinical sign or symptom.

History
Biodata:
 Age: elderly- anemia of chronic diseases e.g. TB, chronic kidney disease (CKD),
and malignancy; in the young, sickle cell disease,
 Sex: female>male (pregnancy and menses)
 Occupation: farmers, herdsmen (prone to parasitic infestation)
 Religion/tribe: vegetarians like Hindus (prone to B12 deficiency)

Presenting complaint(s): most are non-specific symptoms. They include:

 Tiredness, headache, weakness, dizziness, light headedness (due to low level of oxygen
in CNS)

 Tinnitus (can be the only presenting symptom)

 Claudication (due to hypoxia in calf muscles)

 Chest pain (exacerbation of stable angina due to myocardial hypoxia)
 Palpitation (compensatory increase in heart rate to meet body oxygen requirement)
 Other symptoms may suggest the etiology e.g. bleeding diathesis may suggest leukemia
or lymphomas, hematemesis- PUD, CLD etc.
History of presenting complaint(s)
 Course: ?onset of symptom
?progression of symptom
?limitation of activities,?extent of limitation.
?hx of cravings for dirt, paint (pica), ice (pagophagia)-suggests Fe
deficiency
 Causes:
 ?hx of diagnosis of HIV or hx suggestive of HIV (anemia due to HIV)
 Upper GI bleeding associated with long standing hx of epigastric pain
radiating to the back associated with meals (PUD).
 Upper GI bleeding +jaundice +right hypochondriac pain (CLD)
 ?hiccups, body itching, decreased urine production or absent urine
production, hematuria, polyuria, nocturia. (Chronic kidney disease,
CKD)
 ?paroxysmal cough, blood stained sputum, wheeze, body itching, loose
stools (gastointestinal helminthic infestation).
 ?recurrent infections

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  ?recurrent bleeding from minor trauma, ?exposure to radiation or
anticancer (cytotoxic) drugs. (bone marrow aplasia)
 ?long standing fever, cough, weight loss or contact with chronically
coughing adult .(TB)
 Hx of blood donation
 ?frank blood per rectum or blood stained stool (hematochezia) (lower
GI bleeding)
 Complications:
 ?dyspnea on exertion (mild, moderate or severe exertion), orthopnea,
paroxysmal nocturnal dyspnea (PND) and/or ankle swelling. (heart
failure)
 ?confusion, delirium, altered level of consciousness. (shock, if acute
hemorrhage is the cause)
 ?difficulty in swallowing (dysphagia secondary to long-standing Fe-
deficiency anemia, also known as Paterson-Brown-Kelly or Plummer-
Vinson syndrome).
Past medical history:
 ?past admission, reason for the admission.
 ?past surgery (e.g. gatrectomy or tumor excision).
 ?recurrent blood transfusion.

Drug history:
 ?anticoagulant (bleeding)
 ?aspirin or other NSAIDs (Upper Gastrointestinal bleeding)

 ?anticonvulsants e.g. phenytoin (B12 deficiency)

 ?anticancer drugs, chloramphenicol (bone marrow suppression)

Family history:
 ?of similar condition, ?the affected family member
 ?of any other disease condition.
Social history:
 ?alcohol (excessive chronic ingestion is associated with poor nutrition
and decrease dietary intake).
 ?smoking (chronic smoking is associated with many cancers which
can cause anemia of malignancy or chronic disease).
 ?consumption of clay or laundry starch- Iron is rendered less
absorbable.

Examination

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General examination:
 Respiratory distress, cardiac position (?presence of heart failure as a
complication)
 Fever : infection, hemolysis or malignancy
 Pallor: check the conjunctiva, tongue, palms (especially the creases), and soles
of feet.
 Jaundice (?hemolysis or hepatic disease)
 Mouth: angular chelosis and smooth beefy tongue (Fe deficiency)
 Petechiae (thrombocytopenia 20 bone marrow aplasia)
 Lymphadenopathy: Infections and malignancies
 Hand: koilonychias (spoon shaped nail secondary to long-standing Fe
deficiency. anemia).
 Pedal/ankle edema (? heart failure as a complication).

Systemic examination:
 Cardiovascular system: Pulse (tachycardia, low volume pulse, bounding
pulse), BP is reduced, displaced cardiac apex (? Heart failure) usually from
uncompensated anemia
 Abdomen: splenomegaly, hepatomegaly, or any other palpable mass.
 Respiratory system: tachypnea,
 GCS: if low, may be due to decreased perfusion to the brain

Investigations
 Full blood count:
 Low Hb (normal: male=13.5-17.5g/dl, female=11.5-15.5g/dl).
 Low packed cell volume (PCV) or Hematocrit (HCT): normal male
=40-50%, female=35-45%
 Low RBC count: normal male=4.3-6.0x106/μL, female=3.5-
5.0x106/μL
 Mean corpuscular hemoglobin(MCV): normal MCV=80-95fL
Low MCV denotes microcytic anemia (Fe def. anemia, chronic disease
anemia, thalassemia etc.).
Normal MCV denotes normocytic anemia (acute blood loss, renal
failure).
High MCV denotes macrocytic anemia (folate, Vit. B12 def., others:
alcohol, liver disease)
 Mean corpuscular hemoglobin (MCH): normal MCH=30-35g/dL
Low MCH denotes hypochromic anemia (Fe def. anemia, chronic
disease anemia)

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 Normal MCH denotes normochromic anemia (anemia of acute blood
loss, anemia secondary to renal failure).
 Reticulocyte count:
Low reticulocyte count denotes decreased RBC production e.g. bone
marrow suppression, folate or B12 def.
High reticulocyte count denotes increased RBC production e.g.
hemolytic anemia
 Laboratory investigation of iron deficiency anemia: this check for serum
Fe level, total iron binding capacity (TIBC), and serum ferritin level. Some
possible results are summarized below.

Parameter Result Differential Diagnosis

Serum Fe level Low Fe deficiency, anemia of

chronic diseases

TIBC Raised Fe deficiency

Normal/low Anemia of chronic disease

Serum ferritin level Low Fe deficiency

Normal or high Anemia of chronic disease

 Blood film examination:

This is carried out to look at the red call morphology.
 Red cells with normal appearance are seen in anemia due to acute
hemorrhage.
 Abnormally large red cells may be seen which suggests megaloblastic
anemia.
 Abnormally small red cells with faint color and associated pencil-
shaped red cells may be seen in Fe def. anemia or chronic disease
anemia.
 Red cells with abnormal morphology (e.g. sickled, spherocytes,
elliptocytes or poikilocyte) are seen in hemolytic anemia since they are
easily destroyed in the spleen. In addition, red cell fragments might be
seen, which also suggests an ongoing intravascular hemolysis due to
DIC (disseminated intravascular coagulation), microangiopathy, burns,
HUS (hemolytic uremic syndrome, etc.).
 Microscopy: stool, urine, or sputum for microscopic blood loss that can lead
to iron deficiency over time.

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 Stool microscopy for the ova of hookworm.

 Chest x-ray: this can be done when there are features of heart failure.
Cardiomegaly, prominent pulmonary vascular markings, pleural effusion, or
other incidental findings.
 Other investigations:
 Clotting profile if abnormal bleeding is present.
 Upper/lower gastrointestinal endoscopy.
 Bone marrow examination.

Treatment
Treatment depends on the onset of the anemia (sudden or gradual), severity (mild,
moderate, severe) and etiology.

Severe Anaemia <7 g/dl

Moderate Anaemia 7 – 9 g/dl
Mlid Anaemia 10 - 12
 Based on the onset:
 Acute anemia: treat the underlying cause. If mild or moderate, give hematinic. If
severe, offer whole blood transfusion and treat the cause.
 Chronic anemia: In chronic anemia, adaptation has occurred by increasing fluid
reabsorption and consequent intravascular volume expansion.
Treat the underlying cause. If mild or moderate, administer hematinic.
If severe, treat the underlying cause and offer packed cell transfusion. In the
absence of packed cells, sedimented red cells or whole blood can be given,
however a diuretic must be added to avoid volume overload and impending
heart failure.
 Based on severity:
 Moderate to severe anemia is treated by nutritional supplementation and treatment
of the underlying cause.
 Severe anemia is treated by blood transfusion. Whole blood is transfused when
the anemia is acute in onset. However, packed cell transfusion is preferred if the
onset of the anemia is insidious.
 Based on etiology:
 Fe deficiency anemia is treated with iron supplementation and treatment of the
underlying cause. Oral iron supplementation (ferrous sulfate) is administered in
mild to moderate Fe deficiency anemia. Severe iron deficiency anemia is treated
using parenteral iron supplementation (e.g. iron sorbitol, iron dextran).
 Megaloblastic anemia is treated using folate or B12 supplementation.
 Chronic disease anemia: treat/manage the disease. Specific treatment may
be required under some conditions e.g. erythropoietin in CKD.

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Chronic Liver Disease

Definition

Is defined as clinical or pathological spectrum of liver disease of varying etiology lasting for more than six
months and characterized by hepatic necrosis, inflammation with or without fibrosis or neoplastic
transformation

History

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 Biodata

Occupation: health worker

Presenting complaint ( symptoms usually >6months )

 Abdominal swelling/distension

 Yellowish coloration of eyes

 Pruritus

 Amenorrhea

 Abnormal hair distribution(F)

 Hyperpigmentation

It is worthy of note that presenting symptoms are many and non-specific. Careful and detail history is the
key to diagnosis

History of presenting complain

 Character: abdominal swelling- onset; progression; ever regressed? Spontaneous or with

medications; painful or not; no. of episodes; swellings elsewhere;

 Course

 When and how the symptoms starts, associations, worsening episodes and
improvement. Clark all symptoms thoroughly.

 Slow onset of symptoms and rapid development/deterioration

 Cause

 Fever, recurrent intermittent jaundice, recurrent malaise, anorexia, nausea, vomiting

upper abdominal discomfort and weight loss; patient is a known IVDU, hx of needle stick
injuries, multiple sexual partners, hx of blood transfusion, hx of surgery, scarification
marks, etc. (?hepatitis B or C)

 A young/perimenopausal woman, with amenorrhea, acne, arthralgia + features of c.

hepatitis (autoimmune hepatitis)

 History of ingestion of poorly stored grains (?Aflatoxin)

 Living in riverine areas and past history of childhood hematuria (?schistosomiasis)

 Family history of liver disease (?α1 antitrypsin deficiency) and neurologic/dystonic

symptoms(?Wilson’s disease)

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  Nonspecific symptoms with hematemesis, jaundice right hypochondriac pain, abdominal
distension in a chronic male alcoholic. Here ask for the type, quantity, duration of use,
and the CAGE questions (?alcoholic liver disease)

 Chronic use of traditional concoctions.(unknown toxins)

 Chronic use of drugs such as methyl dopa(antihypertensive), amiodarone (anitarrhymic),

nitrofurantoin (antibiotic) (?drug induced hepatitis)

 Known or newly diagnosed diabetic with brownish/bronze skin discoloration and joint
pains(Hemochromatosis)

 Inquire about other features suggestive of primary biliary cirrhosis, cardiac cirrhosis and
primary sclerosing cholangitis

 R/O differentials: (refer to the corresponding sections)

 CCF:

 CKD:

 Abdominal TB:

 Nephrotic syndrome

 Complications. Clerk around;

-Synthetic functions impairment

-portal hypertension

-Hepato-renal syndrome

-hepatic encephalopathy (RISC- Reversal of sleep pattern, Increase somnolence, Semi coma, Coma)

-hepatocellular carcinoma (Rt hypochondrial pain in a patient with initial ascites)

 Care

Ask about what was done to the patient right from the onset of symptoms. These include past and
present traditional medication, religious incantations/food restrictions, and hospital admissions.

Social history

Cigarette smoking, alcohol (including locally produced ones) ingestion (? amount) and indiscriminate use
of drugs

Family history

Family history of autoimmune disorders in a female with stigmata of CLD

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 Occupational history

Health workers (Hbv), workers in heavy chemical industries

Past medical and surgical history

Hx of Hospital admissions?

Systemic review

There are often multisystemic effects of chronic liver disease; therefore, all systems must be thoroughly
reviewed.

CHRONIC OBSTRUCIVE PULMONARY DISEASE (COPD)

INTRODUCTION

Chronic Obstructive Pulmonary Disease (COPD) is a group of obstructive lung diseases primarily
characterized by irreversible limitation of airflow usually resulting from an increase in resistance caused
by partial or complete obstruction at any level. Two disease entity fall into this group namely:
Emphysema and Chronic bronchitis

HISTORY

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BIODATA

Age: > 40 years

Race: prevalence now on the increase in Asia and Africa (related to increase in cigarette
smoking)

PRESENTING COMPLAINTS

NB: Both forms co-exist, rarely do they present as separate entity

 Breathlessness

 Cough

 Exercise intolerance

HISTORY OF PRESENTING COMPLAINTS

 Course:

Onset, duration

Note: Chronic bronchitis is diagnosed clinically as a persistent productive cough in most days of the
week for at least 3 consecutive months in at least 2 simultaneous years.

Symptoms aggravated by exercise at the initial stage and later present even at rest.

Cough productive of sputum (may be purulent) seen in chronic bronchitis or in emphysema with chronic
bronchitis

Excercebating factors:

?upper respiratory tract infection

? Changes in weather i.e. temperature changes

? Non-compliance with (or under dosing of) medications

? Cardiac arrhythmias

? Environmental exposure to pollens, fumes, allergens or other irritants

? Left ventricular dysfunction

? Drugs e.g. beta blockers

 R/O differentials:

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? Fever, Cough, weight loss and night sweats > 2 weeks (R/o Tuberculosis)

? Known asthmatic or hx suggestive of attacks when exposed trigger factors (R/o chronic asthma)

? Chest pain, Orthopnea, Paroxysmal nocturnal dyspnea, leg swelling (R/o Congestive Cardiac Failure)

Note: Cor Pulmonale is a complication of COPD

? Copious, purulent mucoid sputum more in the morning (R/o Bronchiectasis)

? Hemoptysis (R/o Lung Cancer)

? Fever, cough (R/o Pneumonia)

 Complications:

Headaches (due to hypercapnia)

Leg swelling (due to hypoxic kidneys or cor pulmonale)

Weight loss (if emphysema only)

Bluish discoloration of mucosae

Hemoptysis

 Care:

What medical care received and if there was significant improvement

DIABETIC EMERGENCIES

These are spectrum of life threatening events that may occur in either type 1 or type 2 diabetic
patients. They are;

1. Diabetic ketoacidosis (DKA)

2. Hyperosmolar hyperglycemic state (HHS)

3. Hypoglycemia

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Both DKA and HHS are characterized by very high blood glucose levels resulting from severe lack of
insulin.

DKA:

Is an acute complication of diabetes mellitus characterized by a triad of hyperglycemia, ketosis and

metabolic acidosis. It mainly complicates type 1 diabetes, where it may be the first manifestation of the
disease and rarely people with type 2 diabetes.

HHS:

It mainly occurs in older people with type 2 diabetes, in about one third of the cases of HHS, it is the
first manifestation of type 2 diabetes. The blood glucose rises to very high levels but acidosis does not
develop, the residual insulin is sufficient to prevent ketogenesis. Elevated blood glucose lead to
increased serum osmolality, this results in dieresis and fluid shift, increased urination causes body wide
depletion of water and electrolytes causing extreme dehydration.

Both have the same principles of management with little differences.

Management includes;

History

Physical examination

Investigations

Definitive treatment

History: it should be short and precise

Biodata ;

Presenting complain(s): polyuria, polydipsia, nausea, vomiting, abdominal pain, altered level of
consciousness, change in breathing pattern.

Ask for history of diabetes, if yes, ask for duration, type of treatment the patient is on (injection or
tablets), is the patient drug compliant? And if regular on follow up.

History of precipitating factors; newly diagnosed diabetic, infection (ask for fever) the commonest is UTI
and URTI. So ask for history of cough, pleuritic chest pain,painful micturition and suprapubic pain (note
that a diabetic can have an infection without any fever due to relative immunosuppression).

Ask for features of myocardial infarction; chest pain, excessive sweating, epigastric pain. It must always
be ruled out in any diabetic presenting with DKA/HHS. Remember diabetics are at risk of silent MI(MI
without any pain).

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Ask for missed dose of insulin, or insulin administration while fasting or taking oral hypoglycemics
without eating.

Physical examination;

Parameters of interest is level of consciousness(delirium, drowsiness and lethargy, atimes comatose ),

hydration status, acetone breath, pyrexia, kussmaul’s breathing(rapid shallow breathing),tachycardia,
normal or low blood pressure, increased capillary refill time.

HEART FAILURE (CCF)

Introduction:
Congestive cardiac failure is a condition in which there is inadequate cardiac output for body’s
needs. it is characterized by:
-Left ventricular dysfunction.
-Exercise intolerance.

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-Breathlessness.
-Fluid retention &
-Decreased longevity.

Biodata:
 Age: most commoner in elderly (It increases with age, affecting 6–10% of people > 65,
reaching 30% in those aged over 80years).
 Sex: males>females.
 Race: commoner among blacks.

Presenting complaint(s)
Presentation depends on the type of heart failure (i.e. whether it is right, left or congestive
cardiac failure).
A. For LHF, cough, breathlessness, tiredness, & exercise intolerance.
B. For RHF, generalized/ankle swelling, right upper abdominal pain/heaviness, abdominal
swelling.
C. For CCF, there is a combination (to a variable extent) of signs of LHF & RHF with
marked severe wasting (cardiac cachexia).
NB.: Cachexia is due to a combination of anorexia, impaired absorption due to low cardiac
output skeletal muscle atropy due to immobility & increased levels of circulating cytokines.

History of presenting complaint

I. Course: onset, duration & progression of the symptoms one after another.
Associated symptoms like orthopnea, PND, production of frothy sputum, hemoptysis, oliguria
(other LHF symptoms); or loss of appetite, nausea, early satiety, neck engorgement and pulsation
(other RHF symptoms).

II. Cause(s):
 Hypertension- history of HTN, when & where diagnosed, on any anti-HTNsives or not,
regular on HTN clinic or not, family hx of HTN, hx of diagnosed renal disease or not.
 Rheumatic valvular heart dx- history of fever with sore-throat (GABHS)/skin rashes in
the past; history of previous cardiac surgery for valve repair.
 Anemia (anemic HF)- history of easy fatigability, palpitation, dizziness.
 Dilated cardiomyopathy and/or peri-partum CM- history of child birth within the last
few months, history of hot-water birth, ingestion of potash pap.
 Ischemic heart disease- preceding history of central/praecordial chest pain,
aching/burning, precipitated by exertion, relieved by rest or nitroglycerine.
 Infective endocarditis- hematuria, tiny blood spots in the finger nails (splinter
hemorrhage), abnormally curved nails (finger clubbing).
 Cor Pulmonale: previous hx suggestive of COPD or other long standing lung disease.
 Diabetes: hx of polyuria, polydipsia, polyphagia and weight gain

NB: history of precipitants of heart failure is ESSENTIAL in patients with acute on chronic heart
failure. Precipitants are listed below

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Rule out differentials
 For the cough
-Bronchial asthma: is pt a known asthmatic?, any history of allergy?, any family history of
asthma in 1st degree?
-COPD: history of long term tobacco smoking, exposure to air pollutants such as NO2, thick
yellowish-green or white-yellow sputum.
 For the body swelling and pedal edema
CLD: history of childhood jaundice associated with fever, history of alcohol ingestion.
CKD: history of oliguria &/or anuria, history of diagnosed DM, renal disease in the past, chronic
ingestion of NSAIDs.
Nephrotic syndrome: frothy urine, early morning facial puffiness later involving whole body.

III. Complications
 Uremia: history of itching, muscle cramps, vomiting, altered consciousness (uremic
encephalopathy).
 Thrombo-embolism: history of leg pain with redness/erythema (DVT), history of
weakness or inability to move any part of the body (stroke).
 Impaired liver function: current history of yellowish discoloration of the eye/ mucosa,
delayed clotting.
 Hypokalemia: weakness, lassitude, constipation (maybe from k+ loosing diuretics or
hyperaldosteronism from activation of rennin angiotensin system).
 Hyperkalemia: hx of weakness, fatigue, or muscle paralysis (not really specific)
 Hyponatremia: history of thirst, dizziness, confusion.
 Arrythmia: (high index of suspicion is required as it may be asymptomatic or present
with non- specific symptoms of palpitation, dizziness, syncope, fatigue e.t.c.)

IV. Care
 Where patient went to after the symptoms first appeared, what was done (drugs,
investigation & results if known).
 Why patient moved to this hospital (self referral, formal referral from the previous
hospital)
 What was done to the patient in this hospital, what he/she is on and if patient has
improved during the care.

Past medical history

History of hospital admission, surgery, blood transfusion in the past? If yes, state reasons.

Drug history
Hx of ingestion of recreational drugs like alcohol or cocaine.

EXAMINATION

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General physical examination:
 Patient lying on cardiac position.
 Acutely ill-looking (respiratory distress, pains)
 Chronically ill-looking (wasting[temporal recession, prominent zygomas, ])
 Palor (due to hemodilution): Conjuctival palor, pale mucous membrane.
 Clubbing: Infective endocarditis, congenital heart disease
 Pedal edema: Right heart failure.
 02 concentration insitu (respiratory distress)
 Urinalysis if patient is bloated to R/O nephrotic syndrome, CKD.
 Weight of patient & compare with that prior to illness if he/she knows.

Cardiovascular system:
 Tachycardia.
 Locomotor brachialis (hypertensive heart disease).
 Normal or low blood pressure
 JVP usually raised (Right heart failure).
 Apex: may be displaced/heaving (hypertension, aortic stenosis); thrusting/diffuse (dilated
cardiomyopathy, mitral regurgitation); dyskinetic ( left ventricular dysfunction)
 Heart sound: S3± gallop rhythm.

HUMAN IMMUNE DEFICIENCY VIRUS (HIV)

HISTORY:

 BIODATA:

 Age: younger population (<25-30yrs, previously); older population (recently, use of antiretroviral
drugs results in HIV patients living longer)

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  Occupation: commercial sex workers, long distance travellers/drivers, health workers

 Marital status: singles

 PRESENTING COMPLAINT(S):

 Acute HIV syndrome: occurs in about 2/3 of individuals with HIV within 3-6 weeks
after primary infection. It is due to rapid replication of the virus. Common
symptoms include:

Fever

Headache

Malaise

Lymphadenopathy

Joint pain (arthralgia)/muscle pain (myalgia)

Weight loss

Anorexia

Nausea/vomiting/diarrhea (especially chronic)

Sore throat

Erythematous maculopapular rash

Meningism

Night sweat

 Clinical latency (asymptomatic stage): persists for an average of 10yrs before the
development of symptomatic disease. It is due to decrease viral load and rise in
CD4 lymphocytes. And 1/3 of patients may develop Persistent Generalized
Lymphadenopathy (PGL). PGL is defined as the presence of an enlarged node >1cm,
in 2 or more extra-inguinal sites, lasting 3months or longer.

 AIDS-related complex (ARC): it occurs before the onset of AIDS & thus regarded as
a prodrome to AIDS & characterized with following constellation of symptoms and
signs:

Fever

Night sweats

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Diarrhea

Weight loss

± Opportunistic infections e.g. oral candidiasis, oral hairy leucoplakia, herpes zoster, recurrent herpes
simplex, seborrhoeic dermatitis, tinea infections.

 Acquired Immune Deficiency Syndrome (AIDS): occurs after an average period of

10yrs, although it can occur at any time during the course (progression) of the
disease. It depicts severe depletion of CD4 count (<200cells/μL) with subsequent
development of all sorts of opportunistic infections.

 HISTORY OF PRESENTING COMPLAINT(S):

 ?details of the symptoms related to the above complaints in order to get a

collection of symptoms attributable to a particular disease entity or its
complication.

 ? the following as it relates to each major complaints:

-on set

-progression

-development of other symptoms

-regression of other symptoms

-limitation of activities

-care sought (may be in the form of drugs or any other form of intervention)

 PAST MEDICAL HISTORY:

 ? History of blood transfusion, frequency, place & time of the transfusion (blood
transfusion exposes patients contracting HIV. However, it depends on the
transfusion frequency & facilities at the center where it is done. For symptoms to be
attributed to a transfusion, time span must be significant enough to allow for
development of symptoms.)

 ? Other transfusion-dependent medical conditions like chronic kidney disease (CKD),

bone marrow malignancies (e.g. leukemia) etc.

 ? History of sexually transmitted infections (STIs): unhealthy sexual practices that

lead to the acquisition of STIs also predispose to the risk of HIV; STIs also cause

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 breach of epithelial linings which increases the risk of HIV acquisition than intact
epithelium.

 ? Past surgery (risk of blood transfusion; organ transplant may transmit HIV)

 ? Past hospital admission, reason & duration

 DRUG HISTORY:

 ? If patient is currently on any drug. Ask about name/description, dosage & for how
long has the drug been taken. This will give an idea whether the patient is on ant-
retroviral therapy (ART). And whether the drugs taken have a possible interaction or
cross toxicity with the drugs to be prescribed. And whether some of the presenting
symptoms are side effects of the drugs the patient is taking. Thus, this emphasis the
need for continuous update of knowledge about drugs, about their action, reaction,
interaction & toxicities.

Examples:

-Cytotoxic chemotherapy (anticancer agents) or immunosuppressive therapy (for transplant patients)

may lead to severe immunosuppression that may lead to the development of opportunistic infections
which can mimic AIDS.

-Chloramphenicol and Zidovudine can have a combined suppressive effect on bone marrow.

-Rifampicin (anti TB) may reduce the serum levels of some anti-retroviral drugs (ARVs).

-HIV can affect renal function and cause CKD (HIV associated nephropathy, HIVAN). So, when
nephrotoxic drugs are used in HIV management (e.g. streptomycin & amphotericin B) there is a
combined effect on the kidney. Thus, there is need for continuous monitoring of renal function.

 ? History of drug allergy; ask about the name of the drug or its description.

 FAMILY HISTORY:

o ? Of a similar condition (especially in spouse).

o ? Monogamous or polygamous family setting, if married.

o ? Spouse(s) or co-wives in first or second order of marriage (first order marriage=first

marriage in life time; second order marriage=marriage to a different person after a previous
one; and so on).

o ? History of STDs in spouse(s) or co-wives.

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 o ? Death of spouse(s); ask if cause of the death was diagnosed or not.

o ? Any other family disease e.g. Diabetes mellitus, hypertension, allergy etc.

 SOCIAL HISTORY:

I. ? Extramarital relationship; ask if multiple; ask about history of STDs in sexual

partner(s); ask about death of a sexual partner; ask if cause of the death was
diagnosed or not.

II. ? Long distance travel; frequency of the travel; duration of stay before returning
home.

III. ? Illicit drugs use (esp. intravenous drugs).

IV. ? Sharing of sharps

V. ? Smoking or alcohol ingestion.

 SYSTEMIC REVIEW:

 ? Symptoms that have not been asked in all the systems: (CNS, CARDIOVASCULAR,
RESPIRATORY, GASTROINTESTINAL, GENITOURINARY & MUSCULOSKELETAL SYSTEMS).

PEPTIC ULCER DISEASE

Peptic Ulcer Disease is generally characterized by burning upper abdominal pain often worsened by
hunger and relieved by meals.

Presenting Complain: Epigastric pain, nausea, vomiting

History of presenting complaint:

COURSE

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Pain : Often of sudden onset, localised at the epigastrium and may radiate to the back. More severe
early in the morning. Precipitated by NSAIDs, spices, tea, sour drinks, fried oily food etc. More severe
during meals (gastric ulcer) or some 2-3 hrs after meals (doudenal ulcer).

Vomiting: Contains recently ingested food +/- blood.

CAUSE

? Use of Non-steriodal anti inflammatory drugs

? Family history of similar illness

? Burns ( curling’s ulcer)

? Head injury (Cushing’s ulcer)

? Hx of cigarette smoking

R/O differentials:

Gastritis: Difficult to differentiate unless on endoscopy

Gastroesophageal reflux disease: typical symptoms include heart burn, regurgitation, dysphagia with or
without atypical symptoms (cough, chest pain, wheeze)

Chronic pancreatitis: epigatric pain, radiating to the back that is relieved by leaning forward.

DKA: Known diabetic or history suggestive of diabetes.

Acute MI: sudden stabbing chest pain which may radiate to the left shoulder or left jaw + risk factor of
cardiovascular disease.

Acute cholecystitis: egigastric pain which may radiate to the right scapular + fever

Cholelithiasis: epigastric pain that is colicky, not relieved by antacids, emesis, or flatuds may also radiate
to the right scapular +/- jaundice

gastric cancer- long standing hx of epigastri pain, vomiting, anorexia, epigastric mass and weight loss.

COMPLICATIONS

? History of melaena (passage of black tarry stools)

? Hx of vomiting of blood (NSAID induced ulcers may only present with bleeding)

? Hx of sudden abdominal pain which is severe and pt may collapse with or without
haematemesis (perforation)

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Past medical history: Hx of surgery (gastric ca can mimic PUD)

Drug history: NSAIDs, steroids

Social & family hx : Hx of smoking, alcohol ingestion

Family hx of PUD or malignancy

TUBERCULOSIS

History

Biodata:

Age: elderly

Occupation: health workers

Presenting complaint:

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  Cough>3/52, breathlessness, hemoptysis, fever, night sweats, weight loss, chest pain.

History of presenting complain:

Course:

 chronic cough productive of mucoid sputum that does not respond to full course of antibiotics
or recurs after a course or courses of antibiotics ± hemoptysis

 chest pain may be pleuritic

 ± wheeze (from compression of the bronchus by enlarged LN)

Cause/risk factors

 Sustained intimate contact with a chronically coughing adult or patient on anti-TB

 Drugs: patients on steroids

 Conditions: DM, CKD, malignancy, HIV, alcoholism, gastric surgery

 Poverty, malnutrition, overcrowding (from social hx)

Complications

 Pleural TB: pleuritic chest pain

 TB adenitis: Hx of neck swelling

 TB spine: Hx of back pain aggravated by straining or cough, band-like sensation followed by

weakness and finally sphinsteric disturbance

 Milliary TB: progress hx of fever, malaise, and weight loss

 TB meningitis: headache, vomiting, irritability, depressed consciousness, coma

 Abdominal TB: abdominal pain, distension, diarrhea/constipation

 TB pericarditis: features of HF, breathlessness, ↑JVP, leg swelling

 GU TB: dysuria, hematuria, flank pain/mass, epididimo orchitis, endometritis

 Skin TB: skin changes includes- Lupus vulgaris, Scrofuloderma, Tuberculosis vesicular cutis,
Tuberculous gumma, Tuberculitis, Erythema nodosum

 TB adrenalitis: fatigue, lightheadedness upon standing, mood changes, salt craving

Care:

 Investigations and medications so far and outcome

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R/O differentials

 Bronchogenic Ca: similar symptoms but with significant smoking

 Bronchiectasis: copious sputum that worsens on sitting up

 Psittacosis: exposure to paultry

 Heart failure: Hx of PND, orthopnea, production of frothy sputum

 Lung abscess: swinging fever, cough productive of purulent fowl smelling sputum, chest pain

 Occupational lung disease: Hx of exposure

 Pneumocystis carini: HIV+, dry cough, oral candidiasis,

 Histoplasmosis: closely resembles TB with batwing appearance on CXR in HIV+ pt

 Karposi sarcoma: HIV+ pt; closely resemble TB, skin lesions may be present

 Sarcoidosis: dry cough, external manifestations like hepatosplenomegaly, and

keratoconjunctivitis

TETANUS

Introduction: Tetanus is a neurologic disorder, characterized by increased muscle tone and spasms,
which is caused by tetanospasmin, a powerful protein toxin elaborated by Clostridium tetani (know the
biology). Tetanus occurs in several clinical forms, including generalized, neonatal, and localized disease.
The median time of onset is 7 days

History:

Biodata

 Age: (neonates-neonatal tetanus, elderly: depressed immunity)

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  Sex: Male>female (due to occupation)

 Address: rural>urban

 Race: black>Caucasians

 Occupation: >farmers

Presenting complain:

 Abnormal body movement in form of spasm, lock-jaw, or convulsion

 Dysphagia

 Neck and back stiffness

 Neck pain

 Grimace facial expression (Risus sardonicus)

 Arching of the back (opisthotonus)

 fever

Hx of presenting complain

 Course:

o there may be a preceeding hx of trauma (3-14 days)

o the spasms are painful and do not impaire with the level of consciousness, they may be
spontaneous or provoked by slight stimulation

 Cause:

o hx of penetrating or burn injury (even a trivial injury is significant)

o hx of otitis media

o hx of an ulcer (sore) on any part of the body

 R/O differentials

o drug hx: especially anticonvulsants (to r/o epilepsy), antiemetic (phenothiazine,

metochlopramide) and strychnine poisoning

o hx of dog bite (r/o rabies)

o hx of fever associated with headache, neck pain and stiffness (r/o encephalitis or
meningitis)

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 o when pt had last meal (r/o hypoglycemia)

o hx of spider bite (r/o widow spider envenomation)

o hx of injury to the head (r/o SAH)

 complication

o hx of fracture and additional injuries from violent spasm

o hx of profuse sweating, fever, palpitation (autonomic dysfunction)

o hx of cough and difficulty in breathing (r/o aspiration pneumonia or pulmonary

embolism)

o hx of calf muscle pain/swelling (suggest DVT)

o passage of coca cola coloured urine- rhabdomyolysis which may lead to ARF

o hx of pressure sores

 care

o what was done to the patient so far both at home and in the hospital and improvements
so far

 past medical and surgical hx

o hx of resent surgical wounds- may give portal of entry

o hx of thyroid surgery- r/o hypocalcemia which may mimic tetanus

o hx of instrumentation and other procedures

o hx of drug allergy

 family and social hx

o take a good social hx to r/o conversion disorder

Examination

Patient is usually conscious (GCS 15/15), may be dehydrated. Signs of autonomic dysfunction may be
present such as tachycardia and hypertension.

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 Acute meningitis

Introduction

An infection of the meningial covering of the brain & spinal cord, often fatal with significant morbidity &
mortality hence is a medical emergency. Duration of symptoms is usually within hours to days

Biodata

High in developing countries due to:

 Poor hygiene

 Climate (hot, dry and dusty) but decreases with onset before rain

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Presenting complain (PC)

 Fever

 Headache

 Neck stiffness

 Can’t open eyes in light (photophobia)

 Vomiting

 Drowsy or Loss of consciousness

(N/B atypical presentation -lethargy with absence of classical presentation- in elderly &
immunocompromised patient)

History of presenting of complaint

Course

? Onset, duration, and course of symptom

? Coma and focal neurological signs (severe bacterial meningitis)

? Purpuric rash and very rapid, abrupt onset of obtundation and circulatory collapse (meningococcal
meningitis with septicemia)

?unwell for weeks or months with recurrent fever, sweating, joint pain and transient rash (chronic
meningococcemia)

Cause

Infections

 Exposure to pt with similar illness- (meningococcal meningitis)

 Hx of URTI, SCD, Splenectomy, Alcoholism--- (S. pneumonia)

 Immunocompromised, Hospital acquired infection, Recent brain surgery or head injury

(gram – ve organism, staph aureus)

 intake of unpasteurized milk, raw vegetables consumption and soft cheese - (L

monocytogenes)

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  TB meningitis:? Chronic cough, night sweat and fever. Hx of contact with chronically
coughing adult. Hx of immunosuppression.

 ?ear pain/ discharge (R/O otitis media)

 ? Painful parotid swelling (R/o mumps)

 Painful rash and ulceration of mouth, hands, feet, buttocks and thighs. (R/o echovirus=
hand-foot-mouth syndrome)

 ? Trauma/ skull fracture, neurosurgical procedure - r/o direct innoculation

Non-infectious

Neoplasm (malignant meningitis) - anorexia, anemia and asthenia

? SLE

Complications

b. Shock (oliguria, hyperpyrexia, impaired consciousness, hyperventilation, collapse rapid

thread pulse etc.)

c. Coma

d. Seizures

e. Cerebral abscess

f. Decreased hearing or deafness

g. DIC (bruising and bleeding)

h. Renal failure (oliguria, decrease urine output, hyperkalemia and metabolic acidosis)

i. Pericarditis (septic or reactive)

j. Septic arthritis

k. Peripheral gangrene

Care

Care sought including use of traditional medications, investigations and results, plans and treatment

Past medical and surgical history

 Diagnosis of the following conditions; pneumonia, TB, otitis media, DM, HIV and cancers

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  Previous surgery

Family history and social history

 Socioeconomic status, environmental hygiene, ventilation, alcohol ingestion and cigarette

smoking

 Hx of similar illness in the family

Examination

 General

 Temperature

 PR, RR and BP

 Kernig’s sign(extension at the knee with hip joint flexed causes spasm of the
hermstrings)

 Brudzinski’s sign(passive flexion of the neck causes flexion of the hips and knees)

 Neck stiffness

 Rashes and Petechial hemorrhages (meningococcal meningitis)

 lymphadenopathy

 CNS

Do a detailed Neurological examination including GCS

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