CONTENTS 2- Woman's Health

* Emergency : Emergency in Family

* Part One : Internal medicine * Part Five : Psychiatry
A- CVS : 1- Mental disorders
1- HTN 2- Somatization
2- Dyslipidemia*
3- ECG* * Part Six : Community Medicine
B- RS : - URTI 1- Periodic health evaluation*
C- ES : 2- Family Planning
1- DM 3- Geriatric medicine
2- Thyroid 4- Smoking
3- Osteoporosis 5- Communication
D- GI : - Hepatitis 6- Evidence based medicine*
E-Hematology: - Anemia
F- MSS : - MSS problems
G- Dermatology Problems
* Symptoms :
* Part Two : Surgery 1- Fatigue & General tiredness
1- Minor Injury* 2- Obesity
2- Urology 3- Headache
4- Dizziness
* Part Three : Pediatrics 5- Red Eye
1- Baby well being & Immunization 6- Chest Pain
2- Child with Fever 7- Dyspnea
8- Abdominal Pain *
* Part Four : Obs & Gyne 9- Dyspepsia*
1- Breast problems
 Emergency in primary care
A. Diabetic Ketoacidosis :
- A medical emergency where insulin deficiency
 Hyperglycemia + Electrolyte disturbances 
Ketonemia + Metabolic acidosis .
- Acute complications of diabetes
- Mostly with Type 1 DM
* Mechanism:
- Lack of insulin  ↑ glucagon 
gluconeogenesis & glycogenolysis  ↑ glucose
in the blood.
- High glucose levels spill over into the urine,
taking water and solutes (such
as sodium and potassium) along with it in a
process known as osmotic diuresis. 
dehydration, polyuria , polydipsia.
- Dehydration  2ndary Hyperaldosteronism 
↑ K+ loss
- Lack of insulin  release of free fatty
acids from adipose tissue (lipolysis)  converted
in liver to Ketone bodies  Metabolic acidosis
- Acidosis  forces H+ into cells displacing
K+
- Body tries to compensate by Hyperventilation
(Kaussmaul breathing)
* Triggering and Risk Factors :
1- Infection
2- Infarction ( cardiac , cerebral ,mesenteric )
3- Insulin ( low dose in noncompliance patient )
4- Intraabdominal process ( pancreatitis )
5- Intoxication ( alcohol )
6- Idiopathic
7- Physical stress and drugs ( glucocorticoids ,2nd
generation antipsychotic )
* Symptoms :
1- nausea, vomiting
2- Abdominal pain
3- Polyuria
4- Thirst
5- Shortness of breath
6- Weakness
* Signs
1- Dehydration
2- Kussmaul Breathing
3- Hypotension
4- Tachycardia
5- Lethargy/cerebral edema/possibly coma
6- ketotic odor ( fruity smell )
7- Abdominal tenderness
*Investigations:
1.Urinalysis for ketones
2.Ketones can be measured in urine
(acetoacetate) and also in the blood (β-
hydroxybutyrate).
3.Arterial Blood gases; to access the severity
of acidosis
4. Blood sample; for urea and creatinine
5. Infection screen; CBC, blood and urine
culture, CRP, chest Xray.
* Diagnosis :
- Mild:
blood pH mildly decreased to between 7.25
and 7.30 (normal 7.35–7.45);
serum bicarbonate decreased to 15–18 mmol/l
(normal above 20);
 the patient is alert
- Moderate:
 pH 7.00–7.25,
 bicarbonate 10–15,
 mild drowsiness may be present
- Severe:
pH below 7.00,
bicarbonate below 10,
stupor or coma may occur
* Management
1- Fluid replacement :
- isotonic saline given at rate 15-20ml/kg/hour
for the first several hours (1-3)
- Once the serum glucose below 200-250mg/dl
change to one-half normal saline with dextrose
(D5 1/2NS ) at rate sufficient to replace free
water loss induced by osmotic diuresis .
2- Glucose and electrolytes :
- Administer short-acting insulin: IV (0.1
units/kg)
- Assess patient: What precipitated the episode
- Replace K+
 Continue above until patient is stable=
glucose goal is 150–250 mg/dL
- Administer long-acting insulin as soon as
patient is eating
-------------------------------------
B.Hypertensive crisis * Management:
- Increase in blood pressure to very high levels  It is important that the BP be lowered
≥180/120 mm Hg which mostly results in target smoothly, not too abruptly.
organ damage. - The initial goal is to lower BP by 25% of the
- If there is no evidence of target organ damage, mean arterial BP within minutes to 2 hours and
the condition is a hypertensive "urgency" rather stabilize BP to approximately 160/100 over the
than "emergency" . next 2 to 6 hours.
 Organ damage - Excessive reduction in blood pressure can
1. Major neurological changes precipitate coronary, cerebral, or renal ischemia
2. Hyertensive encephalopathy and possibly infarction.
3. Cerebral infarction - Sodium Nitroprusside is the most commonly
4. Intracranial haemorrhage used IV drug. It has an almost immediate
5. Acute LV failure antihypertensive effect.
6. Aortic dissection - Oral agents such as Captopril, Clonidine,
7. Renal failure Labetalol can be used but they all have a delayed
onset of action. Therefore they are used when
*Causes : blood pressure control is achieved
1. One main cause is the discontinuation of - Hydralazine is reserved for use in pregnant
antihypertensive medications patients.
2. Autonomic hyperactivity ---------------------------------------------
3. Stroke C. Myocardial Infarction :
4. Heart attack * occurs most often in the early morning hours,
5. Heart failure because of :
6. Kidney failure 1- the increase in catecholamine-induced platelet
7. Aortic aneurysm aggregation
8. preeclampsia and eclampsia 2- increased serum concentrations of
9. Drug use (cocaine, amphetamine.) plasminogen activator inhibitor-1
(PAI-1) that occur after Awakening
* Signs & Symptoms: * evaluation and initial management should take
1. headache, vomiting and/or subarachnoid or place promptly
cerebral hemorrhage  due to increased ICP. * the benefit of early prviding care decrease the
2. Chest pain, dyspnea motility & morbidity .
3. Headache, epistaxis
4. Confusion, altered mental status. * Risk factors:
5. Arrhythmias 1.previous cardiovascular disease
6. Papilledema must be present before a 2.old age
diagnosis can be made. 3.Smoking & excessive alcohol consumption.
7. eyes may show retinal hemorrhage or 4. Dyslipidemia,
an exudate. & hypertensive retinopathy. 5. DM + HTN
8. left ventricular dysfunction 6.lack of physical activity
9. The kidneys will be affected, resulting in 7.Obesity
hematuria, proteinuria, and acute renal failure. 8. chronic kidney disease
9. use of cocaine and amphetamines
* Investigation :
- CBC ± clotting screen. *Clinical presentation
- U&Es, creatinine. 1- Sudden severe retrosternal pain that
- Liver and TFTs. lasts >30 min radiating to the neck, lower jaw or
- Blood sugar measurement. left arm.
± Cardiac enzymes and fasting blood lipids. 2- Pain is not relieved by Nitroglycerin or rest.
3- Nausea, and vomiting.
4- Shortness of breath.
5- diaphoresis.
6- Palpitation.
7- Light headedness.
 Silent in DM , HF patient & they come with :
1-VF
2-Syncope
3-Stroke
4-Confusion
* Diagnosis : 2 of 3
1) Typical symptoms.
2) Rise in cardiac enzymes
3) ECG change : Pathological Q waves, ST
elevation or depression on ECG.
4)Coronary intervention.
Cardiac enzymes:
1- Troponin T & I
- preferred enzymes, they are are highly
sensitive and specific for cardiac damage.
- Serum levels increase within 3-12 hours from
the onset of chest pain, peak at 24-48 hours, and
return to baseline over 5-14 days
2. Creatine kinase (CK-MB)
- CK-MB levels increase within 3-12 hours of
onset of chest pain, reach peak values within 24
hours, and return to baseline after 48-72 hours
3. Myoglobin
- It may be detected as early as two hours after
an acute myocardial infarction. This enzyme high
sensitivity but poor specificity
* Management:
When the patient with suspected acute MI
reaches the emergency department (ED)
evaluation and initial management should take
place promptly, because the benefit of
reperfusion therapy is greatest if therapy is
initiated early.
 The initial evaluation of the patient ideally
should be accomplished within 10 minutes of his
or her arrival in the ED; certainly no more than
20 minutes should elapse before an assessment is
made.
 On arrival in the ED the patient with
suspected acute MI should immediately receive
(1) oxygen by nasal prongs; & Obtain IV access
for CBC, cardiac enzymes, electrolytes, KFT.
(2) sublingual nitroglycerin (unless systolic
arterial pressure is less than 90 mm Hg or heart
rate is less than 50 or greater than 100 beats per
minute [bpm]);
(3) adequate analgesia (with morphine sulfate or
meperidine); and
(4) aspirin, 160 to 325 mg orally.
(5)A 12-lead electrocardiogram (ECG) should
also be performed. ST-segment elevation (equal
to or greater than 1 mV) in contiguous leads
provides strong evidence of thrombotic coronary
arterial occlusion and makes the patient a
candidate for immediate reperfusion therapy,
either by fibrinolysis or primary percutaneous
transluminal coronary angioplasty (PTCA).
Symptoms consistent with acute MI and left
bundle branch block (LBBB) should be managed
like ST-segment elevation. In contrast, the
patient without ST-segment elevation should not
receive thrombolytic therapy. The benefit of
primary PTCA in these patients remains
uncertain
6- Antiemetic drugs (metoclopramide).
7- Anti platelet (clopidogrel).
9- B-blocker(Atenolol) ,, ACEI
10 -Unfractionated Heparin
Reperfusion therapy( restores blood flow
through blocked arteries, typically after a heart
attack)
1.Thrombolytic agents: These agents are given
in the first 12 hours, but best given in the first 4
hours after MI attack. They are given only in
STEMI and are contraindicated in NSTEMI
and unstable angina. They are indicated before
necrosis appears ( Q wave on ECG).
(streptokinase, urokinase, plasminogen activator).
2.PTCA (Percutaneous coronary intervention)
3.CABG (Coronary artery bypass surgery)
-------------------------------------------------
D. Pulmonary Edema :
- a condition caused by accumulation of fluid
within the parenchyma and air spaces of the
lungs, affecting gas exchange making it difficult
to breath.
* Causes:
1. Cardiogenic causes: left ventricular failure.
2. Non cardiogenic causes: lung infection,
kidney disease, hypertensive crises, neurogenic
causes
 6. No exacerbations
* Sx & Sign
1. Extreme shortness of breath, dyspnea, * Clinical presentation :
orthopnea, and PND. 1. Severe shortness of breath.
2. Anxiety. 2. chest tightness or pain.
3. cough with pink frothy sputum. 3.coughing or wheezing.
4. Excessive sweating. 4. Retractions.
5. Chest pain. 5. Difficulty in talking. Blue lips, finger nail.
6. Confusion 6. Pale, sweaty face. Feeling of anxiety or panic.
7. Crackles 7. Low peak expiratory flow (PEF) readings .
8. Abnormal heart sounds 8. Worsening symptoms despite use of a quick-
9.Tachycardia relief inhaler.
10. Tachypnea  Physical examination :
11. Pallor or cyanosis. 1. General appearance of the patient.
2. Vital signs.
* Tests and diagnosis 3. level of alertness.
1- Chest x-ray: Fluid in the alveolar walls, 4. Hydration status.
Kerley B lines, increased vascular shadowing and 5. Respiratory distress.
possibly pleural effusion. 6. Wheezing.
2- Arterial blood gases: low oxygen saturation. 7. Signs of hypoxemia.
3- Echocardiogram: Changes in the ventricles 8. Pulsus paradoxus.
maybe present.
4- ECG: Signs of a heart attack or problems with * Management :
the heart rhythm. 1. Oxygen: high dose by mask 8-10L/min to
keep the saturation above 95%.
* Management :
1) ABC + Semi-setting position 2. Nebulized Salbutamol.
 High flow oxygen by mask (CPAP, VPAP). 3. IV Salbutamol: It is used when the patient’s
tidal volume is reduced
 IV line access and draw blood samples.
2) Preload reducers: these drugs decrease the 4. Ipratropium Bromide :
pressure caused by fluid going to the heart and - It is an anticholinergic bronchodilator with no
lungs. e.g. nitroglycerin and diuretics. systemic atropine-like effects and no inhibition of
3) Afterload reducers: These drugs dilate the mucociliary clearance.
- It has good synergy with beta2 agonist.
blood vessels and take a pressure load off the
heart's left ventricle. e.g. Enalapril and captopril. - Ipratropium can be mixed with salbutamol in
4) Analgesia (morphine sulfate), decreases the nebulizer.
anxiety and causes vasodilation. 5. Corticosteroids:
- Reduce the severity of acute severe asthma.
----------------------------------------------
- Reduce the inflammation in bronchial mucosa.
E. Exacerbation of Asthma
- Defined as an acute or sub acute episode of - Potentiate the relaxation of bronchial smooth
progressive worsening of symptoms of asthma, muscle by Beta2 –agonists.
including shortness of breath, wheezing, cough, - Reduce mucous production.
- The most important drug in treating asthma
and chest tightness usually at night or after
exercise.(minor, life-threatening). - Decreases recruitment and activation of
inflammatory cells
- Up-regulates B2 receptors
*Controlled asthma:
1. Day time symptoms: non or ≤ 2 /week - Decreases microvascular permeability
2. No limitations of activity - Decreases mucus production
3. No nocturnal symptoms  Management if PEF < 40% , Severe :
4.Need for reliever : non or ≤ 2/week 1. Oxygen
5. Normal lung function 2. Nebulized SABA and ipratropium hourly or
continuous
3. Systemic steroids
4. Consider adjunctive therapy (magnesium
sulfate ± heliox)
PEF < 25% Life threatening
--PFT is not necessary
1. Oxygen
2. Nebulized SABA & ipratropium
3. Systemic steroids
4. Adjunctive therapy
5. ICU admission & consider mechanical
ventilation

* Prevention of subsequent attacks of asthma

1. Avoidance of triggering factors.
2. Environmental control.
3. Prompt recognition and treatment of
exacerbation factors.
4. Patient and parents education.
5. Monitor PEFR at home.
6. Development plan for management at home.
7. Development good communication and good
relationship between the physician and he
patient.

Stage Symptoms Night PFT

symptoms

Mild < 2/week < 2/month PEF / FEV1 N

intermittent
PEF var. < 20%

Mild > 2/week > 2/ month PEF / FEV1 N

persistent not daily PEF var. 20-30%

Moderate Daily symptoms > 1/week PEF/FEV1 60-80%

persistent
PEF var. > 30%

Severe Cont. symptoms Frequent PEF/FEV1 < 60%

persistent
PEF var. > 30%
 HYPERTENSION
* General Characteristics : - Causes : Acc. To Age
1- Definition :  Children and adolescents
Sustained elevation of systemic arterial blood 1. Renal parenchymal disease, such as
pressure, equal to or greater than 140/90. a. Glomerulonephritis, including (acute
2- Types of hypertension: postinfectious glomerulonephritis , Alport syndrome
-Type 1 hypertension: , IgA nephropathy , minimal change disease , lupus
*manifested by vasoconstriction and high renin nephritis , membranoproliferative
levels. glomerulonephritis
*common in young white people membranous nephropathycongenital
*responds better to ACEIs,ARBs and beta abnormalities )
blockers. b. Reflux nephropathy
-Type 2 hypertension: 2. Coarctation of aorta
* sodium retnsion and low rennin "excessive sodium  Adults 19-39 years old
reabsorption". 1. Thyroid disease
* common in young black people. 2. Renal artery stenosis caused by
*responds better to diuretics and calcium fibromuscular dysplasia
channel blockers. 3. Renal parenchymal diseases
3- CAUSES :  Adults 40-64 years old
* Primary HTN 1. Thyroid disease
- Accounts for 95% of cases. 2. primary hyperaldosteronism
- Elevated BP without an identified cause. 3. Cushing disease
- Cause unknown, but it’s a complex process 4. pheochromocytoma
that results from a variety of physiological and 5. obstructive sleep apnea (OSA)
environmental factors.  Adults ≥ 65 years old
1.Heredity: interaction of genetic, and 1. atherosclerotic renal artery stenosis
environmental factors . 2. Renal failure
2.High salt diet. 3. hypothyroidism
3.Altered renin-angiotensin mechanism. ** Features of secondary HTN:
4.Stress which activate the sympathetic system. 1. Early or late onset of HTN (<20, >50).
5.Insulin resistence and Hyperinsulinemia. 2. History of tachycardia, sweating and
headache.
* Secondary HTN
- Accounts for 5% of cases. 3. Past or family history of renal disease.
- Specific cause of HTN can be identified. 4. Resistant HTN in a compliant patient.
-Causes: in General 5. Symptoms of sleep apnea.
1. Renal: any cause of chronic kidney 6. History of amphetamine, cocaine, or
alcohol abuse.
disease
renovascular hypertension 7. Use of OCP, NSAID, coticosteroids.
2. Endocrine: 8. History of hirstuism or easy bruising .
Cushing syndrome,primary
hyperthyroidism,hyperparathyroidism,pheochro 4- Consequences (Hypertension is a risk factor
mocytoma for ) :
1. coronary artery disease (CAD)
3. obstructive sleep apnea (OSA)
2. heart failure
4. coarctation of aorta
5. Medications: 3. aortic regurgitation
NSAID.OCP,MAOI,antihistamine, 4. atrial flutter
decongestants, alcohol. 5. peripheral arterial disease (PAD)
6. stroke Based on 3 or more visits with 2
7. intracerebral hemorrhage measurements at each visit.
8. transient ischemic attack (TIA) Confirm
9. mild cognitive impairment (MCI) - within two months if readings are within 140-
10. chronic kidney disease 159/90-99.
- Within one month if readings are within
5- Epidemiology : Who is most affected: 160-179/100-109.
- onset generally at age 20-50 years, but - Within one week if readings within
prevalence increases with increasing age. 180-199/110-119.
-Incidence/Prevalence: - One reading if more than 200/120
prevalence of hypertension OR
 general population > 25% b. BP>= 140/90 with the Presence of end- organ
 people aged 60-69 years >50% damage.
 people ≥ 70 years old >75% .
-------------------------------------------------- * Ambulatory blood pressure values consistent
* Clinical Entities : with hypertension
1- History: > 135/85 mm Hg when awake
- generally asymptomatic. > 120/75 mm Hg when asleep
- usually diagnosed incidentally during
routine visits. 4- Investigations
- Clinical manifestation include: ischemic A.Recommended by most guidelines :
heart disease, stroke, peripheral vascular disease, 1. Fasting blood sugar.
renal insufficiency, retinopathy characterized by 2. S.Creatinine
exudates or hemorrhage, and, in severe HTN, 3. S.potassium
papilledema. 4. U/A.
2- Classification: 5. Lipid profile.
A. based on JNC 8 : 6. ECG, may consider echo if abnormal
- Normal : Blood Pressure < 120/80 mm Hg ECG.
- Prehypertension: BP 120-139 / 80-89 mm B.Recommended by some
Hg. 1. S. Ca
- Stage 1 hypertension: 2. S. Na
BP 140-159 / 90-99 mm Hg. 3. S.Uric acid
- Stage 2 hypertension : 4. Urine microalbumine
BP ≥ 160 / ≥ 100 mm Hg; evaluate within 1 month 5. Hb or PCV
OR if > 180/110 mm Hg , within 1 week. C.Other tests may be ordered based on clinical
B. based on ESH/ESC : findings
- Optimal BP < 120 / 80 mm Hg 1.Coarctation of aorta (CT- angiography,
- Normal BP 120-129 / 80-84 mm Hg echocardiography, or MRI)
- high normal BP 130-139 / 85-89 mm Hg 2. Cushing syndrome suspected -
- grade 1 hypertension - dexamethasone suppression test or 24-hour urinary
BP 140-159 / 90-99 mm Hg free cortisol
- grade 2 hypertension - 3. parathyroid disease suspected - serum
BP 160-179 /100-109 mm Hg parathyroid hormone
- grade 3 hypertension - 4.Pheochromocytoma suspected - plasma or
BP ≥ 180 /110 mm Hg urinary metanephrines
- isolated systolic hypertension - 5. primary aldosteronism suspected - plasma
SBP ≥ 140 mm Hg and DBP < 90 mm Hg aldosterone and plasma renin activity
6.Renovascular hypertension (renal artery
stenosis) suspected - duplex ultrasonography, CT
3-Diagnosis of HTN established if:
a. Mean of BP >=140 /90 mmHg. angiography, or magnetic resonance angiography
(MRA)
7. Sleep apnea suspected - sleep study or
nocturnal pulse oximetry
8. thyroid disease suspected -
thyroid-stimulating hormone (TSH)
4-Comlications:
Target organ complication:
1.CVS: angina, LVH, aortic aneurysm,
atherosclerosis
2. CNS: stroke, intracerebral hemorrhage
3. Nephropathy.
4. Retinopathy.
4- Management :
A. Goals of the therapy :
-The ultimate goal of antihypertensive
therapy is to reduce morbidity and mortality.
- Treating the SBP and DBP to targets that
are below 140/90 mmHg is associated with a
decrease in the risk of cardiovascular complications .
- target blood pressure (BP) < 140/90 mm Hg
recommended for most patients.
- In patients with HT and DM or renal
disease the BP goal is still <140/90 mmHg .(JNC 8).
B. BENEFITS OF LOWERING THE BP
In clinical trials , antihypertensive therapy has been
associated with reductions in the risks of:
- stroke by 35 – 40%
- MI by 20 – 25%
- HF by 50%
C. Treatment
1.LIFE STYLE MODIFICATION
- The first step in treatment
- Lifestyle modification alone effectively
controls about 10% of patients.
- Adoption of a healthy lifestyle is critical for the
prevention of high blood pressure, and is an
important part in the management of hypertension
patients.
1- Weight loss:can reduce blood pressure
(BP) by about 1 mm Hg per kg lost
2- Adoption of the DASH Eating plan:
Dietary approach to stop hypertension eating plan
(can reduce BP by 8-14 mm Hg )
Limiting the intake of saturated fat,
cholesterol and total fat.
 Include fruits, vegetables and low fat
dairy products in the diet.
 Avoiding red meat, sweets and sugar-
containing beverages.
 Increasing k , Ca , Mg , protein and fiber
content of diet.
 Restricting salt intake to <2.4 g/day
reduces BP by mean 5-10/2-3 mm Hg.
3- Emerging in regular aerobic physical
activity , such as brisk walking at least 30 minutes a
day most days of the week.
4- Limiting alcohol intake.
5- Counselling to quit smoking.
2. Pharmacological treatment
* Start medications from the beginning, one med for
stage 1, 2 for stage 2
* initial antihypertensive therapy typically starts
with 1 of 5 drug classes :
1. Thiazide-type diuretic - recommended option for
all patients in most guidelines.
2. Angiotensin-converting enzyme (ACE)
inhibitor - recommended option either for nonblack
patients or all patints.
3. Angiotensin receptor blocker (ARB) -
recommended option for nonblack patients or all
patients.
4. Calcium channel blocker - recommended
option for all patients in most guidelines.
5. beta blockers - recommended option in
some guidelines for patients < 60 years old) but not
recommended as initial option in American or
British guidelines, and may increase risk of adverse
cardiovascular events compared to other
antihypertensive drugs
* Most patients will require two or more
antihypertensive medications to achieve adequate
control .
- add drugs (from other classes than initial therapy)
if target blood pressure levels not achieved with
monotherapy.
- ACE inhibitor and ARB combination not
recommended.
D.Recommendations for medical NICE Guidlines
- aged >=55 YO , the first choice for initial therapy
should be either a CCB or a thiazide diuretic
- < 55YO , the first choice for initial therapy
should be an ACE inhibitor or ARB.
- If treatment with 3 drugs is required , the
combination of a CCB , ACE inhibitor and a
thiazide diuretic should be used
- If BP remains uncontrolled on adequate
doses of 3 drugs consider adding a fourth and/or
seek an expert advise .
 initial treatment with ACE inhibitor or ARB often
recommended for patients with diabetes, chronic
kidney disease, or coronary artery disease
 ACE inhibitor and beta blocker
recommended in patients with heart failure.
 HYPERTENSION TREATMENT:
SPECIAL POPULATIONS
* African Americans and Elderly
Thiazide diuretics,or CCB
* Diabetes Mellitus
ACEI plus or minus thiazide diuretics OR
ANY antihyperensive med.
* Congestive Heart Failure
ACEIs, ARBs, Beta blockers, or Aldosterone
antagonists
* Coronary Artery Disease
Beta blockers, CCBs, or ACEIs
* Cerebrovascular Accident
ACEIs and indapamide
* Pregnancy
Methyldopa, nifedipine, or labetalol
E. Follow up and Monitoring
- Patients should return for follow-up and adjustment
of medications monthly until the BP goal is reached.
- More frequent visits for stage 2 HTN or
with complicating co-morbid conditions.
- Serum potassium and creatinine monitored
1–2 times per year.
- BP at goal and stable, followup visits at 3to
6-month intervals.
- Comorbidities, such as heart failure,
associated diseases, such as diabetes, and the need
for laboratory tests influence the frequency
of visits.
- Low-dose aspirin therapy should be
considered only when BP is controlled, because the
risk of hemorrhagic stroke is increased in patients
with uncontrolled hypertension.
------------------------------------------------------
*** CASE STUDY :
1) 47 y/o AA male presents to the office
with URI symptoms. He is taking no
medications with the exception of
pseudoephredrine for his cold. You notice
when looking at his vital signs that his blood
pressure is 180/106. Repeat measurement is
175/103.
What is your initial approach to this patient?
A) Start a chronic antihypertensive since he
is at risk for a stroke within the next couple
of days.
B) Administer clonidine in the office to
reduce the blood pressure to 150/100.
C) Watch the patient over the next 2 weeks
and get additional blood pressure readings
before deciding what to do.
D) Schedule the patient for outpatient labs
and EKG.
The patient returns to your office with six
blood pressure readings taken over a two
week period at a local pharmacy. The
majority of the readings are in the 155/98
range. Only two of the six readings are less
than140/80.
Your best response at this point is to:
A) Start an antihypertensive
B) Send the patient for a 24 hour ambulatory
blood pressure measurement
C) Don’t worry about the blood pressure
readings since they are abnormal due to
stress at work
D) Get a nephrology consult to help in
decision making
The best drug(s) to start this patient on is:
A) An ACEI
B) A thiazide diuretic
C) A calcium channel blocker
D) A beta blocker
E) B and C
F) A,B,C, and D
2) A 58 y/o female with HTN, diabetes
mellitus, ischemic cardiomyopathy, and stage
4 CKD presents for follow-up. Her current
medications are insulin, ASA, metoprolol,
and lisinopril. Her blood pressure is 142/86
and she has significant lower extremity
edema. Her labs reveal a serum K+ of 5.3
What is her target blood pressure?
To achieve her target BP while avoiding
adverse events, the best initial step is:
A) Discontinue lisinopril
B) Furosemide 20mg po qam
C) HCTZ 12.5mg po qam
D) Increase lisinopril
E) Losartan 25mg po daily
---------------------
** ROUND NOTES
** OWN MIND MAP

Dyslipidemia
* General Characteristics : - Secondary
a- Definition : A condition characterized by
elevated serum levels of total cholesterol( TC), low-
------------------------------------------------
density lipoprotein cholesterol (LDL-C)or non-high-
density lipoprotein cholesterol (none HDL-C).
 This is associated with elevated risk for
cardiovascular disease. also lower levels of HDL-C
and, to a lesser extent, elevated triglyceride levels.
b- Lipid Parameter Function:
1.VLDL
- Carries triglycerides to peripheral
cells
- High levels may be associated with
increased CHD risk
2. LDL
- Carries cholesterol to cells ------------------------------------------------------
- High levels linked to increased
*Clinical Entities :
CHD risk
* Symptoms & Signs :
- Primary target of cholesterol-
reducing therapy
3.HDL
- Removes cholesterol from cells
- High HDL considered protective against CHD
- HDL >60 mg/dL decreases CHD risk
4.Lipoprotein(a)
- A complex of LDL and
apolipoprotein(a)
- Prevents LDL from being taken up
* Checking lipids:
by the Liver
1. Non fasting lipid panel  measures HDL and
- Elevated Lp(a) is an independent
total cholesterol
risk factor for premature CHD
2. Fasting lipid panel  Measures HDL, total
5.Triglycerides
cholesterol and triglycerides
- A neutral fat stored in adipose cells
LDL cholesterol is calculated:
- Positively correlated with risk for
LDL cholesterol = total cholesterol – (HDL +
CHD
triglycerides/5)
c. Causes of Hyperlipidemia *Values of Lipids:
- Primary * Total Cholesterol
1. Familial Hypercholestrolemia Abnormally of - < 200 → Desirable
the LDL receptor - 200-239 → Borderline
2. Familial hypertriglyceridemia  High VLDL - ≥240 → High
production, decreased lipoprotein lipase activity * LDL
3. Familial Combined Hyperlipidemia  LDL and - < 100 →Optimal
VLDL, increased secretions of VLDLs
- 100-129 → Near optimal 9- Chronic renal disease
- 130-159 → Borderline 10- Metabolic syndrome
- 160-189→ High *Management and Prevention:
- ≥ 190 → Very High
*HDL
- Low if <40 mg/dL in males and
< 50 mg/dl in females).
>60 high
* Serum Triglycerides
- < 150 → normal
- 150-199 → Borderline
- 200-499 → High
- ≥ 500 → Very High

* Screening :
1- Men over 35 and woman 0ver 45.
2- Anyone with atherosclerotic symptoms regardless
of age
3- Anyone with diabetes regardless of age
4- Family history of premature CVD
5- Inflammatory diseases (lupus, rheumatoid arthritis,
psoroasis)
6- Children of patients with severe dyslipidemia
7- Clinical signs of hyperlipidemia
8- Erectile dysfunction
Treatment of the metabolic syndrome
Treat underlying causes (overweight/obesity
and physical inactivity):
Intensify weight management
Increase physical activity
Treat lipid and non-lipid risk factors if they
persist despite these lifestyle therapies:
Treat hypertension
Use aspirin for CHD patients to reduce
prothrombotic state
Treat elevated triglycerides and/or low HDL
(as shown in Step 9 below)
 Diabetes
Mellitus
* General Characteristics : D. Metabolic Syndrome (MS)
A. Definition : Any Three of the following. (AHA)
* an Endocrine disorder characterized by 1. Central obesity
hyperglycemia resulting from variable degrees of - waist circumference ≥ 102 cm for men and ≥ 88 cm
insulin resistance and deficiency. for women ( USA and Europe).
* DM is a leading cause of morbidity and mortality, > 94 and 80 cm in middle east countries)
costly yet controllable with a prevalence of 17.1% in 2. Triglycerides≥ 150 mg/dl (1.7 mmol/L)
Jordan. 3. HDL-cholesterol:
* Blood sugar management is only part of story. It is men < 40mg/dl (1.03 mmol/L),
important to ensure that Blood pressure and women < 50mg/dl (1.29 mmol/L)
cholesterol level are tightly controlled in order to 4. BP ≥ 130/85mmHg
reduce complications. 5. Fasting glucose≥ 100mg/dl (5.6 mmol/L)
B. Epidemiology
- worldwide prevalence is 9% in men and 7.9% in  Pts should undergo a full cardiovascular risk
women in 2014. assessment and management should be aggressive to
( more than 85% of whom have type 2 variety). reduce the risk of CVD and type 2 D.M
- Type 2 DM is much more strongly inherited than
type 1 DM --------------------------------------------------
- The incidence of T2DM varies significantly among * Clinical Entities
and within different ethnic groups according to their A. Who should be screened for D.M
culture and lifestyles. a) T1DM: no indications for screening
b) T2DM: Testing should be considered in all adults
C. Classification of different types of Diabetes: who are overweight (BMI) ≥ 25 kg/m2) and have
1-T1DM:(beta-cell destruction, usually leading to additional risk factors:
absolute insulin deficiency) 1)Sedentary lifestyle
immune-mediated 2)Family history of DM.
idiopathic 3)Prior history of Pre-diabetes (annual screening)
2-T2DM:(constitutes 85% of all diabetics) is 4)Hypertension, Hyperlipidemia, Coronary artery
characterised by insulin resistance and variable disease.
insulin secretory defects
5)History of gestational DM or delivery of infant
3) Gestational diabetes. weighing over 4.5 kg
4) Other types:
a) Genetic defects in insulin production or action 6)Pregnant ladies
b) Exocrine pancreatic disease 7)History of PCOS
c) Associated with endocrinopathies * Community screening outside a health care setting
d) Drug induced is not recommended
e) Infection * In the absence of the above criteria testing should
* 50% of T2DM are not diagnosed begin at age 45 years
* If results are normal testing should be repeated at
IDDM NIDDM least 3 years intervals
Age <30 >30
Rate of onset Rapid Slow B. Diagnosis of Pre-diabetes
Body WT Thin obese 1.Impaired Fasting Glucose (IFG)
Ketosis Common rare FPG 100- 125 mg/dl (5.6-6.9 mmol/L)
HLA association Present absent 2.Impaired Glucose Tolerance (IGT)
Identical twins <50% >50% 2 hr plasma glucose 140- 199 mg/dl
(7.8- 11.0 mmol/L)
Islet cell mass Greatly reduced Slightly
- Both IFG and IGT are risk factors for future
reduced
diabetes and for
Endocrinopathies occasional rare - cardiovascular disease and associated with insulin
resistance and metabolic syndrome.
- Unless lifestyle modifications are made most people IGT 140-199
with pre-diabetes develop type 2 diabetes within 10 mmol/dl
(7.8-11
years. mmol/L)
DM ≥ 126 mg/dl ≥ 200mg/dl ≥ 200mg/dl
(7 mmol/L) (11.1 (11.1
mmol/L) mmol/L)
(with
symptoms)

C. Criteria for the diagnosis of DM D. Laboratory evaluation for newly diagnosed

1) Fasting Blood Glucose(FPG )≥ 126 mg/dl (7.0 Diabetes
mmol/L) 1) Fasting glucose , Lipid profile, Hba1c,
2) Symptoms of hyperglycemia and a casual plasma Urinanalysis,Kidney function test(KFT).
glucose ≥ 200mg/l) (11.1 mmol/L)
OR 2)Microalbuminuriashould be measured annually.
3) 2 hr plasma glucose ≥ 200 mg/dl (11.1) during an 3) Physical Exam.must include height, weight, blood
oral glucose tolerance test(OGTT). pressure.
4)Vision measurement and exam for retinopathy
*In the absence of unequivocal hyperglycemia, these should be done annually.
criteria should be confirmed by repeat testing on a 5)Baseline neurological and cardiovascular exam
different day should be obtained.
*The classical symptoms of hyperglycemia include 6)The foot exam. should include peripheral pulses,
polyuria, polydipsia or unexplained weight loss. sensation.
*Fatigue,blurred vision, recurrent monilial vaginites 7) Skin exam.for diabetic dermopathy.
may present.
*OGTT is not recommended for routine clinical use. E. Management:
a) Glycemic Goals
 Indications for OGTT
1. HbA1C < 7%
1.Patients with Impaired Fasting Glycemia (IFG)
2.Pregnant women and postpartum (in women with  HbA1C is the pry target for glycemic control.
GDM) 2. Pre-prandial glucose 70-130 mg/dl (3.9-7.2
 OGTT is performed using a 75 oral glucose load mmol/L)
in the morning after a noncaloric 8hr fast. Water is 3. Peak postprandial < 180 mg/dl (<10 mmol/L)
allowed but not coffee or smoking. - Prevention of microvascular complic. Occurs
through optimal glycemic control, normotension and
 Types of Curves when performing OGTT
1.Normal curve avoidance of excess sodium and protein intake.
2.IGT - Prevention of macrovascular complic. is achieved
3.Diabetic curve via aggressive conventional risk factors reduction.
4.Lag storage curve - A recent report indicated that only
5.Flat curve *37% of adult with diagnosed DM achieved an
HbA1C of < 7%
*Hemoglobin A1c(Hba1c)is not recommended for *36% had BdP < 130 /80 mmHg
diagnosis of D.M *48% total cholesterol < 200 mg/dl
 Normal Hba1c does not rule out D.M * 7.3% of diabetic pts achieved all three Rx goals
 Hba1c is the standard indicator of long term sugar
control. b) Treatment of Type 2 DM :
1- Weight reducing regime
* Weight reducing regime + Exercise + lifestyle
Test FPG OGTT Random
measurements
* Majority are overweight, ↑ body weight is
How to >=8 hours >=8 hrs fast At any time associated with ↑ risk of CVD
perform fasting  75g regardless of
before glucose  eating
* Reduction of 5-10% in weight can have a major
2hrs test impact on the clinical course of type 2 DM
* Normal or near normal weight will:
Normal < 100mg/dl < 140 mg/dl a) Optimize insulin sensitivity
(5.6 mmol/L) (7.8 mmol/L)
b) Minimize insulin requirement
c) Minimize cardiovascular risks
IFG 100-125 2- Encourage a healthy lifestyle
mg/dl
(5.6-6.9 a. Diet
mmol/L) - It is basically a diet for healthy living. Patient who
are over weight should follow a hypocaloric diet of
between 500-600kcal/day less than their normal
intake aiming of 0.5kg/week weight loss.
- Recommendation is for high complex CHO, low fat
diet.
- Caloric requirements vary with age, sex, ideal body
weight, level of physical activity and concurrent
illness
1) Low fat, high fiber diet (CHD > 55%, fat < 30%,
Protein 10-15%)
2) Encourage intake of monounsaturated fat.
3) Reduce salt intake.
4) Hypo caloric (500 k cal deficit) diet.
5) Limit alcohol intake < 21 units/week for men
and < 12 units for women.
b. Physical Activity
- Brisk walking for 30 minutes daily or every other
day Swimming or Gardening
- Benefits of exercise:
*Improved glucose control
*↓ C.V risk factors (Hypertension and
hyperlipidemia)
* Weight reduction
*Reduced stress
*Decreased Osteoporosis
c. Stop smoking.
d. Avoid stress.
3- Oral hypoglycemic agents
- The majority of type 2 diabetic patients require oral
hypoglycemic agents.
- At time of diagnosis pancreatic function is 50% of
normal.
1) Biguanides:(↓ HbA1C 1-2%)
Metformin(insulin sensitizers) is the drug of choice
for treatment of type 2 diabetic patient.
-It does not cause hypoglycemia and causes
- less weight gain and improve lipid profile.
- Metformin decrease blood glucose by:
a)Decrease hepatic gluconeogenesis
b)Increase glucose uptake in the muscles
c)Decrease glucose absorption ?
- Daily dose 1.5 –2.5 gm
- Side effects = diarrhoea, nausea, lactic acidosis
(avoid in patient with renal, hepatic and unstable
heart failure).
2) Sulphonylureas:(↓ HbA1C 1-2%)
- Act by stimulation of insulin release from B-cells
of pancreas.
- e.g. Glibenclamide, glipizide, gliclazide.
- Glimepiride once daily with low risk of
hypoglycemia.
- Side effects: weight gain, hypoglycemia, skin
reaction and hematological complications.
3) Thiazolidinediones(Insulin Sensitizers)
- e.g. Pioglitazone and Troglitazone can be used as
monotherapy or in combination with metformin,
sulfonylurea or insulin.
- Dosing independent of food intake and can be used
in end stage renal failure.
- Contraindications: Hepatic Impairement. H.F
4) Newer insulin secretagogues
- e.g. Repaglinide (result in insulin secretion)
Exenatide (enhance insulin secretion)
5) α–Glucosidase inhibitors
e.g. A carbose (lead to reduction in the rise of
postprandial glucose).
6) DPP-4 Inhibitors: Gliptins(increaseincretin
levels which inhibitglucagon release, which in turn
increasesinsulin secretion)
4- Insulin
- Some type 2 diabetic patients may ultimately
require insulin therapy because of :
1) Failure of dietary and medication compliance
2) Final exhaustion of beta cells.
- Basal Insulin accounts for approximately 50% of
total insulin secreted each day where as the
remaining 50% of the insulin is secreted in response
to meals.
- Types of Insulin:
1)Rapid-acting analogue e.g Aspart, Lispro
2)Short-acting e.g Regular
3)Intermediate-acting e.g NPH
4)Long-acting e.g Glargine, Detemir
5)Premixed Insulin
- Combination of depot and regular insulin are
designed indivually for patient . The most popular
plan entails
2/3 of the day’s requirement given s.c before
breakfast as a mixture of 2/3 NPH -insulin and 1/3
Regular insulin.
The remainder third is given before the evening meal
as 2/3 NPH and 1/3 Regular.
- When patient is stable and when close nursing
follow up and patient education and training are
available insulin therapy is initiated on an outpatient
basis for better prediction of outpatient energy,
dietary and insulin needs.
- An average starting estimation of insulin
requirement is about 25 units depending on the mass
of patient.
5- Patient Self-Care and Provider Practices to
improve Outcomes
Pt. counseling, education and motivation are vital for
short term and long term goal achievements.
(I) Patient Self-Care Practices
1. Regular medical appointments to assess control
and for complication surveillance / prevention.
2. Healthful meal planning
3. Regular exercise
4. Regular medication use as prescribed
5. Glucose self-monitoring (take results to
appointment)
6. Adjustment of medication based on glucose results
7. Daily foot check
8. Annual eye check
9. Annual dental check
(II) Provider Office Practices
1. Patient education(team approach)
Nutrition education for patient
Exercise prescription
Glucose self-monitoring
Medication adjustment
Foot Care
2. Askabout
Hyper / Hypoglycemic symptoms
Impotence and autonomic dysfunction symptoms
Cardiac and vascular disease symptoms
3. Each visit
Check weight, Blood Pressure, glucose, condition of
feet , Check glucose self-monitoring results /make
recommendations
4.Referrals
* Annual dilated eye exam
* Family planning for women of reproductive age
* Registered dietitian.
* Diabetes self-management education
* Dental exam
* Mental health professional if needed
5.Laboratory:
- Hba1c measurement every 3-6 months
- KFT,lipids, urine microalbuminyearly or as needed
6. Vaccines Influenza and pneumococcal
F. Complications of Diabetes Mellitus
a) Acute Complications
1) Diabetic ketoacidosis
2) Hyperosmolar Nonketotic Hyperglycemia
3) Hypoglycemia
Prevention of hypoglycemia is a critical
component of diabetes.
 Hypoglycemia may be asymptomatic, mildly
symptomatic or severely symptomatic and require
assistance. Different patients are affected to different
degrees as happens with hypoxia.
 Teaching people with diabetes to balance insulin
use, carbohydrate intake & exercise is imp.
 Clinical manifestations:perspiration, tremor,
hunger, nausea, tachycardia, pallor, irritability,
headache, lethargy, confusion, bizarre behavior. If
severe coma, seizure, permanent neurological
impairment and even death.
 Treatment of hypoglycemia
•If conscious : glucose15-20 g orally preferred
•consume meal or snack once blood glucose
normalizes
•If unconscious or unable to take glucose orally:
1. IVglucosepreferred
–initial bolus -glucose 25 g IVinadults, 10% dextrose
2-4 mL/kg IVinchildren.
2. Glucagon 1mg IM, SC or IV if iv glucose not
available.
4) Lactic acidosis
5) Coma in Diabetic Patient
1) Related to diabetes
Hypoglycemia. Diabetic ketoacidosis, nonketotic
hyperglycemic coma, lactic acidosis.
2) Unrelated to diabetes
Alcohol or other toxic drugs, C.V.A or head trauma,
uremia.
b) Chronic Complications
* Macrovascular Complications of Diabetes
Atherosclerotic vascular disease
(a) Coronary artery disease
(b) MI with sudden death
(c) C.V.A
(d) Peripheral vascular dis.
(e) Intestinal ischemia
(f) Renal artery stenosis
Up to 80% of pts. with type 2 diabetes will develop
or die of macrovascular disease.
* Microvascular Complications of Diabetes
1) Diabetic nephropathy
2) Peripheral neuropathy
3) Autonomic neuropathy
4) Diabetic retinopathy
G. Prevention & Management of Diabetic
Complications
a) Cardiovascular Complications:
* D.M has 2-3 fold ↑ risk of developing CVD
* Up to 75% of type 2 DM & 35% of type 1 DM die
from CVD
* CVD is the largest contribute to the direct and
indirect costs of diabetes
* Numerous studies have shown the efficacy of
controlling cardiovascular risk factors in preventing
or slowing CVD in people with diabetes
1)Hypertension
* Hypertension affects majority of diabetes pts and is
a major risk factor for both CVD & microvascular
complications
* Lowering BP will reduce the incidence of coronary
heart disease, stroke and nephropathy
* Target BP is: JNC 7 < 130 / 80. JNC 8:140/90
* Multiple drug therapy is generally required
* Medication either ACE inhibitor or ARBs (Calcium
channel blockers are warranted in cases of
intolerance or contraindication to ACE inhibitors
2)Dyslipidemia
*Statin therapy should be added to lifestyle therapy
regardless of baseline lipid levels for diabetic pts
with overt CVD.
* The pry goal in an LDL choles. < 100 mg/dl (2.6
mmol/L).
* consider statin therapy if age > 40 and LDL>70.
3)Antiplatelet agents
* Aspirin therapy(75-160) indicated for high risk
group.(10 year risk of >10%.eg men >50 with
additional risk factor or women >60 with additional
risk factor.
4)Smoking Cessation
Advice all pts not to smoke
b)Diabetic Nephropathy
* Diabetic nephropathy occurs in 20-40% of pts. with
diabetes & is the single leading cause of end-stage
renal disease (ESRD)
* Microalbuminuria (persistent albuminuria in the
range of 30-299 mg/24 hr) is the earliest stage of
diabetic nephropathy and a marker of CVD risk
* The most Useful screening test is the albumin:
creatinine ratio(AC Ratio) on the 1stmorning urine
sample. More than one positive test is required over a
few weeks or months
* Control of diabetes and BP will reduce the risk or
slow the progression of nephropathy
* ACE inhibitors usage is associated with significant
reduction in progress to overt proteinuria & ↑
regression to normoalbuminuria
c) Diabetic Retinopathy (DR)
* DR is the leading cause of blindness and diabetic
pts have 10% chance of acquiring blindness from
retinopathy
* Glaucoma, cataracts and other disorders of the eye
occur earlier & more frequently in people with
diabetes
* Screening by yearly fundoscope exam or fundal
photography
* Laser photocoagulation is indicated in pts with
proliferative diabetic retinopathy(PDR), macular
edema and some cases of NPDR.
d)Diabetic Neuropathy
* Distal symmetrical polyneuropathy,
mononeuropathy, autonomic
neuropathy are the main types
* Up to 30% of diabetic develop neuropathy
* 50% may be asymptomatic
* Numbness, parasthesia, pain, absence sensation,
ulcer may occur
* Tricyclic antidepressants, capsaicin,
anticonvulsants (carbomazepine,Gabapentin,
pregabalin) may help to control Pain
e)Foot Care
* Foot ulcer occurs in 5-10% of diabetic patient
* Three pathoPhysiologic process result in injury
predisposition and potential amputation
a)Neuropathicb) Ischemiac) Sepsis
* Foot self-care education includes cleaning &
drying, nails cutting,shoes, sockets, smoking, avoid
hot objects, never go barefoot,taking advise for any
foot problem
f) Skin changes
Most dermopathy occurs in type 1 DM.
Diabetic dermopathy, A canthosis nigricans.
Necrobiosis lipoidica, skin may become thick and
waxy,
----------------------------------
**Gestational D.M
- women who develop DM during pregnancy.
- Screening is performed at 24-28 wks by one step or
two-step approach
Based on ADA either of:
one step approach: FBS then 75 g glucose and test
at 1hr, and 2 hrs.
If one is abnormal of FBS>92, 1hr >180, 2hr >153
mg/dl.
Or Two step approach:
Challenge test:50 gram glucose then test at 1 hr
If >135-140, do 100 gm 3 hr test.
Diagnose if 2 abnormal of: FBS>95, 1 hr>180, 2
hr>155, 3 hr >140 mg/dl.
- The glycemic control target for GDM is
preprandial ≤ 100 mg/dl and either
1 hr post meal ≤ 155 md/dl (8.6 mmol/L) or
2 hr post meal ≤ 130 mg/dl (7.2 mmol/L)
- Uncontrolled DM is associated with spontaneous
abortion and major fetal abnormalities. In majority
gestational DM resolve after pregnancy but is likely
to recur.
 Upper Respiratory Tract Infection(URTI)
* General Characteristics :
- URTIs : inflammation of the respiratory mucosa
from the nasal cavity down to the bronchus. (above
the level of the carina).
- Includes : common colds , influenza , sinusitis ,
rhinitis , tonsillitis , otitis media , pharyngitis ,
laryngitis,epiglottitis,Tracheitis and croup.
- Epidemiology:
- children will have 5 URTIs/ year and adults 2-
3/year.
- 70-80 % of these infections are caused by viruses ;
rhinoviruses and adenoviruses are the most common.
----------------------------------------------
* Clinical Entities :
- Management principles:
*Viral infections need ONLY symptomatic treatment
, NO need for antibiotics(Abs).
Why not to use Abs for viral infections ?
1. Promotes Abs resistance.
2. Adverse reactions such as allergy and anaphylaxis
3. Patients do not need Abs to feel satisfied
4. Costly
 Why to use Abs for bacterial infections?
1. To prevent suppurative complications
2.To prevent rheumatic fever
3. To speed up recovery
4.To reduce spread to others
* Viral URTIs :
1. Influenza
2. Common cold
3. Mild acute sinusitis
4. Mild acute otitis media
*Bacterial URTI :
need ABs for treatment in addition to the
symptomatic treatment.
1. GABHS pharyngitis
2. Moderately to severe acute sinusitis
3. Moderately to severe acute otitis media
4. Special cases ( pertussis , epiglottitis )
1) Common Cold :
- a self-limiting , viral infectious disease of the upper
respiratory system.
- Incidence : most frequent infectious disease in
humans ; 2-4 infections / year in adults and 6-12 in
children.
- Transmitted by droplets and close personal contact /
airborne.
- usually occurs in the fall and winter months.
- Causative agents :
1. Rhinovirus (50%) ,
2. Coronavirus (10-20%),
3. Adenovirus (5%) ,
4. others :RSV , parainfluenza virus.
5. Bacterial infections are unlikely:
Mycobacterium leprae, Klebsiella rhinoscleromatis,
Pseudomonas mallei (glanders), Rhinosporidium
seeberi (rhinosporidiosis), Leishmania mexicana
(leishmaniasis) .
- Symptoms:
1. The first symptom is usually a sore or “scratchy
throat”  followed soon after by nasal stuffiness and
discharge ( rhinorrhea ) , sneezing and coughing.
 The throat is usually sore for a brief time. The
cough symptoms are usually worse on the 4th or 5th
day of illness , while the nasal symptoms improve.
 Symptoms generally last for 7 to 10 days. Cough
may continue up to 4 weeks.
**If the nasal discharge becomes viscous and
green with time ; it doesn’t mean superimposed
bacterial infection . It’s a normal course of common
cold.
- Management:Symptomatic Treatment :
a) comfort is the goal of treatment which may
include:
1. nasal suction for infants
2. steam/mist inhalation
3.nasal irrigation
4. humidified air
5. consume extra fluids (warm fluids may be soothing
for irritated throats
6. consume nutritious diet as tolerated
7. elevate head of bed
8. salt water gargle for sore throat .
9. get adequate rest
10.Vitamin C may reduce duration of common cold
in children.
11. Zinc syrup associated with reduced duration of
cold symptoms in children
12.Honey may reduce nocturnal cough and sleep
disruption in children with acute cough, and might be
more effective than dextromethorphan or
diphenhydramine
b) Medication :
1. Antipyretics: no evidence that fever or antipyretic
treatment affects illness course or neurologic
complications
2. Ibuprofen appears more effective than
acetaminophen for reducing fever in single-dose
comparisons and ibuprofen and acetaminophen
appear to have similar analgesic effects .
Combined or alternating acetaminophen and
ibuprofen regimens may be more effective than
either monotherapy for reducing fever in children.
*Ibuprofen approved for use( by FDA) after
6 months of age.
*Paracetamol: may be used after 2-3 months of age.
3.Nasal Decongestants and Antihistamines:
*Nonprescription medicines (antihistamines and
antitussives) do not appear effective for acute cough
in children )
*FDA recommends against use of nonprescription
cough and cold products in children < 2 years old
and supports not using them in children < 4 years
old.
*nonprescription cough and cold preparations may
not be safe in children
4.Aspirin is contraindicated in children with viral
infections due to association with increased risk for
Reye Syndrome
5. Antibiotics :
*Abs do not appear to reduce symptoms of common
cold or acute purulent rhinitis.
* No role of antibiotics in common cold ( viral
infection ).
C) Prevention:
1-Wash hands after contact with common cold
patients.
2- Do not touch any surfaces or objects that may
have been contaminated.
3- Keep fingers out of eyes and nose.
- Complications:
1.Acute otitis media (most common in children)
2.Pharyngitis
3.Sinusitis
4.Bronchitis and pneumonia
5.Conjunctivitis
6. Adenitis
7. Aggravation of asthma
----------------------------
2) Influenza :
* viral infection that affects mainly the nose ,
throat , bronchi , and occasionally lungs.
* Influenza causes annual epidemics that peak
during winter.
*Seasonal influenza
- Acute viral infection caused by influenza type
A , B and C.
- Type A and B are constantly changing due to
mutations ( antigenic drift and shift ) , more
serious than type C.
Currently influenza A (H1N1) and A (H3N2)
subtypes are circulating among humans.
-Type C is stable , it’s cases occur much less
frequently than type A and B.
*Transmitted by droplets and close person
contact / airborne.
-Signs and symptoms
1.Following an incubation period of 1-2 days
flu presents with abrupt onset of fever
(39 – 40 c) ,muscle aches , headache and fatigue.
2.The individual may have respiratory symptoms
such as a dry cough , sore throat , and
occasionally a runny nose.
3.Other symptoms related to systemic illness
include chills and sweats , loss of appetite ,
diarrhea and vomiting.
- Prognosis:
*These symptoms generally improve over two to
five days, though may last one or more weeks.
*Some patients experience postinfluenzal
asthenia (persistent weakness or becoming tired
easily) which may be present for several weeks
following the illness.
* A dry cough (post viral cough syndrome) may 3. Isolation of patient until 24 hours of afebrile
also persists for several weeks. period.
4.Vaccination:most effective measure of
- Complications: prevention .
1. Bronchitis  Influenza vaccine
2. Sinus infections - Annual vaccine
3. Ear infections - Two types :
4. Pneumonia 1-Injectable : killed vaccine
5. Encephalitis 2-Nasal spray : live but weakened virus
 Highest risk of complications occurs among : - 70% protection in 1 year.
1.Children < 2 years - Reduces severe complications by 60% , and
2.Adults 65 years or older death by 80%.
3.Medical chronic illnesses - Recommended for :
4.Immunocompromised patients 1. all persons ≥ 50 years old
5. pregnant women 2. Infants and children aged from 6 months to 4
-Treatment: years.
1)Bed rest 3. women who are or will be pregnant during
2) Antipyretic/Analgesics the influenza season.
3)Fluid intake 4. adults who have chronic pulmonary (including
4)Antiviral treatment: asthma) or cardiovascular (except isolated
* antiviral treatment recommended as soon as hypertension), renal, hepatic, neurological,
possible (and not delayed while awaiting hematologic, or metabolic disorders (including
diagnostic confirmation) for patients with diabetes mellitus)
confirmed or suspected influenza who: 5. household contacts and caregivers of children
1.have severe, complicated, or progressive illness < 5 years old.
2.require hospitalization 6. Immunocompromised patients and
3.are at higher risk for influenza complications immunosuppressive treatment.
Drugs : 7. Health care professionals.
1-oseltamivir 8. residents of nursing homes and other long-term
- adult dosing 75 mg orally twice daily for 5 days care facilities.
- weight-based dosing used for oseltamivir in 9. persons who are morbidly obese (body mass
children up to age 12 index ≥ 40 kg/m2
2-zanamivir
- 10 mg (2 inhalations) twice daily for 5 days in *Common cold Vs Influenza:
patients aged ≥ 7 years - Influenza is different from the common cold in
-not recommended in patients with airways that it causes a more severe illness , with fever ,
disease headache , significant fatigue and muscle aches
- not approved for children aged < 7 years and systematic manifestations.
3-peramivir - It’s less likely to cause sneezing or a blocked
- dosing 600 mg IV single dose in patients aged ≥ nose with thick nasal discharge.
18 years
- not approved for children or adolescents. ---------------------------------------------
- amantadine and rimantadine not recommended 3) Pharyngitis/Tonsillitis:
due to widespread resistance. - It is an inflammation of the pharynx, w/o
tonsilles.most commonly caused by viral or
- Prevention: bacterial infection.
1.Frequent hand washing. -Causative agents :
2.Wear masks and gloves. 1. Viral : adenovirus (80% most common ) ,
enterovirus , EBV , herpes simplex virus.
2. Bacterial : GABHS (5-15%), mycoplasma.
 GAS uncommon in children younger than 2-3
years, and the peak is between 5-11 years.
- Peak Winter to early Spring.
- Spread by direct contact.
-Clinical presentation:
1. The main symptom is a sore throat.
2. Other symptoms may include:
- Fever
- Headache
- Joint pain and muscle aches
- Skin rashes
- Swollen lymph nodes in the neck
 Bacterial Vs. Viral Presentation
*Viral Infection:
-Clinically: Gradual, more likely to have
rhinorrhea, cough, diarrhea, hoarseness of voice.
- Adenovirus: conjunctivitis, most common cause
in children < 3 years of age.
- Coxsackieviruses: ulcer on posterior pharynx,
herpangina (mouth blisters).
- EBV: prominent tonsils with white exudates,
posterior cervical LN enlargement, Palatal rash,
Hepatosplenomegaly, high fever and fatigue.
* Bacterial Infection:
- Clinically: Rapid onset fever, prominent throat
pain, headache, abdominal pain, vomiting,
dysphagia and malaise.
- On exam: Pharynx are erythematous, tonsils
enlarged with yellow-blood tinged exudate,
petichia may be present on soft palate, anterior
cervical lymph nodes enlarged and tender.
* Investigations :
1. Rapid Antigen Test (RAT)
- Sensitivity of RAT against culture varies
between 61-95%.
- Specificity of RAT 88-100%
- Takes 10 min to be performed
-ve results should be confirmed by culture.
2.Throat Culture
- 20-40% of those with negative throat
culture will be labeled as having GABHS.
- +ve culture makes the Dx of GABHS,but
–ve culture does not rule out.
* Management of Pharyngitis :
Why we treat GAS pharyngitis
1. decrease risk of Rheumatic fever, but not
of PSGN.
2. shorten duration of illness.
3.decrease risk of complication (mainly
abscess).
1.Supportive Measures
*Encourage fluid intake
*Acetaminophen or NSAID may reduce pain.
*Benzydamine oral rinse or mouth spray may
reduce pain and improve symptoms.
 Other supportive measures without direct
evidence include
- topical analgesics (such as nonprescription
throat sprays) and anesthetics (such as viscous
lidocaine 2%)
- warm salt water gargles
- throat lozenges, hard candy, or frozen desserts
- soft foods or cold thick liquids such as ice
cream
- Humidifier.
2. Bacterial Pharyngitis:
*Antibiotics:
 Penicillin V 500mg twice daily for 10 days
oral or once IM benzathine penicillin 1.2 million
unit.
- safe , cheap , narrow spectrum , no
resistance.
 or amoxicillin 500mg twice daily for 10 days.
 If penicillin allergic:
- Cephalexin or azithromycin or clarithromycin
or clindamycin.
3. Corticosteroids such as dexamethasone 0.6
mg/kg orally may hasten pain relief in acute
pharyngitis.
4. Carriers:
Small RCTs suggest that intramuscular
benzathine penicillin combined with four days of
oral rifampin (Rifadin) or a 10-day course of oral
clindamycin effectively eradicates the carrier
state
5.Tonsillectomy
Recommended for recurrent severe sore throat if
more than 6 episodes in past year,more than 4
episodes per year in 2 years or more than 2 per
year in 3 years.
* Differential diagnosis
1. Infectious mononucleosis, when a
membranous exudate is present.
2. Diphtheria, especially in the underimmunized.
3. Herpangina, with many vesiculoulcerative
lesions in the anterior pillars & soft palate.
4. Agranulocytosis, yellowish dirty white
exudates covering the tonsils & post pharyngeal
wall.
5. Kawasaki disease.
* Complication of GAS pharyngitis:
1- Otitis media
2- Glomerulonephritis and Rheumatic Fever
may follow streptococcal infection.
3- Monoarthritis.
4- Mesenteric adenitis (viral or bacterial)
abdominal pain with or without vomiting.
5- In debilitated children, large chronic ulcers in
the pharynx (viral or bacterial)
6- Rheumatic Fever
 Major Criteria:
- Polyarithritis
- Carditis
- Sydenham Chorea
- Subcutaneous nodules
- Erythema Marginatum
 Minor Criteria:
- Fever of 38.2–38.9 °C (101–102 °F)
- Arthralgia: Joint pain without swelling
(Cannot be included if polyarthritis is present as a
major symptom)
- Raised ESR or CRP
- Leukocytosis
- ECG showing features of heart block, such as
a prolonged PR interval (Cannot be included if
carditis is present as a major symptom)
- Previous episode of rheumatic fever or inactive
heart disease
 According to revised Jones criteria, the
diagnosis of rheumatic fever can be made when:
2 major criteria, or 1 major criterion plus 2
minor criteria, are present along with evidence of
streptococcal infection: (elevated or rising ASO
titre or DNAase).
Exceptions are chorea and indolent carditis,
each of which by itself can indicate rheumatic
fever.
-----------------------------------------
4) Sinusitis:
* Inflammation of mucosa of paranasal
sinuses.
- Most commonly it is viral, especially post
common cold,: Rihnovirus, Influenza virus,
parainfluenza virus.
- Could be bacterial: Strep. Pneumoniae, H.
Influenzae, M. Catarrhalis, Staph. Aureus.
- Risk Factors:
1. Allergic rhinitis or hay fever
2. Cystic fibrosis.
3. Day care, Weakened immune system from
HIV or chemotherapy
4. Changes in altitude (flying or scuba diving)
5. Large adenoids, Nasal polyps
6. Smoking
7. Nasogastric and nasotracheal intubation
*Clinical presentation:
- The symptoms of acute sinusitis in adults
usually follow a cold that does not improve, or
one that gets worse after 5 - 7 days of symptoms.
1. Mucopurulent Rhinorrea
2. Nasal congestion
3. Facial pain, pressure and fullness
4. Decrease sense of smell
- Signs :
1. Looking in the nose for signs of polyps
2. Shining a light against the sinus
(transillumination) for signs of inflammation
3. Tapping over a sinus area to find infection
(tenderness), very painful
* Diagnosis of Sinusitis:
 Clinically
- We use radiological evaluation if there is
warning signs:
1. Severe swelling and redness of the tissues
around the eye
2. Limitations of eye movement
3. Swelling of the forehead
4. High fever
5. Altered consciousness
6. Radiological evaluation:
7. Regular x-rays of the sinuses are not
recommended.
8. CT scan of the sinuses for suspected
complications.
* Complications of Sinusitis:
1. Periorbital cellulites
2. Meningitis
3. Brain abscesses
4. Cavernous sinus thrombosis
5. Osteomylitis of frontal bane.
* Treatment of Sinusitis:
1. Analgesics and antipyretics as needed
2. Intranasal corticosteroids.
3. Consider intranasal saline with either
physiologic or hypertonic saline.
4. Decongestants and antihistamines: lack
evidence for effectiveness unless evidence of
allergic component.
5. antibiotics for acute bacterial sinusitis:
-most cases resolve without antibiotic treatment.
-only consider treatment with antibiotics if
patient meets criteria for acute bacterial
sinusitis.
- consider watchful waiting without antibiotics in
patients with uncomplicated mild illness (mild
pain and temperature < 101 degrees F [38.3
degrees C]) with assurance of follow-up .
- if decision made to treat with antibiotics,
amoxicillin is first-line therapy for most patients
 Criteria for acute bacterial sinusitis:
1) persistent symptoms or signs lasting ≥ 10 days
without evidence of clinical improvement .
2) severe symptoms or signs of high fever (≥ 39
degrees C and purulent nasal discharge or facial
pain lasting for ≥ 3-4 consecutive days at
beginning of illness.
3) worsening symptoms or signs characterized by
new onset of fever, headache, or increase in nasal
discharge following typical viral upper
respiratory infection that lasted 5-6 days and
were initially improving ("double-sickening") .
- Antibiotic choice
1. Amoxicillin or amoxicillin clavulanate is
preferred first-line treatment
(500 mg/125 mg orally 3 times daily or 875
mg/125 mg orally twice daily).
2. Alternative choices: levofloxacin,doxycyclin.
For chronic or recurrent sinusitis addition of
intranasal steroid accelerates recovery.
---------------------------------------------------
5- Otitis Media
*Suppurative or acute otitis media (AOM):
- usually a complication of eustachian tube
dysfunction that occurs during a viral URTI.
--streptococcus pneumoniae, Haemophilus
influenzae, and Moraxella catarrhalis are the
most common organisms isolated from middle
ear fluid.
*Non-suppurative or secretory otitis media or
otitis media with effusion (OME)
- Usually non infective
- Cultures are sterile, but in 30% same organisms
* Recurrent otitis media
- 3 times in 6 months or more than 4 times in a
year
* Chronic otitis media
Foul-smelling otorrhea.
Risk factors:
1. Age: 6-20 months- decrease with age
2. Male gender
3. Low socioeconomic status
4. Exposure to smoking and day care attendance
5. More in cold weather
6. Bottle feeding while sleeping, breast feeding
(protective)
7. Congenital anomalies: Down syndrom, cleft
palate.
 Clinical Presentation:
1) In infants, are nonspecific and include fever,
irritability, excessive crying and poor feeding.
2) In older children and adolescents, fever,
otalgia (acute ear pain), otorrhea (ear drainage);
after spontaneous rupture of the tympanic
membrane. Signs of a common cold are often
present.
3) Nausea, Vomiting, dizziness, fever.
4) TM exam: red, bulge, loss of land marks,
decrease mobility (by pneumatic otoscopy),
apparent light reflex, perforation.
Normal tympanic membrane:
1. Shiny
2. Translucent.
3. +ve light reflux
4. No air fluid border
5. No bulge.
 Complication of Otitis Media :
1. Chronic suppurative otitis media
2. Acute mastoiditis
3. Facial paralysis
4. Cholesteatoma (cyst like lesion in middle ear,
tend to expand and cause bone resorption)
5. Intracranial complications: meningitis,
abscess, lateral sinus thrombosis
6. Conductive hearing loss and possible
developmental sequelae.
 How to manage it?
- Natural history of OME is spontaneous
resolution … days-months.
- Prompt surgical referral for structural
damage to TM or ME (e.g. cholesteatoma).
 Surgical referral for children with OME with
hearing loss independent on OME, speech or
language disorder, developmental delay and
uncorrectable visual impairment.
- Antihistamines, decongestants, or steroids
should not be used in the management of
OME in children.
 Treatment of Otitis Media:
1. Give drugs to decrease pain (oral-topical
analgesics)
2. Antibiotics :Indications:
1)moderate or severe otalgia
2) otalgia for ≥ 48 hours
3) temperature ≥ 39 degrees C (102.2 degrees
F)
4) age < 24 months and bilateral AOM
5) Antibiotic therapy can be deferred in
children two years or older with mild
symptoms.
 Antibiotic Choice:
*Amoxicillin 90mg/kg/days…first choice.
*Amoxicillin 90 mg/kg/day plus clavulanate 6.4
mg/kg/day in 2 divided doses…second choice if
not improving on amoxicillin after 2-3 days.
* Other choices: if allergy to amoxicillin or not
improving.
*Cefdinir(omnicef),cefuroxime(zinat),ceftriaxone
(rocephen)and Cefpodoxime.
If the patient fails to respond to the initial
management option within 48-72 hours, clinician
must reassess to confirm AOM and exclude other
causes of illness. If AOM is confirmed in:
- Patient initially managed with observation,
begin antibacterial therapy.
- Patient initially managed with antibacterial
agent, change the agent.
- If treatment failed: tympanocentesis and culture
may be needed
- Clinician should encourage the prevention of
otitis media through decrease the risk factors.
--------------------------------------------
6- Croup:
- LaryngoTracheoBronchitis
- Caused by ParaInfluenza virus
- Age: 3 months – 5 years, peak 2 year
- More in male
- More in Winter
- Clinical presentation:
1. Some Rhinorrhea, mild cough, low grade
fever,
2. 1-3 days then characteristic barking cough,
hoarseness and inspiratory stridor (70%
obstruction)
3. Worse at night, usually resolve in 1 week.
4. Exam: hoarseness of the voice, mild
tachypnea, child prefer to sit upright, more
symptoms with crying and agitation.
 ( seal-like )Barking cough is the hallmark of
croup among infants and young children,
whereas hoarseness predominates in older
children and adults. * Diagnosis:
* Diagnosis of Croup: Clinical
-Diagnosis is usually based on history, physical, - Large cherry red swollen epiglottis by
and response to treatment. laryngoscope
- sudden onset of barking cough, hoarseness, and - Lateral neck x-ray: thumb sign
inspiratory stridor in a child (especially if aged 6- (swollen epiglottis)
36 months)
- absence of atypical findings (for example, * Treatment of Epiglottitis:
wheezing, drooling, or toxic appearance) 1. It is a Medical Emergency : establish airway
- improved respiratory symptoms after treatment by intubation, rarely tracheotomy regardless of
with corticosteroids, with or without nebulized the degree of obstruction.
epinephrine 2. Antibiotics: broad-spectrum second- or third-
* Treatment of Croup: generation cephalosporins recommended.
 Airway management is the priority: 3. Corticosteroids :IV dexamethasone or
1.Use cool mist budesonides aerosols.
2. corticosteroids usually indicated for children 4. Oxygen and IV fluid.
with croup. ------------------------------------------------------
- corticosteroids improve croup symptoms and 8-Laryngitis
reduce return visits or readmissions. - An inflammation of the larynx, manifests in
- Dexamethasone 0.6 mg/kg orally or both acute and chronic forms.
intramuscularly given once.  Acute : less than 3 weeks
- Or prednison oral for 3 days. Chronic : last more than 3 weeks
3. Epinephrine(racemic)nebulizer- for - Acute laryngitis has an abrupt onset and is
children with severe croup usually self-limited.
------------------------------------------------- - The etiology of acute laryngitis includes vocal
7. Epiglottitis: misuse, exposure to noxious agents, or infectious
*A life-threatening disease. agents.
*Caused by H. Influenzae, S. pneumoniae, - The infectious agents are most often viral but
S. aureus sometimes bacterial
* now uncommon, because the H. influenzae * Causes:
type B vaccine is a routine childhood a. Infection (usually viral upper respiratory
immunization. tract infection)
* Clinical Presentation: 1. Rhinoviruses
1. high fever and sore throat. 2. Parainfluenza viruses
2. Dyspnea, progressive upper airway obstruction 3. Respiratory syncytial virus
in hours. 4. Adenoviruses
3. On Exam: Toxic, ill looking, difficulty 5. Influenza viruses
swallowing, drooling, hyper extended neck 6. Measles virus
(tripod sign) 7. Mumps virus
4. Stridor is a late sign 8. Bordetella pertussis
9. Varicella-zoster virus
* Complications: b. Gastroesophageal reflux disease
the airway may become totally obstructed , c. Environmental insults (pollution)
empyema or epiglottic abscess. d. Vocal trauma
e. Use of asthma inhalers

*Clinical Presentation :
- Generally associated with hoarseness or loss of
voice.
- Symptoms: hoarseness of the voice,Fever
Swollen lymph nodes, dysphagia, odynophagia,
dyspnea, rhinorrhea, postnasal discharge, sore
throat, congestion, fatigue, and malaise.

*Complications: rarely respiratory distress

* Treatment:
a. voice rest, analgesia,cool mist,hydration.
b. Nebulized epinephrine or oral steroid for
sever cases.
 Minor Injuries inPrimary Care
A. Skin Injuries :
Types Definitions
1- Scraped skin caused by friction against
Abrasion: a rough surface.
involves only the epidermis,
characterized by Minimal bleeding,
pain, and usually do not scar.
2- 2- Straight or jagged skin tear; caused
Laceration: by blunt trauma (e.g., fall, collision)
Clinical features: Little to profuse
bleeding; ragged edges may not readily
3- Incision: align.
3- a sharp cut with clean edges, caused
by a clean, sharp-edged object such as
aknife, razor, blade,scalpelor glass
splinter
4- Bite or Broken skin caused by penetration of
puncture sharp object
wound Typically more bleeding internally
than externally, causing skin
discoloration
5- Burn Thermal dynamic injury, may progress
two to three days after initial injury
6- Avulsion is an injury in which a body structure
is forcibly detached from its normal
point of insertion by eithertrauma or
surgery.
Management
Skin irrigation and removal of foreign bodies, topical
antibiotic, occlusive dressing; aggressive injuries may
require topical and oral antibiotics and consultation
with plastic surgeon for skin grafting.
Sutures, stapling, tissue adhesive, bandage, or skin
closure tape
High-pressure irrigation and removal of foreign
bodies, tetanus prophylaxis with possible antibiotics;
human bites to the hand require prophylactic
antibiotics; plantar puncture wounds are susceptible
to pseudomonal infection
Depends on degree and size; in general, first-degree
burns do not require therapy (topical nonsteroidal
anti-inflammatory can be helpful); deep second-and
third-degree burns require topical antimicrobials and
referral to burn subspecialist
most commonly refers to a surface trauma where all
layers of theskin have been torn away, exposing the
underlying structures (i.e.,subcutaneous
tissue,muscle,tendons, orbone.
 Wound Suture Size Time of
Location removal (days)

Face 5-0 or 6-0 3-5

* Treatment of Minor Skin Injuries:
1. The first step in the care of cuts, scrapes
(abrasions) is to stop the bleeding. Scalp 3-0 or 4-0 5-7
-Most wounds respond to gentle direct pressure with
a clean cloth or bandage. Hold the pressure
Trunk & 4-0 or 5-0 7-10
continuously for approximately 10-20 minutes.
Extremities
2. Thoroughly clean the wound with soap and water.
 There is no evidence that antiseptic irrigation is
superior to sterile saline or tap water Over Joint 3-0 or 4-0 10-14
 Hydrogen peroxide and povidone-iodine Surface
(Betadine) products may be used to clean the wound
initially, but may inhibit wound healing if used long-
term. Palms or Soles 3-0 or 4-0 14-21
3. Remove any foreign material in the wound, such
as dirt, bits of grass, which may lead to infection.
 Tweezers can be used (clean them with alcohol
first) to remove foreign material from the wound
edges, but do not dig into the wound as this may push
bacteria deeper into the wound.
4. Cover the area with a bandage to help prevent
infection and dirt from getting in the wound.
 A first aid antibiotic ointment can be applied to
help prevent infection and keep the wound moist.
 Any redness, swelling, increased pain, fever, or
pus draining from the wound may indicate an
infection.
5. Pain management:
* Paracetamol, hydrocodone or other opioids.
 NSAID may delay bleeding; so try to avoid them
6 . Do Not Forget to:
1. Control bleeding. 8. Tetanus Prophylaxis
2. Palpate for foreign body.
3. Check for fracture.
4. Check for tendon, nerve, vessel or duct injury.
5. Exclude substance abuse, physical abuse,HIV or
hepatitis(B or C).
7. Suture selection and timing of removal :

---------------------------
B. Muscle and tendons Injuries
- Strains : are caused by overstretching or tearing the
tendons or muscles that help support and move a
joint. Many strains are minor -just small tears in the
tissue -but some can be severe.
- Sprains : are likewise caused by overstretching or
tearing, but they occur in ligaments.
- Bruises: happen when a muscle, ligament, or
tendon sustains a blow forceful enough to injure
capillaries, so they break open and cause blood to
collect under the skin and in the injured tissue. Most
bruises are minor and heal with treatment at home.
But some can be severe and take weeks or months to
heal. Bruising can even occur in vital organs, if the
injured tissue is a vital organ.
* Evaluation & Management of Muscle and
tendons Injuries
1. Skip the heroics.
2. Don't wait.
3. Begin RICE immediately.
Rest:Cut back on normal daily activities and avoid
putting weight on the injured body part.
 Ice:Use an ice pack on the injured area for 10 to
20 minutes at a time, anywhere from four to eight
times per day. Don't use the ice pack for longer than
20 minutes, and wrap it in a T-shirt or thin towel so
you don't burn your skin.
 Compression:To reduce pain and swelling, wrap
the injured area with an elastic bandage not too
tightly, though.
 Elevation:Use pillows or blankets to raise the
injured limb above the level of the heart to minimize
swelling.
** Delaying RICE treatment could mean more pain
and swelling and a longer recovery period.
------------------
C. Head Trauma
- Head injuries include both injuries to the brain and
those to other parts of the head, such as the scalp and
skull
- Head injuries are generally classified as closed or
open (penetrating).
- Brain injuries may be diffuse, occurring over a wide
area, or focal, located in a small, specific area.
- Brain injury can be at the site of impact, but can
also be at the opposite side of the skull due to a
counter-coup effect
 Traumatic subdural hematoma, a bleeding
below the dura mater which may develop slowly
 Traumatic extradural, or epidural hematoma,
bleeding between the dura mater and the skull
 Traumatic subarachnoid hemorrhage
 Cerebral contusion, a bruise of the brain
 Concussion, a loss of function due to trauma
 A severe injury may lead to a coma or death
* Shaken Baby Syndrome-a form of child abuse (it
can cause brain injury , retinal hemorrhage ,
developmental and behavioral defects ).
** Red Flags of Head Trauma
1.Becomes very drowsy
2. Behaves abnormally
3. Develops a severe headache or stiff neck
4. Loses consciousness, even briefly
5. Vomits more than once
6. There is severe head or face bleeding
7. The person stops breathing
8. changes in vision, taste or smell
9. muscle weakness
10. inability to concentrate
11. decreased reading comprehension
12. diminished auditory comprehension
13. irrational fears
14. problems with judgment
----------------------------------------------
Needle stick injury-Post exposure prophylaxis
(PEP):
1) HIV
* Post exposure prophylaxis is Indicated if:
- Source patient is individual with known HIV
infection or
- unknown HIV status who is epidemiologically at
higher risk of having HIV.
* HIV testing should be performed in all patients
before starting antiretroviral PEP.
-Antiretroviral PEP should beinitiatedas soon as
possible afterexposure:
-Within 72 hours
-given for 28-day.
* Drugs:
-Tenofovir 300 mg plus emtricitabine 200 mg orally
once daily.
Plus:
-raltegravir 400 mg orally twice daily for 4 weeks.
* Follow-up with HIVantigen/antibody testing at 3
and 6 months.
2)Hepatitis B post exposure prophylaxis
 go back to slide #32 there is a table
3) Hepaitis C Post Exposure prophylaxis
For HCV PEP , the HCV status of the source and the
exposed person should be determined.
if HCV positive source, or source unknown but high
risk, follow-up HCV testing should be performed to
determine if infection develops by testing HCV Ab at
baseline and then at 3 and 6 months.
-------------------------------------------------