Echinococcus genus of tapeworms has nine recognized species, but four are of primary public health concern in humans. These species cause three main forms of the disease, known collectively as echinococcosis or hydatid disease.
The main species and the diseases they cause are:
Echinococcus granulosus sensu lato This species complex is the most common cause of human echinococcosis worldwide, causing cystic echinococcosis (CE), also known as hydatid disease or hydatidosis. The larval stage forms slow-growing, fluid-filled, unilocular (single-chambered) cysts, typically in the liver or lungs.
Echinococcus multilocularis This species is found in the northern hemisphere and causes alveolar echinococcosis (AE). This form is more aggressive, behaving like a malignant tumor by growing in an infiltrative, multilocular pattern (many small, interconnected vesicles) primarily in the liver, and can spread to other organs.
Echinococcus vogeli and Echinococcus oligarthrus These species are limited to Central and South America and are responsible for the rare polycystic echinococcosis (PE) or neotropical echinococcosis. E. vogeli typically causes large, polycystic growths in the liver and abdomen, while E. oligarthrus rarely infects humans and is found in the orbit or heart.
Two other species, Echinococcus shiquicus (found in the Tibetan fox) and Echinococcus felidis (found in African lions), have been identified but their potential for human infection is currently unknown or not reported.
The main species and the diseases they cause are:
Echinococcus granulosus sensu lato This species complex is the most common cause of human echinococcosis worldwide, causing cystic echinococcosis (CE), also known as hydatid disease or hydatidosis. The larval stage forms slow-growing, fluid-filled, unilocular (single-chambered) cysts, typically in the liver or lungs.
Echinococcus multilocularis This species is found in the northern hemisphere and causes alveolar echinococcosis (AE). This form is more aggressive, behaving like a malignant tumor by growing in an infiltrative, multilocular pattern (many small, interconnected vesicles) primarily in the liver, and can spread to other organs.
Echinococcus vogeli and Echinococcus oligarthrus These species are limited to Central and South America and are responsible for the rare polycystic echinococcosis (PE) or neotropical echinococcosis. E. vogeli typically causes large, polycystic growths in the liver and abdomen, while E. oligarthrus rarely infects humans and is found in the orbit or heart.
Two other species, Echinococcus shiquicus (found in the Tibetan fox) and Echinococcus felidis (found in African lions), have been identified but their potential for human infection is currently unknown or not reported.
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معادلات مهمة في الطوارىء و الرعاية :
1. Corrected Sodium (للـ Hyperglycemia)
Na_corrected = Na_measured + 1.6 × (Glucose - 100) / 100
(أو ≈ +2 لكل 100 مجم/ديسيلتر فوق 100)
مثال: Glucose 400 → +4.8–6 mEq/L للـ Na
2. Corrected Calcium (للـ Hypoalbuminemia)
Ca_corrected = Ca_measured + 0.8 × (4 - Albumin g/dL)
(أو +0.2 لكل 1 g/dL انخفاض الألبومين تحت 4)
مثال: Albumin 2 → +1.6 mg/dL للـ Ca
3. Serum Osmolality (Calculated)
Osm_calc = 2 × Na + Glucose/18 + BUN/2.8
(جميعها في mg/dL، Na في mEq/L)
Normal: 275–295 mOsm/kg
Osmolar gap = Measured Osm - Calculated Osm (>10 يشير لـ toxins زي methanol، ethylene glycol).
4. Anion Gap (AG)
AG = Na - (Cl + HCO₃)
Normal: 8–12 mEq/L (بدون K) أو 12–16 لو مع K.
Corrected AG لو albumin منخفض: AG + 2.5 × (4 - Albumin)
5. Delta Ratio (Δ/Δ or Delta-Delta) – لتقييم Mixed Metabolic Acidosis
Delta Ratio = (AG - 12) / (24 - HCO₃)
<0.4: Hyperchloremic normal AG acidosis
0.4–0.8: Mixed high AG + normal AG acidosis
1–2: Pure high AG metabolic acidosis (الأكثر شيوعًا)
2: Mixed high AG acidosis + metabolic alkalosis (أو chronic resp. acidosis)
6. ازاي تعرف الـ pH صح ولا غلط؟ (في ABG)
أول حاجة: قارن pH بالـ [H+] المتوقع (تقريبي):
pH 7.00 → [H+] ≈ 100 nmol/L
pH 7.40 → [H+] ≈ 40
pH 7.20 → [H+] ≈ 63
لو الـ [H+] مش مطابق للـ pH → الـ sample غلط (خطأ في القياس أو تأخير).
تاني حاجة: استخدم Henderson-Hasselbalch:
pH = 6.1 + log([HCO₃] / (0.03 × PaCO₂))
لو الـ pH محسوب مش مطابق للـ measured → خطأ في الـ ABG.
تالت حاجة: لو metabolic acidosis موجود (HCO₃ منخفض)، شوف الـ Delta Ratio:
لو قريب من 1–2 → الـ acidosis متسق (pure HAGMA).
لو خارج النطاق → mixed disorder (مش متسق مع pH لوحده).
7. Dehydration بالتحاليل (أهم علامات)
•BUN/Creatinine ratio >20:1 (prerenal azotemia).
•Sodium مرتفع (> 145) لو free water loss.
•Hematocrit مرتفع or HCT/albumin
•Uric acid مرتفع أحيانًا.
•Serum Osmolality مرتفع (>295).
•Urine specific gravity >1.020 أو Urine Osm >500–600.
•Fractional excretion of urea <35% (أحسن من FENa في dehydration) لأن الكلى بتعمله reabsorption في حالة الdehydration
1. Corrected Sodium (للـ Hyperglycemia)
Na_corrected = Na_measured + 1.6 × (Glucose - 100) / 100
(أو ≈ +2 لكل 100 مجم/ديسيلتر فوق 100)
مثال: Glucose 400 → +4.8–6 mEq/L للـ Na
2. Corrected Calcium (للـ Hypoalbuminemia)
Ca_corrected = Ca_measured + 0.8 × (4 - Albumin g/dL)
(أو +0.2 لكل 1 g/dL انخفاض الألبومين تحت 4)
مثال: Albumin 2 → +1.6 mg/dL للـ Ca
3. Serum Osmolality (Calculated)
Osm_calc = 2 × Na + Glucose/18 + BUN/2.8
(جميعها في mg/dL، Na في mEq/L)
Normal: 275–295 mOsm/kg
Osmolar gap = Measured Osm - Calculated Osm (>10 يشير لـ toxins زي methanol، ethylene glycol).
4. Anion Gap (AG)
AG = Na - (Cl + HCO₃)
Normal: 8–12 mEq/L (بدون K) أو 12–16 لو مع K.
Corrected AG لو albumin منخفض: AG + 2.5 × (4 - Albumin)
5. Delta Ratio (Δ/Δ or Delta-Delta) – لتقييم Mixed Metabolic Acidosis
Delta Ratio = (AG - 12) / (24 - HCO₃)
<0.4: Hyperchloremic normal AG acidosis
0.4–0.8: Mixed high AG + normal AG acidosis
1–2: Pure high AG metabolic acidosis (الأكثر شيوعًا)
2: Mixed high AG acidosis + metabolic alkalosis (أو chronic resp. acidosis)
6. ازاي تعرف الـ pH صح ولا غلط؟ (في ABG)
أول حاجة: قارن pH بالـ [H+] المتوقع (تقريبي):
pH 7.00 → [H+] ≈ 100 nmol/L
pH 7.40 → [H+] ≈ 40
pH 7.20 → [H+] ≈ 63
لو الـ [H+] مش مطابق للـ pH → الـ sample غلط (خطأ في القياس أو تأخير).
تاني حاجة: استخدم Henderson-Hasselbalch:
pH = 6.1 + log([HCO₃] / (0.03 × PaCO₂))
لو الـ pH محسوب مش مطابق للـ measured → خطأ في الـ ABG.
تالت حاجة: لو metabolic acidosis موجود (HCO₃ منخفض)، شوف الـ Delta Ratio:
لو قريب من 1–2 → الـ acidosis متسق (pure HAGMA).
لو خارج النطاق → mixed disorder (مش متسق مع pH لوحده).
7. Dehydration بالتحاليل (أهم علامات)
•BUN/Creatinine ratio >20:1 (prerenal azotemia).
•Sodium مرتفع (> 145) لو free water loss.
•Hematocrit مرتفع or HCT/albumin
•Uric acid مرتفع أحيانًا.
•Serum Osmolality مرتفع (>295).
•Urine specific gravity >1.020 أو Urine Osm >500–600.
•Fractional excretion of urea <35% (أحسن من FENa في dehydration) لأن الكلى بتعمله reabsorption في حالة الdehydration
Appendicular mass (APP mass) is a complication of acute appendicitis caused by localization of infection by the omentum and bowel loops.
The patient usually presents with right iliac fossa pain, fever, vomiting, and a palpable tender mass after 3–5 days of symptoms.
Investigations include CBC showing leukocytosis and abdominal ultrasound or CT to confirm the diagnosis.
Management is usually conservative by the Ochsner-Sherren regimen: NPO, IV fluids, antibiotics, and close observation.
Interval appendicectomy is commonly done after 6–8 weeks to prevent recurrence.
The patient usually presents with right iliac fossa pain, fever, vomiting, and a palpable tender mass after 3–5 days of symptoms.
Investigations include CBC showing leukocytosis and abdominal ultrasound or CT to confirm the diagnosis.
Management is usually conservative by the Ochsner-Sherren regimen: NPO, IV fluids, antibiotics, and close observation.
Interval appendicectomy is commonly done after 6–8 weeks to prevent recurrence.
Physiological Esophageal Motility — Detailed Explanation
Esophageal Motility is the coordinated muscular activity that transports food from the pharynx to the stomach.
1. Initiation of swallowing
Swallowing begins voluntarily in the mouth.
Once the food bolus reaches the pharynx, swallowing becomes an involuntary reflex controlled by the swallowing center in the medulla.
At this stage:
The upper esophageal sphincter (UES) relaxes
The bolus enters the esophagus
The UES then closes again to prevent air entry and aspiration
2. Primary peristalsis
After the bolus enters the esophagus, a coordinated peristaltic wave begins.
Mechanism:
Circular muscles behind the bolus contract
Muscles ahead of the bolus relax
This creates a downward propulsive movement
The wave travels from the upper esophagus toward the stomach.
Primary peristalsis is initiated by swallowing and occurs even in the absence of gravity.
3. Muscle composition of the esophagus
Upper one-third:
skeletal muscle
Middle one-third:
mixed skeletal and smooth muscle
Lower one-third:
smooth muscle
4. Lower esophageal sphincter (LES) relaxation
Before the peristaltic wave reaches the distal esophagus:
The LES undergoes receptive relaxation
This allows passage of the bolus into the stomach
After passage:
The LES contracts again
Preventing gastroesophageal reflux
Nitric oxide and inhibitory neurons are important mediators of LES relaxation.
5. Secondary peristalsis
If food remains within the esophagus or the esophagus becomes distended:
Secondary peristaltic waves occur
They are triggered locally by distension
No new swallow is required
Function:
Clears retained food or refluxed material
Neural control
Esophageal motility is controlled by:
Vagus nerve
Enteric nervous system
Brainstem swallowing center
Esophageal Motility is the coordinated muscular activity that transports food from the pharynx to the stomach.
1. Initiation of swallowing
Swallowing begins voluntarily in the mouth.
Once the food bolus reaches the pharynx, swallowing becomes an involuntary reflex controlled by the swallowing center in the medulla.
At this stage:
The upper esophageal sphincter (UES) relaxes
The bolus enters the esophagus
The UES then closes again to prevent air entry and aspiration
2. Primary peristalsis
After the bolus enters the esophagus, a coordinated peristaltic wave begins.
Mechanism:
Circular muscles behind the bolus contract
Muscles ahead of the bolus relax
This creates a downward propulsive movement
The wave travels from the upper esophagus toward the stomach.
Primary peristalsis is initiated by swallowing and occurs even in the absence of gravity.
3. Muscle composition of the esophagus
Upper one-third:
skeletal muscle
Middle one-third:
mixed skeletal and smooth muscle
Lower one-third:
smooth muscle
4. Lower esophageal sphincter (LES) relaxation
Before the peristaltic wave reaches the distal esophagus:
The LES undergoes receptive relaxation
This allows passage of the bolus into the stomach
After passage:
The LES contracts again
Preventing gastroesophageal reflux
Nitric oxide and inhibitory neurons are important mediators of LES relaxation.
5. Secondary peristalsis
If food remains within the esophagus or the esophagus becomes distended:
Secondary peristaltic waves occur
They are triggered locally by distension
No new swallow is required
Function:
Clears retained food or refluxed material
Neural control
Esophageal motility is controlled by:
Vagus nerve
Enteric nervous system
Brainstem swallowing center
Ranson Criteria for Acute Pancreatitis
Ranson's criteria are used to predict the severity and mortality risk of acute pancreatitis.
They include 11 parameters:
5 assessed at admission and
6 assessed during the first 48 hours.
At Admission
Within the First 48 Hours
Interpretation
0–2 criteria: Mild pancreatitis (mortality <5%)
3–4 criteria: Moderate disease (mortality ≈15–20%)
5–6 criteria: Severe disease (mortality ≈40%)
≥7 criteria: Very severe disease (mortality approaches 100% in the original study; modern mortality is lower with current ICU care).
Easy Mnemonic
Admission: GA LAW
G = Glucose >200
A = Age >55
L = LDH >350
A = AST >250
W = WBC >16,000
48 Hours: CHOBBS
C = Calcium ↓ (<8 mg/dL)
H = Hematocrit ↓ (>10%)
O = Oxygen (PaO₂ <60 mmHg)
B = BUN ↑ (>5 mg/dL)
B = Base deficit >4 mEq/L
S = Sequestration of fluid >6 L
Exam Pearl
Ranson score cannot be completed until 48 hours after admission, so it is less useful for early risk stratification.
In current practice, BISAP is often preferred for early assessment because it can be calculated within the first 24 hours, while the Revised Atlanta Classification is used to define disease severity.
Ranson's criteria are used to predict the severity and mortality risk of acute pancreatitis.
They include 11 parameters:
5 assessed at admission and
6 assessed during the first 48 hours.
At Admission
Within the First 48 Hours
Interpretation
0–2 criteria: Mild pancreatitis (mortality <5%)
3–4 criteria: Moderate disease (mortality ≈15–20%)
5–6 criteria: Severe disease (mortality ≈40%)
≥7 criteria: Very severe disease (mortality approaches 100% in the original study; modern mortality is lower with current ICU care).
Easy Mnemonic
Admission: GA LAW
G = Glucose >200
A = Age >55
L = LDH >350
A = AST >250
W = WBC >16,000
48 Hours: CHOBBS
C = Calcium ↓ (<8 mg/dL)
H = Hematocrit ↓ (>10%)
O = Oxygen (PaO₂ <60 mmHg)
B = BUN ↑ (>5 mg/dL)
B = Base deficit >4 mEq/L
S = Sequestration of fluid >6 L
Exam Pearl
Ranson score cannot be completed until 48 hours after admission, so it is less useful for early risk stratification.
In current practice, BISAP is often preferred for early assessment because it can be calculated within the first 24 hours, while the Revised Atlanta Classification is used to define disease severity.
BISAP Score (Bedside Index for Severity in Acute Pancreatitis)
The BISAP score is a simple bedside tool used within the first 24 hours of admission to predict the risk of severe acute pancreatitis and mortality.
BISAP Criteria (1 point each)
B – BUN >25 mg/dL (8.9 mmol/L)
I – Impaired mental status
Glasgow Coma Scale (GCS) <15
S – SIRS (Systemic Inflammatory Response Syndrome)
Presence of ≥2 of the following:
Temperature >38°C or <36°C
HR >90/min
RR >20/min or PaCO₂ <32 mmHg
WBC >12,000/mm³, <4,000/mm³, or >10% bands
A – Age >60 years
P – Pleural effusion
Seen on chest X-ray or CT scan
Interpretation
Advantages over Ranson
✅ Can be calculated within the first 24 hours.
✅ Simple (only 5 variables).
✅ Comparable accuracy to Ranson for predicting severe disease and mortality.
Easy Mnemonic
BISAP = B-I-S-A-P
B = BUN >25
I = Impaired mental status
S = SIRS
A = Age >60
P = Pleural effusion
Sources
The BISAP score is a simple bedside tool used within the first 24 hours of admission to predict the risk of severe acute pancreatitis and mortality.
BISAP Criteria (1 point each)
B – BUN >25 mg/dL (8.9 mmol/L)
I – Impaired mental status
Glasgow Coma Scale (GCS) <15
S – SIRS (Systemic Inflammatory Response Syndrome)
Presence of ≥2 of the following:
Temperature >38°C or <36°C
HR >90/min
RR >20/min or PaCO₂ <32 mmHg
WBC >12,000/mm³, <4,000/mm³, or >10% bands
A – Age >60 years
P – Pleural effusion
Seen on chest X-ray or CT scan
Interpretation
Advantages over Ranson
✅ Can be calculated within the first 24 hours.
✅ Simple (only 5 variables).
✅ Comparable accuracy to Ranson for predicting severe disease and mortality.
Easy Mnemonic
BISAP = B-I-S-A-P
B = BUN >25
I = Impaired mental status
S = SIRS
A = Age >60
P = Pleural effusion
Sources
Indication of transfer of the patient to burn center :
(1) second-or third-degree burns greater than 20% TBSA in patients age 10 to 50 years old;
(2) second- or third-degree burns greater than 10% TBSA in patients younger than 10 years or older than 50 years;
(3) third-degree burns greater than 5% TBSA in any age;
(4) any second- or third-degree burn to hands, feet, face, eyes, genitalia, perineum, or skin over major joints;
(5) any electrical or chemical burn; and
(6) any concomitant inhalation injury or multiple trauma.
(1) second-or third-degree burns greater than 20% TBSA in patients age 10 to 50 years old;
(2) second- or third-degree burns greater than 10% TBSA in patients younger than 10 years or older than 50 years;
(3) third-degree burns greater than 5% TBSA in any age;
(4) any second- or third-degree burn to hands, feet, face, eyes, genitalia, perineum, or skin over major joints;
(5) any electrical or chemical burn; and
(6) any concomitant inhalation injury or multiple trauma.