DR. AKOON BOL

✅ Acid–Base Disorders

Step 1: Look at pH
• pH ↓ (7.45) → Alkalosis

✅ Step 2: Look at PaCO₂ and HCO₃⁻

Use them to identify if the problem is respiratory (PaCO₂) or metabolic (HCO₃⁻).

✅ If pH and PaCO₂ move in OPPOSITE directions → Respiratory disorder
• pH ↓ & CO₂ ↑ → Respiratory acidosis
• pH ↑ & CO₂ ↓ → Respiratory alkalosis

✅ If pH and HCO₃⁻ move in SAME direction → Metabolic disorder
• pH ↓ & HCO₃⁻ ↓ → Metabolic acidosis
• pH ↑ & HCO₃⁻ ↑ → Metabolic alkalosis

✅ Compensation

Metabolic disorders → lungs compensate (change CO₂)

Metabolic acidosis
• CO₂ should ↓ to match ↓ HCO₃⁻
• Quick rule:
Expected CO₂ ≈ 1.5 × HCO₃ + 8 (±2)
(Winter’s formula)

Metabolic alkalosis
• CO₂ should ↑
• For every ↑1 mmol/L in HCO₃⁻ → CO₂ ↑ by 0.7 mmHg

Respiratory disorders → kidneys compensate (change HCO₃⁻)

✅ Respiratory acidosis (CO₂ ↑)

Acute: HCO₃ ↑ by 1 mmol/L per 10 mmHg CO₂
Chronic: HCO₃ ↑ by 4 mmol/L per 10 mmHg CO₂

✅ Respiratory alkalosis (CO₂ ↓)

Acute: HCO₃ ↓ by 2 mmol/L per 10 mmHg CO₂
Chronic: HCO₃ ↓ by 4 mmol/L per 10 mmHg CO₂


. Akoon Bol Akoon

PLACENTA PREVIA

Definition:
Placenta previa is a condition where the placenta implants low in the uterus, covering partially or completely the internal cervical os.
→ Causes painless vaginal bleeding in late pregnancy.

Symptoms (Classic Presentation)
• Painless bright-red vaginal bleeding in the 2nd half of pregnancy (usually >20 weeks)
• No abdominal pain
• Uterus soft, non-tender
• May have recurrent bleeding episodes

Risk Factors
From the document:
• Previous placenta previa
• Prior uterine surgery (C-section, D&C)
• Multiparity
• Multiple gestation
• To***co use
• Advanced maternal age (AMA)

Diagnosis:
Do NOT perform digital vaginal exam until placenta position is confirmed.
Preferred tests from document:

1. Transvaginal Ultrasound — Gold Standard
• Confirms placental location
• Used to rule out placenta previa in late pregnancy

2. Other evaluations
• CBC to assess blood loss
• Type & screen / cross-match
• Fetal heart monitoring
• No digital exam until previa excluded (ALERT in document)

Differential Diagnosis:
Conditions causing bleeding in late pregnancy (from document):
• Placental abruption → painful bleeding
• Vasa previa → minimal bleeding + fetal distress
• Bloody show of labor
• Placenta accreta spectrum (often associated with previa)
• Uterine rupture (bleeding + abnormal FHR + contractions)

Treatment
Initial Management
• Stabilize mother (ABC)
• IV access, fluids, possible blood transfusion
• Type & screen/cross-match
• Continuous fetal monitoring
• No vaginal exams
• If Rh-negative → RhoGAM (from general bleeding management)

Expectant Management (if stable & preterm)
• Pelvic rest (no s*x, no digital exam)
• Avoid heavy activity
• Monitor bleeding
• Corticosteroids if

Pheochromocytoma

Definition:
A tumor of the adrenal medulla that overproduces catecholamines (epinephrine & norepinephrine), causing episodic sympathetic surges.

Classic Presentation (Think: “PHEO”)

P → Palpitations
H → Headache
E → Episodic sweating
O → Orthostatic hypotension (between hypertensive crises)

PLUS:
• Episodic hypertension
• Tremor
• Anxiety / panic-like spells
• Tachycardia

Diagnostic Tests (Ordered by Priority)

1️⃣ Best Initial Test
• Plasma free metanephrines

2️⃣ Confirmatory Test
• 24-hour urine metanephrines & catecholamines
(More accurate than urine VMA)

3️⃣ Imaging (after biochemical confirmation)
• CT or MRI of adrenal gland

4️⃣ If imaging negative or extra-adrenal suspected
• MIBG scan (nuclear imaging)

Management

1️⃣ First line (before surgery):
• Phenoxybenzamine (α-blocker)
→ Prevents hypertensive crisis during surgery

2️⃣ After adequate α-blockade
• Add β-blocker (if needed for tachycardia)
Never start β-blocker first.

3️⃣ Definitive treatment
• Surgical removal (usually laparoscopic adrenalectomy)

🔑 Key “Exam Triggers”
• Episodic HTN + headache + sweating = Think pheochromocytoma
• Orthostatic hypotension between episodes
• Alpha-block first → then beta-block
• Elevated metanephrines = most sensitive test


. Akoon Bol Akoon

Here is a clear, concise, and easy-to-study explanation of an Asthmatic Attack (Acute Asthma Exacerbation).

Asthmatic Attack

An asthmatic attack is a sudden worsening of asthma symptoms caused by narrowing and inflammation of the airways.

🫁What Happens During an Attack
• Airway inflammation
• Airway muscle tightening (bronchospasm)
• Increased mucus production
→ Leads to difficulty breathing

🚨 Triggers
• Dust, smoke
• Pollen, molds
• Exercise
• Cold air
• Viral infections
• Strong odors/perfumes
• Stress or emotional upset
• Certain medications (NSAIDs, beta-blockers)

🫁Signs & Symptoms
• Shortness of breath
• Wheezing
• Chest tightness
• Persistent coughing
• Difficulty speaking (severe attack)
• Rapid breathing
• Use of accessory muscles
• Cyanosis (late/very severe sign)

🫁Diagnosis (Clinical)
• Peak flow measurement ↓
• Oxygen saturation ↓
• Wheezing on auscultation
• Sometimes silent chest in severe attacks (very dangerous)

🛑 Emergency Management (Acute Attack)

1️⃣ First Line
• Short-acting bronchodilator
• Salbutamol / Albuterol nebulizer or inhaler

2️⃣ Add-on if needed
• Ipratropium bromide (anticholinergic)
• Oxygen if SpO₂ < 94%
• Corticosteroids:
• Oral: Prednisolone
• IV: Hydrocortisone

3️⃣ Severe Attack
• Magnesium sulfate IV
• Continuous nebulization
• Possible intubation if impending respiratory failure

🚨Severity Signs

Mild
• Can speak in sentences
• Wheezing present

Moderate
• Breathless
• Speaks in phrases
• PEFR 40–60%

Severe
• Speaks in words only
• PEFR < 40%
• Tachycardia
• Oxygen saturation < 90%

Life-Threatening
• Silent chest
• Confusion
• Cyanosis
• Bradycardia
• Respiratory arrest risk

🫁Long-Term Prevention
• Daily inhaled corticosteroids
• Long-acting bronchodilators
• Avoid triggers
• Asthma action plan
• Regular check-ups


. Akoon Bol Akoon

Routes of Administration 💉💊

These are the ways medications can be given to enter the body and produce an effect.

📌Oral (by mouth)
• Examples: tablets, capsules, syrups
• Advantages: convenient, safe, easy
• Disadvantages: slow absorption, affected by food or stomach acid

📌Sublingual (under the tongue)
• Example: nitroglycerin tablet
• Fast absorption through mouth tissues
• Avoids destruction by stomach acid

📌Buccal (between gum and cheek)
• Example: buprenorphine
• Absorbed through oral mucosa, bypasses liver metabolism

📌Parenteral (by injection)

💉 Includes:
• Intradermal (ID): into the skin (e.g., TB test)
• Subcutaneous (SC): into fat tissue (e.g., insulin)
• Intramuscular (IM): into muscle (e.g., vaccines)
• Intravenous (IV): into a vein (e.g., emergency drugs, fluids)

📌Inhalation
• Example: nebulizers, inhalers
• Rapid absorption via lungs

📌Rectal
• Example: suppositories, enemas
• Used when patient can’t swallow or is vomiting

📌Vaginal
• Example: creams, suppositories, tablets for local infection or hormones

📌Topical
• Example: creams, ointments, patches
• Applied directly to skin for local effect

📌Transdermal
• Example: ni****ne or pain relief patches
• Absorbed through skin for systemic effect over time

📌Other specialized routes:
• Intraocular: eye drops
• Intranasal: nasal sprays
• Epidural / Intrathecal: around or into spinal canal (for anesthesia)


. Akoon Bol Akoon

Emphysema overview 🫁🧐🩺👇

Emphysema is a chronic lung disease where the air sacs (alveoli) are damaged and lose their elasticity, causing difficulty in exhaling air.
It’s one of the main types of Chronic Obstructive Pulmonary Disease (COPD).

🫁Causes:
• Smoking (most common cause)
• Long-term exposure to air pollution, chemical fumes, or dust
• Genetic condition (Alpha-1 antitrypsin deficiency)

🫁Pathophysiology (What happens):
• Alveoli walls are destroyed → fewer and larger air sacs
• Less surface area for oxygen exchange
• Air gets trapped → lungs become overinflated → “barrel chest” appearance

🫁Symptoms:
• Shortness of breath (especially on exertion)
• Chronic cough (often dry)
• Wheezing
• Fatigue
• Barrel-shaped chest
• Cyanosis (bluish lips/fingertips in severe cases)

🫁Treatment:
• Stop smoking 🚭 (most important step)
• Bronchodilators (e.g., salbutamol)
• Corticosteroids (to reduce inflammation)
• Oxygen therapy (if oxygen level is low)
• Pulmonary rehabilitation (breathing exercises)
• Surgery (in severe cases — lung volume reduction or transplant)

🫁Complications:
• Respiratory failure
• Pneumothorax (collapsed lung)
• Cor pulmonale (right-sided heart failure due to lung disease)


. Akoon Bol Akoon

Polycystic Kidney Disease (PKD)

Definition:
Polycystic kidney disease is a hereditary disorder characterized by the growth of numerous fluid-filled cysts in both kidneys, leading to progressive renal enlargement and loss of kidney function. The main forms are autosomal dominant PKD (ADPKD) and autosomal recessive PKD (ARPKD) .

Symptoms:
• Flank or abdominal pain (from cyst rupture, bleeding, or enlargement)
• Hematuria (blood in urine)
• Hypertension (often the earliest sign)
• Enlarged kidneys palpable on examination
• Recurrent urinary tract infections or nephrolithiasis (kidney stones)
• Progressive renal insufficiency

Diagnosis:
• Imaging: Ultrasound, CT, or MRI showing multiple bilateral renal cysts
• Family history: Often positive for PKD
• Genetic testing: May confirm mutations in PKD1 or PKD2 genes
• Screening: MRI or MRA for intracranial aneurysms in selected cases 

Differential Diagnosis:
• Simple renal cysts
• Acquired cystic kidney disease (seen in long-term dialysis)
• Medullary sponge kidney
• Tuberous sclerosis

Treatment:
There is no cure for PKD, but management aims to slow progression and treat complications:
• Blood pressure control (ACE inhibitors or ARBs)
• Adequate hydration (>3 L/day to suppress vasopressin) 
• Avoid nephrotoxic drugs
• Treat infections and stones aggressively
• Low-protein diet to reduce renal workload 
• Tolvaptan (vasopressin receptor antagonist) in selected patients to slow cyst growth
• Dialysis or kidney transplantation for end-stage kidney disease (ESKD)

Follow-up:
• Monitor blood pressure and serum creatinine at least twice yearly
• Regular imaging if symptoms change or complications are suspected
• Counseling about genetic risks for family members
• Nephrology referral for progression prevention and long-term management 

Dr. Akoon Bol Akoon

Acidosis

Definition:
Acidosis is a condition characterized by an abnormal increase in the acidity (decrease in pH) of blood and other body tissues.

It is categorized as:
• Metabolic acidosis: Decreased bicarbonate (HCO₃⁻) and low pH.
• Respiratory acidosis: Increased CO₂ (carbon dioxide) due to hypoventilation.

Symptoms:
• Nausea, vomiting
• Fatigue, lethargy
• Rapid breathing (especially in metabolic acidosis)
• Confusion or altered mental status
• Headache
• Cardiac arrhythmias (in severe cases)

Diagnosis:
• Arterial blood gas (ABG):
• pH < 7.35
• Metabolic acidosis: ↓ HCO₃⁻
• Respiratory acidosis: ↑ PaCO₂
• Serum electrolytes: Anion gap calculation
• Urinalysis: May show acid-base abnormalities (especially in renal causes)

Differential Diagnosis:
For metabolic acidosis:
• Diabetic ketoacidosis (DKA)
• Lactic acidosis
• Renal failure
• Toxin ingestion (e.g., methanol, ethylene glycol)
• Diarrhea (loss of bicarbonate)

For respiratory acidosis:
• Chronic obstructive pulmonary disease (COPD)
• Respiratory depression (e.g., opioids, neuromuscular disease)
• Obstructive sleep apnea

Treatment:
• Identify and treat the underlying cause
• DKA → insulin and fluids
• Sepsis/lactic acidosis → antibiotics, fluid resuscitation
• COPD exacerbation → bronchodilators, steroids, oxygen
• Sodium bicarbonate may be considered in severe metabolic acidosis (controversial)
• Ventilatory support for respiratory acidosis

Follow-Up:
• Monitor ABGs, serum electrolytes, and clinical status
• Address chronic causes (e.g., dialysis in chronic renal failure)
• Educate patient on triggers (e.g., medication adherence in COPD, glycemic control in diabetes)


. Akoon Bol Akoon

❇️ Abdominal pain referral areas based on common conditions affecting different organs:

🔷Right Upper Quadrant (RUQ) – Hepatitis, Cholecystitis (Liver and Gallbladder issues).

🔷Epigastric Region (Middle Upper Abdomen) – Peptic ulcer, Pancreatitis (Stomach and Pancreas issues).

🔷Left Upper Quadrant (LUQ) – Splenic injury.

🔷Left Flank (Side Abdomen) – Renal and ureteric pain (Kidney issues).

🔷Periumbilical (Center Abdomen) – Bowel obstruction, Aortic aneurysm (back pain).

🔷Right Flank – Renal and ureteric pain (Kidney issues).

🔷Right Lower Quadrant (RLQ) – Appendicitis.

🔷Suprapubic (Pelvic Region) – Pelvic pain (Ovarian cysts, Pelvic inflammatory disease, etc.).

🔷Left Lower Quadrant (LLQ) – Diverticulitis.

Thanks 🙏
Dr. Akoon Bol Akoon

ABG (Arterial Blood Gas) in Clinical Practice
Definition
ABG means Arterial Blood Gas.
It is a vital test that shows how well the lungs and kidneys are maintaining the acid–base balance, oxygenation, and ventilation of the body.
It helps detect problems like respiratory failure, metabolic acidosis, and oxygen imbalance.

🟦 Main Parameters and Normal Values
🔹 pH: 7.35 – 7.45 → shows acid–base balance
🔹 PaCO₂: 35 – 45 mmHg → represents respiratory component (ventilation)
🔹 HCO₃⁻: 22 – 26 mEq/L → represents metabolic component (renal)
🔹 PaO₂: 80 – 100 mmHg → represents oxygenation
🔹 SaO₂: 95 – 100% → percentage of hemoglobin saturated with oxygen
🔹 Base Excess (BE): −2 to +2 mEq/L → indicates metabolic compensation
🔹 Anion Gap (AG): 8 – 12 mEq/L → helps detect type of metabolic acidosis

Step-by-Step Interpretation

🟢 Step 1 — Check the pH
If pH < 7.35 →Acidemia
If pH > 7.45 → Alkalemia
If pH is 7.35–7.45 → Normal (may be compensated)

🔵 Step 2 — Identify the Primary Disturbance
If pH is low and PaCO₂ is high → Respiratory Acidosis
If pH is high and PaCO₂ is low → Respiratory Alkalosis
If pH is low and HCO₃⁻ is low → Metabolic Acidosis
If pH is high and HCO₃⁻ is high → Metabolic Alkalosis

🟣 Step 3 — Check for Compensation
The body tries to restore normal pH.

Respiratory Acidosis → Kidneys increase HCO₃⁻ to compensate
Respiratory Alkalosis → Kidneys excrete more HCO₃⁻
Metabolic Acidosis → Lungs blow off CO₂ (hyperventilation)
Metabolic Alkalosis → Lungs retain CO₂ (hypoventilation)

👉 If compensation is absent or inadequate → there is a mixed disorder.

🟫 Step 4 — Evaluate Oxygenation
PaO₂ between 80–100 mmHg →Normal
PaO₂ between 60–80 mmHg → Mild hypoxemia
PaO₂ between 40–60 mmHg → Moderate hypoxemia
PaO₂ below 40 mmHg →Severe hypoxemia

➡️ PaO₂/FiO₂ ratio
More than 300 → Normal
Less than 300 → Impaired gas exchange
Less than 200 → ARDS (Acute Respiratory Distress Syndrome)

⬛ Step 5 — Calculate the Anion Gap
Formula: AG = Na⁺ − (Cl⁻ + HCO₃⁻)
Normal value = 8 – 12 mEq/L

If AG > 12 →High Anion Gap Metabolic Acidosis (DKA, lactic acidosis, renal failure, toxins)
If AG normal → Normal Anion Gap (Hyperchloremic) Metabolic Acidosis (diarrhea, renal tubular acidosis)

Common Clinical Patterns

Respiratory Acidosis → Seen in COPD, asthma, hypoventilation, or airway obstruction.
ABG: pH ↓, PaCO₂ ↑, HCO₃⁻ ↑ (if chronic).

Respiratory Alkalosis → Seen in anxiety, pain, fever, sepsis, hypoxia.
ABG: pH ↑, PaCO₂ ↓, HCO₃⁻ ↓ (if chronic).

Metabolic Acidosis → Seen in DKA, renal failure, shock, diarrhea.
ABG: pH ↓, HCO₃⁻ ↓, PaCO₂ ↓ (compensation).

Metabolic Alkalosis → Seen in vomiting, diuretics, hypokalemia.
ABG: pH ↑, HCO₃⁻ ↑, PaCO₂ ↑ (compensation).

🟪 Mnemonic: ROME Rule
ROME = Respiratory Opposite, Metabolic Equal

If pH and PaCO₂ move in opposite directions →Respiratory
If pH and HCO₃⁻ move in the same direction →Metabolic

Examples:
🟥 Respiratory Acidosis → pH ↓, PaCO₂ ↑
🟩 Respiratory Alkalosis → pH ↑, PaCO₂ ↓
🟧 Metabolic Acidosis → pH ↓, HCO₃⁻ ↓
🟦 Metabolic Alkalosis → pH ↑, HCO₃⁻ ↑

🟤 ABG in Critical Care
COPD Exacerbation → Respiratory Acidosis (chronic + metabolic compensation)
Sepsis or Shock → Metabolic Acidosis (lactic acidosis)
Anxiety or Pain → Respiratory Alkalosis
Vomiting → Metabolic Alkalosis
Salicylate Toxicity → Mixed Metabolic Acidosis + Respiratory Alkalosis
DKA → High AG Metabolic Acidosis
Cardiac Arrest → Severe Metabolic Acidosis + Hypoxemia

🩶 Normal ABG Values Summary (for memory)
pH → 7.35 – 7.45
PaCO₂ → 35 – 45 mmHg
HCO₃⁻ → 22 – 26 mEq/L
PaO₂ → 80 – 100 mmHg
SaO₂ → 95 – 100%
Base Excess → −2 to +2 mEq/L
Anion Gap → 8 – 12 mEq/L

🩷 Quick Clinical Tips
Low pH + High CO₂ → Respiratory Acidosis
High pH + Low CO₂ → Respiratory Alkalosis
Low pH + Low HCO₃⁻ → Metabolic Acidosis
High pH + High HCO₃⁻ → Metabolic Alkalosis
Always check O₂ level and compensation
Always calculate Anion Gap in every metabolic acidosis

Thanks
Dr. Akoon Bol Akoon

Visceral Leishmaniasis (Kala-azar)

Definition:
A severe systemic disease caused by the Leishmania donovani complex, transmitted by the bite of infected female sandflies. It mainly affects the spleen, liver, and bone marrow.

Etiology:
• Causative agent: Leishmania donovani, L. infantum, or L. chagasi
• Vector: Female Phlebotomus or Lutzomyia sandfly
• Reservoir: Humans, dogs, and rodents

Pathophysiology:

After the sandfly bite, Leishmania parasites invade macrophages in the reticuloendothelial system (spleen, liver, bone marrow), causing massive organ enlargement and pancytopenia.

Symptoms (Mnemonic: “She Had No Fever But She Complained of Weakness”)

⭐ Splenomegaly
⭐ Hepatomegaly
⭐ Night sweats
⭐ Fever (often irregular or prolonged)
⭐ Blackening of skin (hence “Kala-azar” meaning “black fever”)
⭐ Scaly skin
⭐ Cough
⭐ Weakness and weight loss

Investigations:
• CBC → Pancytopenia (↓WBC, ↓RBC, ↓platelets)
• Serology: rK39 antigen test (rapid diagnostic test)
• Bone marrow or splenic aspirate: Amastigotes seen inside macrophages (“Leishman-Donovan bodies”)
• PCR for species confirmation (if available)

Treatment:
• First-line: Liposomal amphotericin B
• Alternatives: Miltefosine, sodium stibogluconate, paromomycin
• Supportive: Nutrition, management of anemia/infection

Thanks
Dr. Akoon Bol Akoon