Acid base , electrolytes Flashcards
(160 cards)
1
Q
What is Liddle syndrome and what are its key clinical features⁉️
A
➡️ Liddle syndrome is a genetic tubular disorder
➡️ Characterized by:
🔹 Hypertension
🔹 Hypokalemia
🔹 Metabolic alkalosis
⚠️ Low renin and low aldosterone ➡️ Pseudohyperaldosteronism
2
Q
What is the underlying pathophysiology of Liddle syndrome⁉️
A
➡️ Overactivation of ENaC channels in the collecting duct
➡️ normally regulated by aldosterone
➡️ In Liddle syndrome ➡️ ENaC is active without aldosterone
ENaC = epithelial sodium channel
3
Q
What is the treatment of choice for Liddle syndrome⁉️
A
💊 Amiloride
➡️ Blocks ENaC directly
4
Q
What are the three diagnostic steps in acid-base balance disorders⁉️
A
🚩 Step 1: Determine if it’s acidosis or alkalosis (based on pH)
🚩 Step 2: Determine if it’s respiratory or metabolic (based on HCO₃⁻ and PCO₂)
🚩 Step 3: Assess compensation:
➡️ Is it appropriate?
➡️ If not, is there a mixed disorder❓
5
Q
What are the normal reference values in acid-base interpretation⁉️
A
✅ pH: 7.35–7.45
✅ PCO₂: 35–45 mmHg
✅ HCO₃⁻ (bicarbonate): 22–26 mEq/L
6
Q
How is acidosis vs alkalosis determined in acid-base disorders⁉️
A
➡️ Check pH:
🔹 pH < 7.35 = acidosis
🔹 pH > 7.45 = alkalosis
🔹 pH normal but abnormal CO₂ & HCO₃⁻ = mixed disorder
7
Q
How do you determine whether the acid-base disorder is metabolic or respiratory⁉️
A
➡️ Examine HCO₃⁻ and pCO₂:
🔹 ↓HCO₃⁻ = metabolic acidosis
🔹 ↑pCO₂ = respiratory acidosis
🔹 For metabolic alkalosis: predicted pCO₂ ≈ HCO₃⁻ + 15 (compensation check)
8
Q
How is the Anion Gap (AG) calculated, and what does it represent⁉️
A
➡️ AG = [Na⁺] + [K⁺] - [Cl⁻] - [HCO₃⁻]
➡️ It represents unmeasured anions contributing to metabolic acidosis
9
Q
Why should the anion gap be corrected in hypoalbuminemia⁉️
A
➡️ Albumin contributes to the anion gap, so a low albumin level underestimates the true gap
10
Q
How is the corrected anion gap calculated in hypoalbuminemia⁉️
A
✅ For every 1 g/dL decrease in albumin, add 2.5 mmol/L to the calculated anion gap
11
Q
What are common causes of hypoalbuminemia⁉️
A
🔸 Nephrotic syndrome
🔸 Severe liver disease
🔸 Malabsorption disorders
12
Q
What are the causes of high Anion Gap metabolic acidosis ⁉️
A
➡️ MUD PILES mnemonic:
🔹 Methanol
🔹 Uremia
🔹 Diabetic ketoacidosis
🔹 Paracetamol (acetaminophen)
🔹 Isoniazid
🔹 Lactic acidosis
🔹 Ethanol
🔹 Salicylates
13
Q
How is the Delta Ratio calculated and interpreted in metabolic acidosis⁉️
A
➡️ Delta ratio=[Patient AG-normal AG]:[normal
HCO3-patient HCO3]
➡️ Interpretation:
🔹 <1 ➡️ combined AG+non AG acidosis
🔹 1–2 ➡️ Pure high AG metabolic acidosis
🔹 >2 ➡️ High AG acidosis + metabolic alkalosis
⚠️normal values are usually between 1-2
14
Q
When should the osmolar gap be checked⁉️
A
⚠️ If poisoning is suspected; an osmolar gap >12 supports poisoning
15
Q
What acid-base disturbance does salicylic poisoning cause⁉️
A
✅ High anion gap metabolic acidosis and respiratory alkalosis
16
Q
How does compensation occur in metabolic acidosis⁉️
A
✅ Hyperventilation decreases PaCO₂ to balance pH
17
Q
Why is metabolic acidosis ruled out when bicarbonate is normal⁉️
A
➡️ In metabolic acidosis, HCO₃⁻ should be low
18
Q
Why is respiratory alkalosis unlikely if PCO₂ is high⁉️
A
➡️ In respiratory alkalosis,PCO₂ should be low
19
Q
How does the body compensate for chronic respiratory acidosis⁉️
A
➡️ Chronic respiratory acidosis → ↑ HCO₃⁻ as compensation
20
Q
What acid-base imbalance defines respiratory acidosis⁉️
A
➡️ Acidemia (low pH) with elevated PCO₂
21
Q
How does the body compensate for respiratory acidosis⁉️
A
➡️ By increasing bicarbonate (HCO₃⁻) to counteract acidemia
22
Q
What are the typical lab findings in respiratory acidosis⁉️
A
🔹 Low pH
🔹 High PCO₂
🔹 Elevated bicarbonate (in compensated cases)
23
Q
What acid-base disturbance can sodium bicarbonate intoxication cause⁉️
A
➡️ Metabolic alkalosis
24
Q
What is the expected bicarbonate compensation in acute respiratory alkalosis⁉️
A
✅↓2 mEq/L HCO₃⁻ for every ↓10 mmHg PCO₂
➡️ Minimal compensation due to limited time for renal adjustment
25
What is the **expected bicarbonate compensation in chronic respiratory alkalosis⁉️**
✅**↓4 mEq/L HCO₃⁻ for every ↓10 mmHg PCO₂**
➡️ Reflects slower renal compensation over time
26
What **clinical situations** commonly cause **respiratory alkalosis due to hyperventilation⁉️**
🚩 **Panic attacks**
🚩 **Pain**
🚩 **Hypoxemia**
🚩 **Pregnancy**
🧠 All can lead to **↓PCO₂ → respiratory alkalosis**
27
What **acid-base disorder is caused by salicylate (aspirin) toxicity⁉️**
✅ **Mixed** high anion gap **metabolic acidosis** + **respiratory alkalosis**
➡️ CNS stimulation ➡️ early hyperventilation (alkalosis)
➡️ Later: salicylate accumulation ➡️ lactic + ketoacidosis
28
What does a **pH of 7.3 indicate in acid-base balance⁉️**
🔶 **pH < 7.35 ➡️ Acidemia**
➡️ Suggests the presence of **acidosis as the primary process**
29
How can we **identify the primary cause of acidemia in acid-base disorders⁉️**
✅ Stepwise approach:
🔹 Check **HCO₃⁻ = (low)** ➡️ **Metabolic acidosis**
🔹 Check **PCO₂ = (slightly low)** ➡️ **Respiratory alkalosis expected**
🔹 Since **PCO₂ is not low enough,** it suggests **inadequate compensation**
30
How is **compensation assessed in metabolic acidosis,** and what suggests a mixed disorder⁉️
**Metabolic acidosis ➡️ ↓ pH, ↓ HCO₃⁻**
➡️ **Compensation = ↓ PCO₂**
➡️ **Expected PCO₂ = HCO₃⁻ + 15**
➡️ **If measured PCO₂ > expected ➡️ combination of metabolic acidosis with respiratory acidosis**
## Footnote
💡 Assessing this helps identify a combined acid-base disorder
31
How is **pCO2 compensation** calculated for **metabolic acidosis⁉️**
✅ **Expected pCO2 = HCO3 + 15**
OR
✅ **using formula: 1.5 × HCO3 + 8 ± 2**
32
What is **Winter’s formula and what does it estimate⁉️**
➡️ **Winter’s formula:**
Expected pCO₂ = (1.5 × HCO₃⁻) + 8 ± 2
It estimates the expected pCO₂ in metabolic acidosis to **check for adequate respiratory compensation**
33
**Why is it important to compare actual pCO₂ to Winter’s formula in metabolic acidosis⁉️**
✅ To determine if the lungs are **compensating appropriately** or if there is an **additional respiratory disorder** (acidosis or alkalosis)
34
**In metabolic acidosis with HCO₃⁻ = 12, what does a pCO₂ of 40 mmHg indicate⁉️**
➡️ Expected pCO₂ = 26–30 mmHg. A pCO₂ of 40 mmHg is **higher than expected,** indicating a **superimposed respiratory acidosis**
35
**In metabolic acidosis with HCO₃⁻ = 12, what does a pCO₂ of 20 mmHg indicate⁉️**
➡️ Expected pCO₂ = 26–30 mmHg. A pCO₂ of 20 mmHg is **lower than expected,** indicating a **superimposed respiratory alkalosis**
36
How does **vomiting affect acid-base balance⁉️**
✅ It leads to **proton loss and bicarbonate retention,** resulting in **metabolic alkalosis**
37
Why does **urine become alkalotic and potassium-rich during vomiting⁉️**
✅ **Bicarbonate filtration exceeds absorption capacity, leading to alkaline urine and potassium excretion**
38
**What happens when vomiting stops⁉️**
➡️ **Hypovolemia, potassium and chloride deficiency persist, and alkalosis continues due to increased bicarbonate reabsorption
39
What **electrolyte abnormalities** are typically seen **with vomiting⁉️**
👉🏻 **Hypokalemia**
👉🏻 **Hypochloremia**
👉🏻 **Metabolic alkalosis**
40
Why is **urine chloride important in metabolic alkalosis assessment⁉️**
✅ It helps **determine if the cause is renal or non-renal**
41
What does **very low urine chloride indicate in metabolic alkalosis⁉️**
✅ **A renal cause is ruled out,** meaning the **kidneys are functioning properly**
42
What are the **typical urine findings in dehydration⁉️**
➡️ **Low urine sodium** → The kidney reabsorbs sodium to maintain intravascular volume.
➡️ **High urine osmolarity** → The kidney conserves free water, concentrating the urine.
43
What **clinical signs indicate dehydration⁉️**
🔸 **Low blood pressure**
🔸 **Orthostatic hypotension**
🔸 **Low skin turgor**
🔸 **Decreased jugular venous pressure (JVP)**
44
What is a **common side effect of ARBs (e.g., valsartan)⁉️**
➡️ **Hyperkalemia** due to RAAS axis blockade
45
What is the **definition of hyperkalemia⁉️**
✅ Potassium level **above 5.5 mmol/L;**
❗️ **severe hyperkalemia** is above **6 mmol/L**
46
What are the **main causes of hyperkalemia⁉️**
1️⃣ **Intracellular potassium shift into extracellular fluid**
2️⃣ **Decreased renal potassium secretion** (most common cause)
47
What are the **three main categories of hyperkalemia causes⁉️**
1️⃣ **Pseudo-hyperkalemia** → Lab artifact from potassium release during or after blood draw.
2️⃣ **Re-distribution** → Intracellular potassium shifts due to acidosis, drugs (digoxin, beta-blockers, succinylcholine), and cell necrosis.
3️⃣ **Decreased renal excretion** → Most common; seen with RAAS blockers, hypoaldosteronism, and advanced renal failure.
48
What **conditions can lead to pseudo-hyperkalemia⁉️**
🔹 **Leukocytosis**
🔹 **Thrombocytosis**
🔹 **Erythrocytosis**
🔹 **Cooling of the blood sample**
49
Which **mechanisms contribute to intracellular potassium release (redistribution)⁉️**
🔸 **Non-anion gap metabolic acidosis**
🔸 **Drugs** (digoxin, beta-blockers, succinylcholine)
🔸 **Cell necrosis** (tumor lysis syndrome, rhabdomyolysis)
50
What are **common causes of decreased renal potassium excretion⁉️**
🔸 **RAAS-blocking drugs** (e.g., ARBs, ACE inhibitors)
🔸 **Hypoaldosteronism**
🔸 **Advanced renal failure**
51
Why is **hyperkalemia considered a medical emergency⁉️**
➡️ Because it carries a **high risk of life-threatening cardiac arrhythmias,** such as sinus bradycardia, ventricular tachycardia, ventricular fibrillation, and asystole
52
**How do NSAIDs and ACE inhibitors contribute to hyperkalemia⁉️**
➡️ **They reduce glomerular perfusion pressure, lowering GFR and impairing potassium secretion**
➡️ **ACE inhibitors also suppress aldosterone secretion**
53
What is the **physiological response to low GFR⁉️**
➡️ **Prostaglandin-mediated vasodilation of the afferent artery and angiotensin II-mediated vasoconstriction of the efferent artery to maintain perfusion**
54
What are the **indications to treat hyperkalemia urgently⁉️**
🔸 **Plasma K⁺ > 6.5 mM**
🔸 **Any ECG changes suggestive of hyperkalemia**
55
Which **ECG findings may indicate severe hyperkalemia⁉️**
🚩**Sinus bradycardia**
🚩**sinus arrest**
🚩 **slow idioventricular rhythm**
🚩 **ventricular tachycardia or fibrillation, and asystole**
56
What is the **first ECG change seen in hyperkalemia⁉️**
⚠️ **Peaked T waves** due to altered myocardial repolarization
57
What **ECG abnormalities develop as hyperkalemia worsens⁉️**
🔸 **Prolonged PR interval**
🔸 **QRS widening**
🔸 **Loss of P waves**
🔸 **Sine wave pattern** (leading to VF or asystole)
58
What is the **first-line treatment for hyperkalemia with ECG changes or potassium >6.5 mmol/L⁉️**
✅ **IV 10% calcium gluconate, 10 mL over 2–3 minutes;** repeat if ECG remains abnormal
59
Which **immediate treatments promote potassium redistribution into cells⁉️**
✅ **IV insulin** (10 units) with **IV dextrose solution**
✅ **Inhaled beta-2 agonist (albuterol)** 10–20 mg in 4 mL normal saline over 10 minutes
60
**What treatments promote potassium excretion⁉️**
✅ **Potassium-binding resins** (Kayexalate, polystyrene sulfonate)
✅ **Diuretics** (Fusid)
✅ **Hemodialysis** (for refractory cases)
61
**How should insulin and dextrose be administered in hyperkalemia⁉️**
➡️ **IV insulin 10 units followed by IV 50% dextrose 50 mL**
➡️ **10% dextrose at 50–75 mL/hour**
⚠️ **If glucose >200–250 mg/dL, give insulin without dextrose**
⚠️ **NEVER give dextrose without insulin!**
62
What are the **3 key steps in the acute treatment of hyperkalemia and examples of each⁉️**
➡️ **Membrane stabilization:** Calcium gluconate
➡️ **Shift K⁺ into cells:** Insulin + dextrose, β₂ agonist (e.g. albuterol)
➡️ **Eliminate K⁺:** Kayexalate (resins), diuretics, dialysis
63
Name **three conditions that impair renal potassium excretion⁉️**
➡️ **ACE inhibitors / ARBs / Spironolactone**
➡️ **Acute or chronic kidney disease**
➡️ **Addison’s disease** (primary adrenal insufficiency)
64
**List five causes of potassium shifting out of cells into the plasma⁉️**
➡️ **Acidosis**
➡️ **β-blockers or digoxin toxicity**
➡️ **Tumor lysis syndrome**
➡️ **Rhabdomyolysis**
➡️ **Hyperkalemic periodic paralysis**
65
When should **calcium gluconate doses be repeated in hyperkalemia⁉️**
🚨 **If ECG changes persist or recur after initial improvement**
## Footnote
⚠️ It raises the threshold for cardiac electrical activity, stabilizing the myocardium membrane and reducing the risk of arrhythmias
66
How do **beta-agonists (Ventolin) and insulin help lower potassium levels⁉️**
✅ They **shift potassium from the extracellular fluid into cells,** reducing serum potassium
67
Which **treatments help eliminate potassium from the body⁉️**
➡️ **Diuretics** → Increase renal potassium excretion.
➡️ **Potassium binders (Kayexalate)** → Remove potassium via the digestive system.
## Footnote
⚠️ They remove potassium rather than just shifting it intracellularly, leading to a **slower effect**
68
How do **beta-blockers like propranolol affect hyperkalemia⁉️**
⚠️ They can **worsen hyperkalemia by inhibiting intracellular potassium uptake**
69
**When is urgent dialysis indicated in hyperkalemia⁉️**
✅ **For severe hyperkalemia unresponsive to treatment,** but calcium gluconate should be given immediately while dialysis is arranged
70
What is the **definition of hypercalcemia⁉️**
➡️ **Serum calcium level >10.5 mg/dL**
71
What are the **causes of hypercalcemia based on PTH levels⁉️**
➡️ **High/Normal PTH:** 🔹Primary hyperparathyroidism
🔹familial hypocalciuric hypercalcemia
➡️ **Low PTH:**
🔹Malignancy (PTHrP, skeletal metastases, multiple myeloma)
🔹Excessive vitamin D (granulomatous diseases,
lymphoma, intoxication)
🔹Excessive calcium intake (milk-alkali syndrome, TPN)
72
What are the **symptoms of hypercalcemia⁉️**
➡️ **CNS:** Fatigue, anorexia, altered mental status
➡️ **GI:** Constipation, abdominal pain, vomiting
➡️ **Renal:** Nephrolithiasis, polyuria, acute kidney injury
➡️ **Cardiac:** Short QT interval, arrhythmias (bradycardia, AV block)
73
What is the **treatment for hypercalcemia⁉️**
🔹 **Hydration** (4–6L normal saline)
🔹 **Bisphosphonates**
🔹 **Calcitonin**
🔹 **RANK-L inhibitors (Denosumab)**
🔹 **Dialysis in CKD cases**
74
How does **bisphosphonate therapy help treat hypercalcemia⁉️**
✅ **It inhibits osteoclast activity, reducing bone resorption**
75
What are the potential **side effects of bisphosphonates⁉️**
🚩 **Jaw necrosis**
🚩 **hypocalcemia**
🚩 **hypophosphatemia**
🚩 **hypomagnesemia**
76
Why is **calcitonin useful for severe hypercalcemia⁉️**
✅ It has a **rapid onset of action but develops tachyphylaxis quickly**
77
How does **vitamin A intoxication affect calcium levels⁉️**
➡️ **It can cause hypercalcemia**
78
What are **common causes of hypercalcemia⁉️**
🔹 **Excessive PTH** (primary hyperparathyroidism, familial hypocalciuric hypercalcemia)
🔹 **Malignancy** (PTHrP secretion, bone metastasis)
🔹 **Excessive vitamin D** (seen in lymphomas, granulomas)
🔹 **Increased bone resorption** (hyperthyroidism, immobilization)
🔹 **Medications** (thiazides, vitamin A)
79
What **renal complications can arise from hypercalcemia⁉️**
✅ **Polyuria,** leading to severe dehydration and acute renal failure
80
What are **symptoms of vitamin A intoxication⁉️**
🔸 **Ataxia**
🔸 **Alopecia**
🔸 **Hyperlipidemia**
🔸 **Hepatotoxicity**
🔸 **Bone and muscle pain**
🔸 **Visual impairments**
🔸 **Hypercalcemia**
81
What is the **most common cause of AKI⁉️**
✅ **Prerenal failure** due to decreased renal perfusion or systemic arterial blood volume
82
What are the **key criteria for diagnosing acute kidney injury (AKI)⁉️**
🔹 **Increase in creatinine by ≥0.3 mg/dL**
🔹 **Increase in creatinine ≥50% from baseline**
🔹 **Urine output <0.5 mL/kg/hour for six hours**
83
What are the **main indications for dialysis in AKI⁉️**
🔸 **Uremia with symptoms**
🔸 **Acidosis**
🔸 **Intoxication**
🔸 **Electrolyte abnormalities** (e.g., hyperkalemia)
🔸 **Volume overload**
84
What are **common causes of pre-renal AKI⁉️**
🔸 **Hypovolemia**
🔸 **Decreased cardiac output**
🔸 **Decreased effective circulating volume** (CHF, hepatorenal syndrome)
🔸 **Impaired renal autoregulation** (due to NSAIDs, ACE inhibitors)
85
What are **common causes of renal AKI⁉️**
➡️ **Glomerular diseases**
➡️ **Tubular and interstitial damage**
➡️ **Vascular causes** (vasculitis, TTP/HUS, malignant hypertension)
86
What are **nephrotoxic causes of tubular and interstitial AKI⁉️**
➡️ **Endogenous toxins:** 🔹Hemolysis
🔹Rhabdomyolysis
🔹Myeloma
🔹Intratubular crystals
➡️ **Exogenous toxins:** 🔹Iodine contrast
🔹Aminoglycosides
🔹Cisplatin
🔹Amphotericin B, PPIs, NSAIDs
87
What are **common causes of post-renal AKI⁉️**
➡️ **Bladder outlet obstruction**
➡️ **Bilateral pelvoureteral obstruction**
➡️ **Unilateral obstruction in a solitary kidney**
88
How is **pre-renal AKI differentiated from acute tubular necrosis (ATN)⁉️**
89
What are the **key treatment approaches for pre-renal AKI⁉️**
➡️ **Treatment according to etiology:**
🔹Hypovolemia -> Volume resuscitation
🔹Hypervolemia -> Diuresis
90
What are the **key treatment approaches for post-renal AKI⁉️**
➡️ **Ultrasound assessment**
➡️ **Urinary catheter placement**
➡️ **Nephrology procedures**
91
What **laboratory findings** support the **diagnosis of rhabdomyolysis⁉️**
🚩 **High CPK levels**
🚩 **Acute kidney injury**
🚩 **Acute tubular necrosis** (dark granular casts)
🚩 **Positive blood on urine stick with no erythrocytes on urine smear** (due to myoglobin detection)
92
What **electrolyte abnormalities are commonly seen in rhabdomyolysis⁉️**
🔹 **Hyperkalemia**
🔹 **Hypocalcemia**
🔹 **Metabolic acidosis**
93
What are **common causes of rhabdomyolysis⁉️**
▪️ Crush injury
▪️ Convulsions
▪️ Infectious diseases
▪️ Medications (statins + fibrates)
▪️ Strenuous exercise
▪️ Inflammatory muscle diseases
▪️ Electrolyte disorders (hypokalemia, hypophosphatemia)
▪️ Long immobilization
▪️ Severe hypothyroidism
▪️ Neuroleptic malignant syndrome
94
What is the **main treatment strategy for rhabdomyolysis-induced AKI⁉️**
✅ **Supportive care,** including large-volume fluids, monitoring kidney function, urine output, and electrolytes
95
How does **chronic hypokalemia contribute to polyuria⁉️**
✅ It can cause **nephrogenic diabetes insipidus (DI),** characterized by decreased renal responsiveness to vasopressin
96
What is **diabetes insipidus (DI) characterized by⁉️**
✅ **Decreased secretion or responsiveness to vasopressin,** leading to **excessive water loss**
97
What are the **two etiologies of diabetes insipidus (DI)⁉️**
➡️ **Central DI:** Due to destruction of the neurohypophysis, leading to decreased vasopressin secretion.
➡️ **Nephrogenic DI:** Due to impaired renal response to vasopressin.
98
What are **common causes of nephrogenic diabetes insipidus⁉️**
➡️ **Drugs:** Lithium, amphotericin B, aminoglycosides
➡️ **Metabolic abnormalities:** Hypercalcemia, hypokalemia
➡️ **Vascular etiologies**
99
What are the **clinical manifestations of DI⁉️**
🔸 **Polyuria**
🔸 **Hypernatremia**
🔸 **Increased plasma osmolarity**
🔸 **Decreased urine osmolarity**
100
**How is central DI treated⁉️**
✅ **Desmopressin** (DDAVP), a synthetic vasopressin analog
101
**How is nephrogenic DI treated⁉️**
✅ **Thiazide diuretics or amiloride**
102
What is the **preferred treatment** for **mild hypernatremia in post-obstructive diuresis⁉️**
✅ **Increase free water consumption**
103
What **IV fluid can be used if additional treatment is required⁉️**
➡️ **Hypotonic solutions, such as 0.45% saline**
104
Why is **3% saline unsuitable for treating hypernatremia⁉️**
➡️ **It worsens hypernatremia and is only appropriate for hyponatremia treatment**
105
What is the **definition of hypernatremia⁉️**
✅ **An increase in plasma sodium concentration to >145 mM**
106
What are the **most frequent symptoms of hypernatremia⁉️**
➡️ **Altered mental status,** ranging from mild confusion to deep coma
107
What are **potential complications of hypernatremia⁉️**
🔸 **Parenchymal/subarachnoid hemorrhages**
🔸 **Subdural hematomas**
🔸 **Osmotic demyelination (rare in acute cases)**
🔸 **Hypernatremic rhabdomyolysis**
108
What is the **best way to correct hypernatremia⁉️**
➡️ **Free water through the gastrointestinal tract** (oral or nasogastric tube)
109
**How common is hypernatremia compared to hyponatremia⁉️**
➡️ **Less common, but associated with high mortality**
110
What are the **main causes of hypernatremia⁉️**
➡️ **Low water intake** (common in elderly patients with reduced thirst or limited access to fluids)
➡️ **Renal water loss** (osmotic diuresis, post-obstructive diuresis, mannitol)
➡️ **Non-renal losses** (fever, exercise, heat, burns, mechanical ventilation, diarrhea)
➡️ **Diabetes insipidus (DI)** (central or nephrogenic)
111
What are the **primary neurological symptoms of hypernatremia⁉️**
⚠️ **Confusion, lethargy, coma**
112
What is the **recommended correction rate for hypernatremia⁉️**
⚠️ **Slow correction (<10 mM/d) to prevent cerebral edema.**
113
What are the **key steps in hypernatremia treatment⁉️**
1️⃣ **Treat underlying causes** (hyperglycemia, hypercalcemia, hypokalemia, diarrhea).
2️⃣ **Administer hypotonic fluids** (preferably free water via oral or nasogastric tube).
3️⃣ **IV fluids if needed** (D5W or hypotonic saline 0.45% or 0.225%).
114
**When might normal saline (0.9%) be used in hypernatremia treatment⁉️**
✅ **In severe hypernatremia** where it is relatively hypotonic, or with severe hypotension
115
Why is **fluid restriction NOT a treatment for hypernatremia⁉️**
➡️ Fluid restriction is used to treat **hyponatremia and SIADH, not hypernatremia**
116
What are the **key features of Bartter's syndrome⁉️**
🔸 **Polyuria**
🔸 **Polydipsia**
🔸 **Increased urine calcium (hypercalciuria)**
🔸 **Hypomagnesemia**
117
What are the **key features of Gitelman’s syndrome⁉️**
🔸 **Hypomagnesemia**
🔸 **Marked hypocalciuria (low urine calcium)**
118
What **metabolic abnormality is common to both Bartter's and Gitelman's syndromes⁉️**
⚠️ **Hypokalemic metabolic alkalosis**
119
What **causes respiratory acidosis⁉️**
🔸 **Severe pulmonary disease**
🔸 **Respiratory muscle fatigue**
🔸 **Abnormalities in ventilatory control**
120
**How is respiratory acidosis recognized⁉️**
✅ By an **increase in Paco2 and decrease in pH**
121
How does the **body compensate** for **primary respiratory disturbances⁉️**
✅ Compensation for primary
respiratory disorders **moves the [HCO3-] in the same direction as the primary change in Paco2**
122
What does a **very elevated bicarbonate level** (e.g., 34 mmol/L) **suggest in respiratory acidosis⁉️**
✅ **Chronic compensation, indicating compensated respiratory acidosis**
123
How is **bicarbonate expected to change in chronic respiratory acidosis⁉️**
➡️ Bicarbonate will rise **at least by 0.4 mmol/L per each 1 mmHg elevation in PCO2**
124
What is the **definition of hyponatremia⁉️**
✅ **Serum sodium level <135 mM**
125
What is the **first step in evaluating hyponatremia⁉️**
➡️ **Exclude pseudohyponatremia by measuring plasma osmolality**
126
**What is pseudohyponatremia⁉️**
➡️ **Low sodium levels despite normal or high plasma tonicity,** caused by interference from substances like lipids or proteins
127
What **conditions can cause pseudohyponatremia⁉️**
👉🏻 **Extreme hyperlipidemia**
👉🏻 **Hyperproteinemia**
👉🏻 **Hyperglycemia**
👉🏻 **Mannitol infusion**
128
**How is true hyponatremia defined based on osmolality⁉️**
✅ **Effective plasma osmolality <275 mOsm/kg**
129
**How does hyperglycemia affect sodium concentration⁉️**
✅ **Water shifts from cells to plasma, lowering serum sodium levels**
130
**How does the treatment approach for hyponatremia vary⁉️**
➡️ **It depends on the etiology, severity, and duration of hyponatremia**
131
What is an **exception to gradual hyponatremia correction⁉️**
➡️ **Severe symptomatic hyponatremia requires urgent correction**
132
What are **common causes of
SIADH** (Syndrome of
Inappropriate Antidiuretic
Hormone secretion)⁉️
➡️ SIADH = **unregulated vasopressin (ADH) release**
🔹 **Paraneoplastic
syndromes** (e.g., small cell lung cancer)
🔹 **CNS diseases** (e.g., stroke, trauma, infection)
🔹 **Pulmonary infections**
🔹 **Medications** (e.g., SSRIs, carbamazepine)
133
**Why does SIADH
cause hyponatremia⁉️**
**Excess ADH**➡️ increase water reabsorption
➡️ **Dilutional hyponatremia**
⚠️ Urine osmolality high despite low serum sodium
134
What **laboratory
findings are typical in SIADH⁉️**
➡️ Plasma:
🔹 **Low plasma osmolarity**
🔹 **Hyponatremia**
➡️ Urine:
🔹 **Increase urine Na** (> 20-
30 mEq/L)
🔹 **Increase urine osmolality:**
▪️ **above 400** mOsm/kg 👉🏻 strongly supports **SIADH**
▪️ **100-400**m0sm/kg suggests 👉🏻 **mixed etiology**
135
What is the **treatment for SIADH-induced hyponatremia⁉️**
🔹 **Water restriction**
🔹 **3% saline infusion (for severe cases)**
136
Why must **sodium correction be done cautiously in hyponatremia⁉️**
⚠️ **To prevent osmotic demyelination syndrome (ODS)**
137
What are **treatment options for chronic SIADH⁉️**
💊 **Oral vaptans** (e.g., tolvaptan)
💊 **Demeclocycline**
💊 **Fludrocortisone**
138
What **symptoms does carbamazepine intoxication cause⁉️**
🚩 **Neurologic, cardiovascular, and anticholinergic symptoms**
## Footnote
👉🏻 It does not affect the calculation of the anion gap
139
What **acid-base disorder** is commonly seen in **COPD and CHF patients on diuretics⁉️**
✅ **Metabolic alkalosis with combined respiratory acidosis**
140
How can **metabolic alkalosis compensation be estimated⁉️**
➡️ **Expected PCO₂ = Bicarbonate + 15**
141
Why does **pregnancy cause respiratory alkalosis⁉️**
✅ pregnancy can cause **hyperventilation** (due to increased progesterone levels) causing **respiratory alkalosis**
142
What **electrolyte abnormality** is commonly seen in **refeeding syndrome⁉️**
✅ **Hypophosphatemia, along with hypomagnesemia and hypokalemia**
143
**What triggers refeeding syndrome⁉️**
✅ **Initiation of enteral or parenteral feeding after prolonged poor nutritional status**
144
What is the **physiological cause of electrolyte shifts in refeeding syndrome⁉️**
➡️ **Carbohydrate loading increases insulin, driving electrolytes into cells**
145
What **deficiency** is commonly **associated with refeeding syndrome⁉️**
✅ **Thiamine deficiency**
146
What are the **neurological symptoms seen in refeeding syndrome⁉️**
✅ **Non-focal neurological symptoms** due to electrolyte imbalances
147
**How can refeeding syndrome be prevented⁉️**
✅ **Gradual refeeding with electrolyte and vitamin supplementation, and close monitoring**
148
**What should be done if refeeding syndrome develops⁉️**
✅ **Slow down or temporarily stop feeding, and correct electrolyte deficiencies**
149
**What is renal tubular acidosis (RTA)⁉️**
✅ **A metabolic disturbance of the distal tubule leading to impaired urine acidification**
150
What are **common clinical manifestations of RTA⁉️**
👉🏻 **Nephrolithiasis** (kidney stones)
👉🏻 **Nephrocalcinosis** (calcium deposition in kidneys)
151
What **type of metabolic acidosis is seen in RTA⁉️**
✅ **Hypokalemic, hyperchloremic metabolic acidosis**
152
Why does **RTA lead to calcium-phosphate stone formation⁉️**
✅ **Impaired urine acidification increases phosphate precipitation, promoting stone formation
153
What is the **basic defect in Type 1,2,4 RTA ⁉️**
**Type 1 RTA 👉🏻 Decreased distal acidification**
**Type 2 RTA 👉🏻 Diminished proximal HCO₃⁻ reabsorption**
**Type 4 RTA 👉🏻 Aldosterone deficiency or resistance**
154
**How does the urine anion gap differ in the types of RTA⁉️**
✅ **Positive in all types** (Type 1, Type 2, and Type 4)
155
What is the **minimum urine pH in each type of RTA⁉️**
🔹 **Type 1:** >5.5
🔹 **Type 2:** Variable, <5.5 if given an alkali load
🔹 **Type 4:** <5.5
156
How do **serum potassium levels differ in RTA types⁉️**
🔹 **Type 1:** Low
🔹 **Type 2:** Low
🔹 **Type 4:** High
157
What is the **percentage of filtered bicarbonate excreted in RTA types⁉️**
🔹 **Type 1:** <10%
🔹 **Type 2:** >15%
🔹 **Type 4:** <10%
158
What are the **typical plasma bicarbonate levels (untreated) in RTA types⁉️**
🔹 **Type 1:** May be below 10 mEq/L
🔹 **Type 2:** Usually 14–20 mEq/L
🔹 **Type 4:** Usually above 15 mEq/L
159
How does **glomerular filtration rate (GFR) differ in RTA types⁉️**
🔹 **Type 1:** Normal
🔹 **Type 2:** Normal
🔹 **Type 4:** Low
160
**Which type of RTA is linked to Fanconi syndrome⁉️**
✅ **Type 2 (Proximal RTA),** with excessive urinary loss of glucose, calcium, phosphate, and uric acid
