1 :

Hint : 💧 Assess dehydration: hypotension

Correct Answers:

  • Hypotension


Rationale :

🔷 Osmotic diuresis in DKA causes large free‑water losses, shrinking intravascular volume.

🔷 Falling preload drops stroke volume/cardiac output, manifesting as hypotension.

🔷 Dry mucous membranes, poor skin turgor, tachycardia, ↑BUN: Cr all align with fluid volume deficit.

🔷 Bradycardia is atypical; the usual compensatory response to hypovolemia is tachycardia.

🔷 Kussmaul respirations reflect metabolic acidosis compensation, not the volume status itself.

🔷 Polyphagia is tied to cellular glucose deficiency, not intravascular volume.


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2 :

Hint : 🧠 Brain–gut axis factors

Correct Answers:

  • Environmental and psychosocial factors can be associated with the onset of this disease.


Rationale :

🔶 IBS is multifactorial—brain–gut axis dysregulation, visceral hypersensitivity, motility and microbiome changes.

🔶 Psychosocial stressors (anxiety/depression), post‑infectious states, and dietary triggers are recognized contributors.

🔶 Blood in stool is not typical of IBS and warrants evaluation for other pathology (e.g., IBD).

🔶 Bile duct disorders are unrelated to IBS pathogenesis.

🔶 While family patterns exist, a “psychiatric history + food allergies” narrative is not an established causal mechanism.

🔶 Management targets lifestyle, diet (FODMAP), gut‑brain therapy, and symptom modulators.


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3 :

Hint : 🧪 Check K⁺ & Cr

Correct Answers:

  • Check serum potassium and creatinine levels.


Rationale :

💠 Lisinopril (ACE‑I) can cause hyperkalemia via reduced aldosterone; monitor K⁺ before/after dosing.

💠 ACE‑Is may raise creatinine (efferent arteriolar dilation); tracking renal function is essential.

💠 Salt substitutes often contain potassium—do not encourage their use with ACE‑Is.

💠 BNP guides HF status, not ACE‑I holding parameters.

💠 Vision checks aren’t a known lisinopril‑specific monitoring need.

💠 Watch for cough/angioedema; teach when to report.


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4 :

Hint : 🧪ESKD → low HCO₃⁻

Correct Answers:

  • pH 7.21, PaCO2 36, HCO3 14


Rationale :

🎗️ESKD reduces acid excretion and bicarbonate regeneration, producing metabolic acidosis.

🎗️ Profile shows low pH with low HCO₃⁻ and near‑normal PaCO₂ (little/early respiratory compensation).

🎗️ Choices B/C are alkaloses; D suggests respiratory acidosis—not the typical ESKD pattern.

🎗️ Chronic kidney disease often shows anion gap acidosis from retained acids (e.g., sulfates, phosphates).

🎗️ Treatment: dialysis, bicarbonate, and addressing CKD‑MBD contributors.


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5 :

Hint : 🦴 Inflammation + steroids = bone loss

Correct Answers:

  • Osteoporosis


Rationale :

❖ RA inflammation (TNF‑α/IL‑6) accelerates osteoclast activity → generalized bone loss.

❖ Glucocorticoids, often used in RA, decrease bone formation and increase resorption.

❖ Reduced mobility and vitamin D deficiency further worsen bone mineral density.

❖ Fracture risk (hip/vertebral) rises; screen with DEXA and institute calcium/vitamin D, bisphosphonates, and weight‑bearing exercise.

❖ Osteoarthritis is a different pathology; hyperglycemia/mucositis are not intrinsic RA complications.


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6 :

Hint : 🍽️ Bind phosphate at meals

Correct Answers:

  • Administer phosphate binders with meals.


Rationale :

◆ CKD‑MBD features hyperphosphatemia and hypocalcemia; binders lower phosphate absorption.

◆ Giving with meals traps dietary phosphate in the gut for excretion.

◆ Managing phosphorus helps parathyroid control and reduces renal osteodystrophy.

◆ Also use active vitamin D analogs and consider calcimined per labs.

◆ Increasing potassium or liberal fluids is unsafe in CKD; monitoring Ca²⁺ is needed but not definitive therapy.


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7 :

Hint : 🦴Expect/manage bone pain

Correct Answers:

  • Ensure the patient understands the risk of bone pain and how to manage it.


Rationale :

🔹 Filgrastim (G‑CSF) commonly causes bone pain from marrow stimulation—teach analgesia strategies.

🔹 It’s given subcutaneously (not IM) daily or per protocol until ANC recovery.

🔹 PRN for infection symptoms is inappropriate; dosing is prophylactic/response‑guided to neutropenia.

🔹 Avoid excessive leukocytosis; follow ANC to titrate/hold per protocol—not to 20,000 targets.

🔹 Teach infection precautions until ANC improves (hand hygiene, avoid crowds).


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8 :

Hint : 🌬️ Hyperventilation → tingling/spasm

Correct Answers:

  • Light-headedness and muscle spasms


Rationale :

🔸 Respiratory alkalosis (often from hyperventilation) lowers ionized calcium, causing paresthesias/spasms.

🔸 Patients report light‑headedness, dizziness, tingling of hands/mouth, and carpopedal spasm.

🔸 Hypoxia drives hyperventilation but is not a hallmark symptom here; lethargy fits acidosis more.

🔸 Respiratory depression/hypotension are not expected effects of alkalosis itself.

🔸 Hyperkalemia is more linked to acidosis, not alkalosis.


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9 :

Hint : 🧪Preformed antibodies—remove graft

Correct Answers:

  • Removal of the transplanted kidney.


Rationale :

💎 Hyperacute rejection occurs minutes–hours from preformed recipient antibodies (ABO/HLA).

💎 Leads to rapid thrombosis and ischemic necrosis of the graft—non‑reversible.

💎 High‑dose steroids/calcineurin dose increases are ineffective once hyperacute rejection is established.

💎 Definitive management is immediate nephrectomy to prevent systemic complications.

💎 Future planning involves cross‑match/antibody screen to prevent recurrence.


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10 :

Hint : 🫁 CO₂ rise = compensation

Correct Answers:

  • Metabolic alkalosis with partial compensation


Rationale :

🔵 pH 7.52 = alkalemia; HCO₃⁻ 30 (elevated) identifies metabolic alkalosis as primary.

🔵 PaCO₂ 55 is elevated, indicating hypoventilatory compensation (retaining CO₂ acid).

🔵 Because pH remains alkalemic, compensation is partial, not full.

🔵 Common causes: vomiting/NG suction, diuretics, excess alkali, hypokalemia.

🔵 Manage by correcting volume/Cl⁻/K⁺ deficits and addressing the underlying cause.


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Total Questions: 10

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