All Clinical Cases

Case History 1

A woman aged 30 years old complains of general fatigue,

breathlessness on exertion, giddiness, headache, anorexia, and
dysphagia. On examination the patient showed pallor of the skin
and mucous membrane, tachycardia, glossitis, spooning of the
nails and edema of the dependent part of the body.

Investigations revealed:

Hemoglobin: 6 g/100 ml

RBC count: 3 million/mm³ of blood

MCHC: 20 g/100 ml cells

MCV: 60 fl

WBC: Eosinophilia

Stool exam: Hookworm ova present

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Question 1: In view of the symptoms and blood parameters given

above which clinical condition the patient is suffering from?
Answer: The patient is suffering from iron deficiency anemia due
to chronic blood loss caused by hookworm infestation.

Question 2: Explain why hookworm infestation may cause this

condition?
Answer: Hookworms attach to the intestinal mucosa and suck
blood. Chronic infestation leads to continuous blood loss,
depletion of iron stores, and ultimately iron deficiency anemia.

Question 3: List any other two causes which may cause a

decrease in the Hb level in a person?
Answer:

1. Nutritional deficiency (e.g., Vitamin B12 or folic acid

deficiency).

2. Chronic diseases (e.g., chronic kidney disease, malignancy).

Question 4: Name two supplement agents which can be used to

treat the condition.
Answer:

1. Oral iron preparations (e.g., ferrous sulfate).

2. Parenteral iron therapy (in severe cases).

Case History 2

A 45-year-old female came to a doctor with a history of swelling of

the limbs and face, intolerance to cold, weakness, and
drowsiness. She further stated that she had gained weight and
developed loss of appetite and constipation.

On examination, there was puffiness of face and extremities, lips

were swollen, and the tongue was enlarged. The skin was rough
and thick. The hair was sparse, rough, and lusterless. Speech was
slow, hoarse, and monotonous. She exhibited poor memory, heart
was enlarged. The ankle jerk was slow and there was delayed
relaxation.

Investigations revealed:

Anemia: 40%

BMR: ↓

Serum cholesterol: 300 mg%

Serum PBI: 2 µg/100 ml

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Question 1: Name the most probable cause of signs, symptoms

and lab findings in the given patient.
Answer: The patient is suffering from Myxedema
(hypothyroidism).

Question 2: Explain the presence of anemia in this condition.

Answer: Anemia in hypothyroidism may occur due to decreased
erythropoietin production, impaired hemoglobin synthesis, and
associated nutritional deficiencies (iron, folate, or B12).

Question 3: Given the neurological involvement, explain the signs

and manifestations in this condition.
Answer: Neurological manifestations include slowed reflexes
(delayed relaxation of ankle jerk), poor memory, lethargy, and
slow monotonous speech, all due to reduced metabolic activity
and decreased CNS excitability.

Question 4: Explain the underlying mechanism of low BMR in this

condition.
Answer: Low BMR occurs because thyroid hormones (T3 and T4)
regulate basal metabolic rate by stimulating oxidative metabolism
and mitochondrial activity. In hypothyroidism, deficiency of these
hormones leads to markedly reduced BMR.

Case History 3

A soldier aged 46 years received a stab wound in the back. There

was wasting of the small muscles of the right hand and loss of all
forms of sensation over a strip along its ulnar border. In the right
leg there was spastic paralysis with an increased knee jerk and
loss of sense of posture and passive movement. On the left side
the motor function was normal, but there was loss of sensibility to
pain and temperature over the entire left half of the body as high
as the level of third rib, but no disturbances of proprioceptive
sensibility. Tactile sensibility was normal over entire body except
along the ulnar border of right arm. He was diagnosed as a case
of Brown-Séquard Syndrome.

Question 1: Where and which side is the lesion?

Answer: The lesion is in the right half of the spinal cord
(hemisection) at the level of T3.

Question 2: Why is the touch sensation normal over entire body?

Answer: Touch sensation is carried by both the dorsal column
(ipsilateral) and anterolateral (contralateral) tracts. Because of
this bilateral representation and overlap, touch sensation is
usually preserved.

Question 3: Describe the physiological basis of motor findings in

this patient.
Answer: The spastic paralysis with exaggerated reflexes in the
right leg is due to damage of the corticospinal tract on the same
side below the lesion, resulting in upper motor neuron signs
(spasticity, hyperreflexia, loss of fine motor control).

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Case History 4

A man aged 34 years noticed tingling sensation in his feet and

later suffered shooting pain in his legs. After several months, he
experienced difficulty while walking in the dark, and when walking
in the light it was necessary to watch the ground to keep from
falling. Although his legs were as strong as ever, he would stagger
and sway from side to side as he walked.

On examination, there was no weakness or atrophy of the

muscles, but when relaxed they did not exhibit the normal tone.
There was complete loss of sense of posture, passive movement,
and vibration in the legs. There was loss of tactile localization and
tactile discrimination.

Question 1: Which tract/tracts are damaged?

Answer: The dorsal column tracts (fasciculus gracilis and
fasciculus cuneatus) are damaged.

Question 2: How do you account for the loss of coordination of the

legs in walking?
Answer: Loss of proprioceptive input from muscles and joints
(carried by dorsal column) results in sensory ataxia, leading to
impaired coordination of movements, especially noticeable when
visual guidance is removed (walking in the dark).

Question 3: Describe the reason for loss of the sense of posture

and passive movement.
Answer: The dorsal column pathway normally carries information
about vibration sense, position sense, and fine touch from
muscles, joints, and skin. Damage to this pathway causes loss of
sense of posture and

Case History 5

A young female exhibits abnormal fatigability of muscles, and

muscular movements that are initially strong but rapidly tire as
the day advances or after vigorous exercise. The symptoms that
appear are ptosis, chewing, swallowing, and speaking weakness.
She was unable to undertake work above the level of her
shoulders. The symptoms showed a remitting course and were
often precipitated by emotion, infection, and pregnancy. Muscular
atrophy is also present in chronic cases.

On examination: CNS normal.

A remarkable recovery was seen after the intramuscular injection

of Neostigmine.

Question 1: What could be the pathophysiology for this condition?

Answer: The patient is suffering from Myasthenia Gravis, an
autoimmune disorder where antibodies are produced against
nicotinic acetylcholine receptors (AChR) at the neuromuscular
junction. This reduces the number of functional receptors,
impairing neuromuscular transmission and causing fatigable
muscle weakness.
Question 2: Explain how the injection of Neostigmine improves
the condition.
Answer: Neostigmine is an acetylcholinesterase inhibitor. It
prevents the breakdown of acetylcholine in the synaptic cleft,
thereby increasing the concentration and duration of action of
acetylcholine at the neuromuscular junction. This improves
muscle contraction in patients with reduced receptor availability.

Question 3: Explain why the symptoms worsen as the day

advances.
Answer: With repeated muscle activity, acetylcholine release
decreases due to presynaptic fatigue, while the reduced number
of functional receptors cannot sustain transmission. Thus,
neuromuscular transmission worsens with sustained use, leading
to fatigability that progresses through the day.

Case History 6

A 68-year-old man comes to his primary care physician

complaining of tiredness and difficulty sleeping. Six months
earlier, the patient experienced myocardial infarction of the
anterior wall of the left ventricle. A stent was placed in the
occluded coronary artery, reestablishing perfusion. The patient
now complains of difficulty sleeping at night and awakening with
shortness of breath. He reports sleeping better using pillows to
elevate his chest and head. The moderate exercise regimen that
he followed after the myocardial infarction is now causing him to
become progressively shorter of breath.

Physical Examination:

Temperature: 37°C

Respiratory rate: 18/min and shallow

BMI: 29 kg/m²

CVS: BP – 100/70 mmHg, PR – 80/min

A third heart sound is evident

Auscultation: crackles at base of lungs, dullness to percussion at

base of lung

Laboratory Studies:

Chest radiography: Enlarged left atrium and ventricle, interstitial

pulmonary edema, and consolidation of lung fields

Echocardiography: Ejection fraction 40%

Arterial blood gas: PO₂ = 85 mmHg, PCO₂ = 40 mmHg, pH = 7.38

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Question 1: What could be the possible cause of this patient’s

third heart sound and crackles at the lung bases?
Answer:

The third heart sound (S₃) is due to rapid passive filling of a stiff
and dilated left ventricle during diastole, a sign of systolic heart
failure.

The crackles are caused by pulmonary edema due to backward

transmission of increased left atrial pressure into pulmonary
capillaries, leading to fluid accumulation in alveoli.

Question 2: What is the normal ejection fraction? Comment on the

ejection fraction of this patient.
Answer:

Normal ejection fraction (EF) = 55–70%.

This patient’s EF is 40%, which is significantly reduced, indicating

systolic dysfunction/left-sided heart failure.
Question 3: Explain why the symptoms worsen during sleep.
Answer:

When lying down, venous return increases because gravity no

longer pools blood in the lower extremities.

This further increases pulmonary venous pressure, leading to

worsening pulmonary congestion and edema at night (orthopnea
and paroxysmal nocturnal dyspnea).

Sleeping with pillows elevates the chest and reduces venous

return, thereby relieving symptoms

Case History 7

A 33-year-old woman comes to her primary care physician

complaining of amenorrhea, headaches, profuse sweating, and
joint pains associated with changes in the sizes of her hands and
feet. The patient reports massive growth of her hands and feet as
well as protrusion of her lower jaw. She believes the shape of her
face has changed, becoming sharper. She also complains of
sudden weakness, even when just "carrying the clothes hamper
upstairs." She first noticed these changes about 6 months ago
when she was home for the holidays and saw some high school
and early college pictures of herself. Her mother brought to her
attention how her features seemed much larger. After that she
says she became more aware of her bodily changes. She came in
because she knows something is wrong and that there is a
definite distinction from how she looks now compared to before.
Her husband and she are also trying to conceive but have been
unsuccessful due to amenorrhea for the past 8 months.

Physical Examination:

Temp: 99.1°F

PR: 65/min

RR: 14/min

BP: 130/80 mmHg

Wt: 59.8 kg

BMI: 24 kg/m²

PE: Marked enlargement of facial features, tongue, feet and

hands; soft doughy handshake; thyroid enlargement and possible
visceral enlargement; loss of visual field.

Laboratory Studies:

Pregnancy test (hCG): Negative

Growth Hormone: 40 ng/mL (normal: 0–5 ng/mL)

Fasting IGF-1: 31 ng/mL (normal: <20 ng/mL)

Prolactin: 100 ng/mL (normal: <20 ng/mL)

Glucose: 1.5 ng/mL

Glucose suppression test: after 75-g glucose, GH was 8 µg/L

(normal: <1 µg/L)

BUN and liver enzymes: Normal

---

Question 1: What is the most likely diagnosis?

Answer: The patient is suffering from Acromegaly, most likely due
to a pituitary adenoma secreting growth hormone (with possible
co-secretion of prolactin).

Question 2: What is the physiological basis of her amenorrhea?

Answer: Elevated prolactin levels inhibit GnRH secretion from the
hypothalamus, leading to decreased LH/FSH and anovulation,
causing amenorrhea and infertility.

Question 3: Explain the basis of her headaches and loss of visual

fields.
Answer: The pituitary adenoma compresses surrounding
structures. Headaches occur due to pressure on the dura and
intracranial structures. Loss of visual fields (classically bitemporal
hemianopia) results from compression of the optic chiasm.

Question 4: Explain why the glucose suppression test result

confirms the diagnosis.
Answer: Normally, an oral glucose load suppresses GH to <1 µg/L.
In this patient, GH remained elevated at 8 µg/L, confirming
autonomous GH secretion typical of acromegaly.

Question 5: What is the role of IGF-1 measurement in this case?

Answer: IGF-1 is a stable marker of GH activity (since GH
secretion is pulsatile). The elevated fasting IGF-1 (31 ng/mL)
confirms chronic GH excess.

Case History 8

A 35-year-old woman comes to her physician's office with the

complaint of recent rapid weight gain and excessive sweating.
What initiated her visit was a recent panic attack that frightened
her. Her face looks swollen compared with the rest of her body.
She complains of recent weakness, backaches and headaches and
her periods have lately been irregular. Over the past month she
has noticed frequent bruising with slow healing. She is not on any
birth control or using any medication except for acetaminophen
for the headaches.

Physical Examination:

PR: 68/min

RR: 14/min

BP: 130/86 mmHg

BMI: 33 kg/m²

PE: Moon face, truncal obesity with thin extremities,

supraclavicular fat pads, depression

Laboratory Studies:

Pregnancy test (hCG): Negative

Glucose tolerance: Abnormal, consistent with insulin resistance

Plasma cortisol levels: 4 pm: 25 µg/dL (↑; normal: 3–15 µg/dL)

Dexamethasone suppression test: Cortisol 35 µg/dL next morning

(↑; normal <5 µg/dL)

24-hour urinary free cortisol: Abnormally high

Plasma ACTH: 7 pg/mL (low; normal >20 pg/mL)

MRI of pituitary: Normal

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Question 1: What is the most likely diagnosis?

Answer: The patient is suffering from Cushing’s syndrome due to
an adrenal cause (ACTH-independent), most likely an adrenal
adenoma or carcinoma.

Question 2: Explain the significance of the dexamethasone

suppression test in this patient.
Answer: Normally, dexamethasone suppresses ACTH and thus
cortisol secretion. In this patient, cortisol increased to 35 µg/dL,
showing lack of suppression, which is diagnostic of Cushing’s
syndrome.

Question 3: What is the physiological basis of her clinical features

(moon face, truncal obesity, thin extremities, bruising, irregular
periods)?
Answer:

Moon face & truncal obesity: Cortisol increases fat redistribution

to face, neck, and trunk.

Thin extremities & weakness: Cortisol causes protein catabolism

and muscle wasting.

Bruising & poor wound healing: Cortisol inhibits fibroblast activity

and collagen synthesis.

Irregular periods: Cortisol suppresses GnRH and gonadotropin

secretion, leading to menstrual disturbances.

Question 4: How do plasma ACTH levels help in differentiating the

cause?
Answer:

Low ACTH with high cortisol = adrenal cause

(adenoma/carcinoma).

High ACTH with high cortisol = pituitary adenoma (Cushing’s

disease) or ectopic ACTH production.
In this case, ACTH is low (7 pg/mL), suggesting primary adrenal
pathology.

Case History 9

A patient comes with a history of excessive drinking of water and

passing of excess of colorless urine very frequently. History
revealed that he had suffered from syphilis previously. The patient
becomes markedly dehydrated when water is withheld.

Investigations of urine revealed:

Urine output: 15 L/24 hours, colorless

Specific gravity: 1002–1004

No sugar, blood, albumin

---

Question 1: What is your diagnosis?

Answer: The patient is suffering from Diabetes Insipidus (central
type, neurogenic), most likely due to damage to the hypothalamo-
neurohypophyseal system secondary to syphilis.

Question 2: What is the cause for the development of polyuria &

polydipsia?
Answer: In central Diabetes Insipidus, there is a deficiency of ADH
(vasopressin) due to hypothalamic/posterior pituitary damage.
This prevents water reabsorption in the distal tubule and
collecting ducts, leading to excretion of large volumes of dilute
urine (polyuria). Excess water loss stimulates thirst, leading to
polydipsia.

Question 3: In what other condition does polyuria occur?

Answer:

Diabetes Mellitus (due to osmotic diuresis by glucose)

Chronic renal failure

Primary polydipsia

Nephrogenic Diabetes Insipidus (renal insensitivity to ADH)

Question 4: How do you manage the condition?

Answer:

Desmopressin (DDAVP) – synthetic ADH analog, given intranasally

or orally.

Adequate water intake to prevent dehydration.

Treat underlying cause (e.g., neurosyphilis with antibiotics).

Thiazide diuretics or indomethacin may reduce urine output in

partial/nephrogenic cases.
Case History 10

A middle-aged individual comes with a history of weakness,

increased thirst, increased excretion of urine, and increased
appetite. He also complains of weight loss and non-healing of a
wound. On examination, the patient was obese and had a fungal
infection in the region of the waist and genitalia.

Investigations revealed:

Urine contained sugar but no ketone bodies

Fasting blood glucose level: 150 mg/100 ml of blood

---

Question 1: What is your diagnosis?

Answer: The patient is suffering from Type 2 Diabetes Mellitus.

Question 2: How do you explain polyuria, polydipsia, and

polyphagia?
Answer:

Polyuria: Due to osmotic diuresis caused by excess glucose in the

renal tubules, which prevents water reabsorption.

Polydipsia: Secondary to dehydration from excessive water loss,

stimulating the thirst center in the hypothalamus.

Polyphagia: Despite high blood glucose, tissues cannot effectively

utilize glucose due to insulin resistance → cellular starvation →
increased hunger.

Question 3: What does absence of ketone bodies suggest?

Answer: Absence of ketone bodies indicates that the patient has
Type 2 Diabetes Mellitus rather than Type 1. In Type 2 DM, insulin
levels are usually sufficient to inhibit lipolysis and ketogenesis,
preventing ketoacidosis.
Case History 11

Patient: 8-year-old boy

Complaints: Polyphagia, polydipsia, polyuria, weight loss, fatigue
Investigations:

Blood glucose (fasting): 250 mg/dL ↑

C-peptide: 0.1 ng/mL (very low → absent endogenous insulin)

Urine: Glucose +, Ketones +, High specific gravity

Diagnosis: Type I Diabetes Mellitus (Insulin-dependent)

---

Q1. Explain the cause of hyperglycemia & glycosuria in the above

patient.

Hyperglycemia:

In Type I DM, autoimmune destruction of pancreatic β-cells →

near-total absence of insulin.

Lack of insulin → ↓ glucose uptake by muscle and adipose tissue.

↑ Hepatic gluconeogenesis and glycogenolysis.

Net effect → marked elevation of blood glucose.

Glycosuria:

When plasma glucose > renal threshold (≈180 mg/dL), excess

glucose spills into urine.

Glucose in urine increases osmotic load → leads to osmotic

diuresis.
---

Q2. Explain the cause of polydipsia & polyuria in the above

patient.

Polyuria:

Due to osmotic diuresis caused by glucose in the renal tubules,

which prevents water reabsorption.

Leads to large volumes of dilute urine.

Polydipsia:

Excessive water loss via urine → dehydration → stimulates

hypothalamic thirst center (osmoreceptors) → excessive drinking.

Case History 12

Patient: 30-year-old woman

Complaints: Neck swelling, anxiety, irritability, weight loss despite
↑ appetite, heat intolerance
Exam: Symmetrical thyroid enlargement, exophthalmos, moist
warm skin, onycholysis
Vitals: T = 38°C, HR = 110/min, BP = 140/90 mmHg
Labs:

TSH ↓ (0.1 mIU/mL)

T4 ↑ (40 µg/dL)

T3 ↑ (280 ng/dL)

Diagnosis: Thyrotoxicosis (likely Graves’ disease)

---

Q1. Why is each of the following symptom consistent with

increased thyroid hormones?

(i) Weight loss despite increased appetite

Thyroid hormones ↑ basal metabolic rate (BMR) by stimulating

Na⁺/K⁺ ATPase and increasing mitochondrial oxidative enzymes.

↑ Lipolysis, ↑ proteolysis, ↑ carbohydrate metabolism → net

catabolism > anabolism.

Even though appetite ↑ (due to increased energy demand),

excessive catabolism causes net weight loss.

(ii) Increased heart rate (tachycardia)

Thyroid hormones ↑ sensitivity of heart to catecholamines

(sympathomimetic effect) by upregulating β₁-adrenergic
receptors.

Direct ↑ in cardiac output via ↑ stroke volume and contractility.

Net result → persistent tachycardia and sometimes palpitations.

(iii) Increased pulse pressure

T3 and T4 cause peripheral vasodilation (due to increased tissue

metabolism and O₂ demand) → decreased diastolic blood
pressure.

Simultaneously, they increase stroke volume and cardiac output →

increased systolic blood pressure.

Together, this widens the difference → increased pulse pressure.

(iv) Increased arterial blood pressure

Increased cardiac output + enhanced sympathetic activity raise
systolic arterial pressure.

Thus, patients may present with hypertension, especially systolic

type.

CASE HISTORY-14

A 88 vear-old man comes to the elinie egenplaining of fatigue and

persistent shortness of breath wiwell becomes worse during
exercise. The panent has history of respiratory infections and has
a chronie cough that is worse in the morning. He worked for 20
years in an altomiebile marnifacturing plant and was laid off years
are The patient has smoked Elgarettes since he was a teenager
Curtently he estimates smoking one pack of cigarettes a day

PHYSICAL ENAMIΝΑΤΙΟΝ

SA

BR: 25 min

BML 28 Kgm

PE Patient is in mild respiratory distress with an elevated

respiratory rate and shallow breaths An end-expiatory wheeze is
heard on auscultation. Otherwise, his lungs appear normal to
auscultation and percussion

Laboratory Studies

Pulmonary function tests

FEV1: 70% of predicted

Peak expiratory flow rate: 60% of predicted

*Forced vital capacity: 90% of predicted

Chest radiograph: Normal

Arterial blood gases
BMI 28 Kg/m

PE: Patient is in mild respiratory distress with an elevated

respiratory rate and shallow breaths An end-expiatory wheeze is
heard on auscultation. Otherwise, his lungs appear normal to
auscultation and percussion.

Laboratory Studies

Pulmonary function tests:

FEVI: 70% of predicted

Peak expiratory flow rate: 60% of predicted

Forced vital capacity: 90% of predicted

Chest radiograph: Normal

Arterial blood gases

*PO,75 mm Hg

*PCO: 42 mm Hg

pH: 7.32

Questions:-

1. Give clinical significance of FEVI

2. Define and classify hypoxia

Q1. Clinical significance of FEV₁

FEV₁ (Forced Expiratory Volume in 1 sec): The volume of air

exhaled in the first second during a forceful expiration after full
inspiration.

Clinical significance:
Normal: ~80% of FVC in healthy adults.

In obstructive lung disease (COPD, asthma): FEV₁ is reduced

disproportionately more than FVC → FEV₁/FVC ratio decreases
(<70%).

In restrictive lung disease: Both FEV₁ and FVC are reduced

proportionally → FEV₁/FVC ratio remains normal or increased.

In this patient:

FEV₁ = 70% predicted (↓)

FVC = 90% predicted (near normal)

→ Obstructive pattern consistent with chronic bronchitis/COPD
due to smoking history.

---

Q2. Define & classify hypoxia

Definition

👉 Hypoxia = deficiency of oxygen at tissue level (Guyton).

Classification (Ganong + Guyton)

1. Hypoxic (Hypoxemic) hypoxia

Cause: ↓ arterial PO₂ (low inspired O₂, high altitude,

hypoventilation, diffusion defect, V/Q mismatch).

ABG: ↓ PO₂, ↓ O₂ saturation.

2. Anemic hypoxia
Cause: ↓ hemoglobin or abnormal Hb (anemia, CO poisoning,
methemoglobinemia).

ABG: PO₂ normal, O₂ content ↓.

3. Stagnant (Circulatory/Ischemic) hypoxia

Cause: ↓ blood flow to tissues (heart failure, shock, local

ischemia).

ABG: PO₂ normal, O₂ delivery ↓.

4. Histotoxic hypoxia

Cause: Tissues unable to utilize O₂ (cyanide poisoning, H₂S

poisoning).

ABG: PO₂ & O₂ content normal, venous PO₂ ↑ (since O₂ not used).

---

✅ In this patient:

ABG shows PO₂ = 75 mmHg (low), PCO₂ = 42 (near normal), pH =

7.32 (mild acidosis) → this is Hypoxemic hypoxia due to
obstructive lung disease (COPD).

CASE HISTORY – 13

A 58-year-old woman is referred to an internist due to high

calcium levels found during treatment for a fracture of her femur.
The patient's femur was fractured at the midshaft by a
compression. The injury should not have been severe enough to
break the bone. During treatment, the patient was noted to have
high calcium levels and was referred for further study.
PHYSICAL EXAMINATION

VS: Temp: 37°C; PR: 80/min; RR: 15/min; BP: 116/76 mm Hg

BMI: 26 Kg/m²

PE: The patient appears healthy and exercised regularly before

the injury. The left femur is immobilized, and the injury appears to
be healing well.

LABORATORY STUDIES

Serum calcium: 14.2 mg/dL (normal: 8.4–10.2 mg/dL)

Serum phosphorus (inorganic): 2.1 mg/dL (normal: 3.0–4.5 mg/dL)

PTH levels: 2200 pg/mL (normal: 230–630 pg/mL)

---

Q1. What is your diagnosis?

The patient has Primary Hyperparathyroidism (most likely due to

a parathyroid adenoma).

This is suggested by:

Hypercalcemia (very high serum calcium: 14.2 mg/dL)

Hypophosphatemia (low phosphorus: 2.1 mg/dL)

Markedly elevated PTH (2200 pg/mL, well above normal range).

The pathological fracture of the femur also supports osteitis

fibrosa cystica / bone resorption due to excess PTH.
---

Q2. Explain the pathophysiology of the fracture and high calcium

levels.

Excess PTH → stimulates osteoclast activity indirectly via

osteoblasts, leading to increased bone resorption.

Continuous PTH action causes:

Loss of cortical bone mass → pathological fractures even with

minor trauma.

Increased serum calcium (released from bone).

Decreased serum phosphate (due to PTH-mediated phosphaturia).

Thus, the fracture is not proportionate to the trauma and is due to

weakened bones from hyperparathyroidism.

---

Q3. What are the systemic manifestations of

hyperparathyroidism?

Bones: Osteitis fibrosa cystica, bone pain, pathological fractures.

Stones: Increased calcium → renal stones (nephrolithiasis).

Groans: Abdominal pain due to peptic ulcers, pancreatitis.

Moans: Neuropsychiatric symptoms (depression, confusion,

fatigue).

Thrones: Polyuria and dehydration due to nephrogenic diabetes

insipidus.

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Q4. Why are serum phosphorus levels low in this patient?

PTH increases renal phosphate excretion by inhibiting sodium-

phosphate cotransporters in the proximal tubule.

Thus, despite high calcium, the patient develops

hypophosphatemia.