pt18

Question 1

What are the main functions of oxytocin?

Answer 1

Stimulates uterine contractions during labor and milk ejection (“let‐down”) in lactation via positive feedback.

Question 2

List the principal anterior pituitary hormones.

Answer 2

Growth hormone (GH), thyroid‐stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), follicle‐stimulating hormone (FSH), luteinizing hormone (LH), prolactin.

Question 3

What is the major function of prolactin, and how is it regulated?

Answer 3

Stimulates milk production; tonically inhibited by hypothalamic dopamine (D2 receptors).

Question 4

What illustrates the three levels of endocrine integration?

Answer 4

Hypothalamic–pituitary–end‐organ axes (e.g., HPT, HPA, HPG) coordinating multiple glands.

Question 5

Outline the hypothalamic–pituitary–thyroid (HPT) axis.

Answer 5

Hypothalamus→TRH→Pituitary→TSH→Thyroid→T3/T4→negative feedback on both hypothalamus and pituitary.

Question 6

What are the main effects of thyroid hormones (T3/T4) in adults?

Answer 6

Increase basal metabolic rate, thermogenesis, and sympathetic nervous system activity.

Question 7

Describe the hypothalamic–pituitary–adrenal (HPA) axis.

Answer 7

Hypothalamus→CRH→Pituitary→ACTH→Adrenals→Cortisol→negative feedback on hypothalamus and pituitary.

Question 8

What are the main functions of cortisol?

Answer 8

Regulates metabolism (gluconeogenesis), suppresses the immune response, and supports stress adaptation.

Question 9

What characterizes Addisonian (adrenal) crisis, and how is it managed?

Answer 9

Acute cortisol deficiency with hypotension, hyponatraemia, hyperkalaemia; treat with high‐dose IV steroids and manage precipitating factors.

Question 10

Distinguish Cushing’s disease from Cushing’s syndrome and describe the dexamethasone suppression test.

Answer 10

• Cushing’s disease: pituitary ACTH‐secreting adenoma (high ACTH, high cortisol)
• Cushing’s syndrome: primary adrenal cortisol overproduction (low ACTH, high cortisol)
• Low‐dose dexamethasone at 11 pm, measure cortisol at 8 am: <50 nmol/L is normal; >100 nmol/L suggests autonomous cortisol secretion.

Question 11

What are the endocrine functions of the pancreas?

Answer 11

Islets of Langerhans secrete insulin (β‐cells) in response to high glucose and glucagon (α‐cells) in response to low glucose.

Question 12

What are the primary actions of insulin?

Answer 12

Promotes glucose uptake and storage in liver, muscle, and adipose tissue; anabolic effects on protein and lipid metabolism.

Question 13

What are the primary actions of glucagon?

Answer 13

Stimulates hepatic glycogenolysis and gluconeogenesis to raise blood glucose levels.

Question 14

What are the key clinical features of type 1 diabetes mellitus?

Answer 14

Onset <40 yrs, often normal/slim weight, autoimmune β‐cell destruction, absolute insulin deficiency, acute presentation with ketoacidosis.

Question 15

What distinguishes type 2 diabetes mellitus?

Answer 15

> 90% of cases, insulin resistance plus secretory defect, adult onset, risk factors include central obesity, inactivity, and family history.

Question 16

How do gut hormones contribute to obesity treatment?

Answer 16

GLP-1 analogues mimic gut‐derived incretins to enhance satiety and reduce appetite; endogenous GLP-1 is often deficient in obesity/type 2 diabetes.

Question 17

What causes hyperprolactinemia and how is it treated?

Answer 17

Pituitary prolactinoma (adenoma) secreting prolactin; treat with D2‐receptor agonists (e.g., cabergoline) or surgical resection if refractory.

Question 18

What are common causes and treatment of hypopituitarism?

Answer 18

Causes: pituitary adenomas, trauma, infiltrative disease, vascular apoplexy, rare congenital (Kallmann’s syndrome). Treatment: lifelong hormonal replacement for deficient axes.

Question 19

How do you localize endocrine lesions using hormone measurements?

Answer 19

Compare end‐organ hormone levels with stimulating (pituitary) or releasing (hypothalamic) hormones; e.g., low T4 + high TSH indicates primary thyroid failure.

Question 20

What are the exocrine functions of the pancreas?

Answer 20

Secretes digestive enzymes (lipase, amylase, trypsin, chymotrypsin) into the duodenum for nutrient breakdown.

Question 21

How do transport proteins affect steroid hormone action?

Answer 21

Steroid hormones bind carrier proteins (e.g., SHBG) to increase half‐life (e.g., cortisol ~60–90 min vs. epinephrine ~1 min).

Question 22

How is pituitary surgery commonly performed?

Answer 22

Transsphenoidal endoscopic approach via the nasal cavity to remove adenomas with minimal invasiveness.

Question 23

What is Kallmann’s syndrome?

Answer 23

Congenital GnRH‐deficiency leading to hypogonadism and anosmia due to failed olfactory neuron migration.

Question 24

Define autocrine, paracrine, and endocrine signaling.

Answer 24

• Autocrine: hormone acts on the same cell that secreted it
• Paracrine: acts on neighboring cells
• Endocrine: travels via bloodstream to distant targets.

Question 25

How does hormone structure influence clinical administration?

Answer 25

Peptides/proteins often require injection (degraded orally); steroids and amines may be given orally as tablets.

Question 26

How are endocrine disorders classified?

Answer 26

Hyper‐ (excess hormone production) vs. hypo‐ (deficient hormone production) syndromes.

Question 27

In hypothyroidism, what pattern of TSH and T4/T3 levels localizes the lesion?

Answer 27

Primary thyroid failure: ↑TSH and ↓T4; secondary (pituitary) failure: ↓TSH and ↓T4.

Question 28

Why do endocrinologists often measure both stimulating and end hormones?

Answer 28

To distinguish whether dysfunction is at the hypothalamus, pituitary, or target gland level based on expected feedback patterns.

Question 29

Define benign prostatic hyperplasia (BPH).

Answer 29

Non-neoplastic nodular enlargement (hyperplasia) of prostate stroma and glands.

Question 30

What drives BPH pathogenesis?

Answer 30

Androgens (testosterone) acting on stromal and glandular hyperplasia.

Question 31

Which lobes enlarge in BPH to compress the urethra?

Answer 31

Lateral and median (transition) lobes.

Question 32

What histological compartments are hyperplastic in BPH?

Answer 32

Fibromuscular stroma (smooth muscle & fibrous tissue) and glandular epithelium.

Question 33

Which four “voiding” symptoms characterize BPH?

Answer 33

Hesitancy, poor stream, dribbling post-micturition, frequency/nocturia.

Question 34

What secondary complications arise in BPH?

Answer 34

Urinary retention, cystitis, bladder hypertrophy, hydronephrosis/pyelonephritis.

Question 35

What are the key examination findings in BPH?

Answer 35

DRE: enlarged, firm, smooth, rubbery prostate; palpable distended bladder on abdominal exam.

Question 36

How is prostate size and residual urine assessed?

Answer 36

Trans-abdominal or trans-rectal ultrasound.

Question 37

How do α-blockers relieve BPH symptoms?

Answer 37

Relax bladder-neck smooth muscle (α₁-receptor blockade) to reduce outflow resistance.

Question 38

What is the role of anti-androgens in BPH treatment?

Answer 38

Inhibit testosterone action (e.g., 5α-reductase inhibitors) to reduce prostate growth.

Question 39

What is TURP and its purpose?

Answer 39

Transurethral resection of the prostate—endoscopic removal of hyperplastic nodules to widen the urethra.

Question 40

How does prostatic artery embolisation work?

Answer 40

Blocks prostatic arterial blood flow → ischemic necrosis → prostate shrinkage.

Question 41

How prevalent is prostate cancer among men?

Answer 41

Second most common male cancer (25% of cases); 1 in 10 men >70 yrs; rare <55 yrs.

Question 42

What risk factors are linked to prostate cancer?

Answer 42

Age-dependent androgen changes, androgen-receptor hypersensitivity, family history.

Question 43

Where in the prostate do most cancers arise?

Answer 43

Peripheral (posterior) zone glands.

Question 44

What histological type is prostate cancer and how is it graded?

Answer 44

Adenocarcinoma, graded by Gleason score (sum of two 1–5 pattern grades).

Question 45

How does prostate cancer spread locally and distantly?

Answer 45

Invades bladder floor/pelvis; metastasizes to bone (spine, pelvis, femur, ribs), liver, lungs.

Question 46

What obstructive symptoms and exam findings suggest prostate cancer?

Answer 46

LUTS like BPH; DRE: hard, craggy prostate; bone pain from metastases.

Question 47

How is prostate cancer diagnosed?

Answer 47

TRUS for size/staging; prostate biopsy + Gleason scoring; PSA and EN2 biomarkers; mpMRI for detailed imaging.

Question 48

What is PSA and its limitation?

Answer 48

Prostate-specific antigen rises in metastases but lacks specificity (also elevated in BPH).

Question 49

What is EN2 and its advantage over PSA?

Answer 49

A Surrey-discovered biomarker, more sensitive and specific than PSA.

Question 50

What are the main treatments for prostate cancer?

Answer 50

Radical prostatectomy; hormone manipulation (LHRH analogues or orchidectomy); radiotherapy.