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MBBS IV - Junior Clerkship WCS > JC40 (Medicine) - Adrenal diseases > Flashcards

JC40 (Medicine) - Adrenal diseases Flashcards

1
Q

3 diseases that cause endocrine hypertension

A

Conn’s syndrome
Cushing’s syndrome
Pheochromocytoma

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2
Q

List all hypothalamic factors and pituitary hormones

A

Anterior lobe:

  • Thyrotropin- releasing hormone (TRH) > Thyroid-stimulating hormone (TSH)
  • Dopamine > inhibit prolactin
  • Corticotropin-releasing hormone (CRH) > ACTH
  • Growth-hormone releasing hormone (GHRH) > Growth hormone (GH)
  • Somatostatin > inhibit Growth hormone
  • Gonadotropin-releasing hormone (GnRH) > FSH and LH

Posterior lobe: Neurohypophysis from PVN and SON in thalamus

  • Oxytocin
  • Antidiuretic hormone (ADH)/ Vasopressin (Vp)
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3
Q

List all cell types in the pituitary and their secretion

A

Lactotrophs - Prolactin

Somatotrophs - Growth hormone

Corticotrophs - ACTH

Thyrotrophs - TSH

Gonadotrophs - FSH and LH

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4
Q

Causes of hypopituitarism

A

Hypopituitarism:

Tumor/ Mass lesion

Surgery/ radiation

Trauma

Ischemic necrosis and Sheehan syndrome

Infection/ inflammation

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5
Q

Action of posterior pituitary hormones

A

Oxytocin

  1. Contraction of uterine smooth muscle at pregnancy (positive feedback loop, expel fetus)
  2. Smooth muscle contraction around lactiferous ducts of mammary glands at lactation (milk expression)

Vasopressin/ ADH

  1. Increase permeability of renal collecting ducts
  2. Trigger by decrease BP or increase plasma osmotic pressure
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6
Q

Anatomical layers and composition of adrenal gland

A

Cortex:

  1. Zone glomerulosa (outer) - Mineralocorticoids: Aldosterone, DOC and 18-hydroxy DOC
  2. Zona fasciculata (Middle, 75% volume) - Glucocorticoids: Cortisol, corticosterone
  3. Zone reticularis (inner) - Mainly Androgens: Dehydroepiandrosterone, Androstenedione, Testosterone, Estrogen, Progestogens

Medulla

  1. Chromaffin cells and sympathetic nerve endings > Secrete Catecholamine (Epinephrine mainly)
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7
Q

Causes of acute and chronic adrenal gland insufficiency

A

Acute primary adrenal insufficiency

  • Waterhouse-Friderichsen Syndrome: overwhelming bacterial infection lead to hypotension, shock, DIC and massive adrenal hemorrhage

Chronic primary adrenal insufficiency

  • Addison Disease: caused by Autoimmune adrenalitis/ TB and infections/ Amyloidosis/ Metastatic cancers
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8
Q

Causes of adrenal hyper-function

Primary adrenal causes?

Secondary causes?

A

Primary adrenal causes:

  • Adrenal hyperplasia
  • Cortical adenomas: Conn’s syndrome (high mineralocorticoids) and Cushing’s syndrome (High Glucocorticoids)
  • Pheochromocytomas or Neuroblastoma

Secondary causes:

  • Function anterior pituitary adenoma (Corticotrophs)
  • Iatrogenic ACTH administration
  • Secondary aldosteronism: Low Na in renal tubules or low renal perfusion pressure > activate renin-angiotensin system > activate aldosterone production in adrenal cortex
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9
Q

List all androgens produced by zona reticularis in adrenal cortex

A

Dehydroepiandrosterone

Androstenedione

Testosterone

Estrogen

Progestogens

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10
Q

Plasma transport of steroids

A

Cortisol (Glucocorticoid)

  • 95% protein bound to Albumin (low, affinity, high amount) and Transcortin (high affinity, low amount)

Aldosterone (Mineralocorticoid)

  • 60% bind to Albumin

Sex steroids

  • Sex-hormone binding globulin
  • Globulin increased by estrogen and decreased by androgens
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11
Q

Outline the Renin-angiotensin-Aldosterone system

A
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12
Q

Systemic effects of Renin-angiotensin-aldosterone system activation

A

Adrenal glands > produce aldosterone for fluid and sodium retention

Kidneys > fluid and sodium retention

Heart > muscle hypertrophy and fibrosis

Brain > increase sympathetic outflow, trigger thirst sensation and ADH release

Blood vessel > Vasoconstriction

Overall effect:

  • Increase effective circulating volume
  • Increase Blood Pressure
  • Increase extracellular fluid volume
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13
Q

Aldosterone

  • MoA
  • Condition caused by excess aldosterone
  • Biochemical stimulating factors
A

MoA

  • Increase Na reabsorption in DCT and ascending loop of Henle > increase exchange of Na from urine for K and H+ ions in plasma > retain Na and increase osmotic pressure in blood

Condition caused by excess aldosterone

  • Excessive dumping of K and H+ ions > HypoKalemia and Alkalosis

Biochemical stimulating factors

  • Angiotensin II
  • ACTH (short-term stimulation)
  • Plasma K: HyperKalemia
  • Plasma Na: HypoNatremia
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14
Q

Physiological stimuli/ suppressors of aldosterone secretion

A

Stimuli:

  • Upright posture
  • Exercise
  • Low Sodium
  • Low blood volume
  • Stress
  • Diuretics

Suppressors:

  • Old age
  • High Sodium loading
  • Volume overload
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15
Q

Causes of primary and secondary hyperaldosteronism

A

Primary:

Secondary: reactive to low Na, low BP, low intravascular volume

  • Renal artery stenosis (stimulate renin and RAA system)
  • Congestive cardiac failure (cardiac RAA system)
  • Liver cirrhosis (decrease albumin, hypovolemia)
  • Nephrotic syndrome (sodium loss)
  • Salt-losing states
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16
Q

Pathological Effects of primary aldosteronism

A

Renal: Polydipsia, Polyuria and nocturia

Neurological: HypoK causes weakness, flaccid paralysis, tetany, parasthesiae

Cardiovascular: Increase BP, Cardiac hypertrophy and fibrosis, Headache, Retinopathy, LV failure or Congestive HF

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17
Q

Investigations for Conn’s Syndrome

A

Preliminary:

  • Exclude other causes of HypoK (e.g. diuretic use, GI loss, renal tubular acidosis)
  • Measure urine K loss
  • Maintain normal Na intake (for renal exchange of K)
  • Stop diuretics, B-blocker and ACEI for >2 weeks before dynamic biochemical tests

Basal tests:

  • Plasma K, Basal aldosterone, Basal Plasma Renin Activity (PRA)

Dynamic biochemical tests:

  • Salt-loading test
  • Postural test +/- Adrenal venous sampling

Radiological imaging: CT/ MRI

18
Q

Compare the basal biochemical test results between adrenal adenoma and hyperplasia

A
19
Q

Salt loading test

  • Indication
  • Procedure
  • Caution
  • Normal response
  • Pathological response
A

Indication: Confirmation of primary aldosteronism

Procedure: 0.9% normal IV saline at 500mL/h for 4 hours in sitting/ recumbent position >> measure renin/ aldosterone after test

Caution: Fluid-overload, monitor pulse and BP

Normal response: Salt loading suppress renin and aldosterone

Pathological response: Failure to suppress renin and aldosterone

20
Q

Postural test

  • Indication
  • Procedure
  • Normal response
  • Pathological response
A

Indication: D/dx adrenal hyperplasia or adrenal adenoma

Procedure: Measure supine/ erect plasma renin and aldosterone

  • Supine measurement: at 8am after 8 hours of recumbence overnight
  • Erect measurement: at 12 noon after 4 hours of standing

Normal response: Supine to upright posture triggers RAA system >> increase renin and aldosterone levels

Pathological response:

  • Adenoma (sensitive to ACTH) - Aldosterone drop 70-90%
  • Hyperplasia (sensitive to angiotensin) - Aldosterone increase 90%
21
Q

Adrenal venous sampling

  • Function
  • Ddx
A

Function: measure aldosterone secretion from both adrenal glands to d/dx primary aldosteronism

Unilateral adenoma: Aldosterone high on lesion side, suppressed in contralateral side

Hyperplasia: Aldosterone high on both sides

22
Q

Treatment options of Primary Aldosteronism

A
  1. Pharmacological
  • Spironolactone/ Eplerenone – Aldosterone antagonists
  • Amiloride/ Triameterene – Act on DCT to block Na reabsorption and K excretion
  • Corticosteroid for adrenal hyperplasia
  1. Surgical resection- for adrenal adenoma
23
Q

List causes of Cushing’s syndrome

A

ACTH-dependent:

  • Cushing’s disease: Pituitary or Hypothalamic cause
  • Ectopic ACTH production: neoplastic cause

Non-ACTH dependent

  • Adrenal adenoma
  • Adrenal carcinoma
  • Steroid administration/ Iatrogenic
24
Q

Compare the ACTH and Cortisol levels between ACTH-dependent and ACTH-independent Cushing’s syndrome

A

ACTH-dependent: Cushing’s disease/ Ectopic ACTH production >> High ACTH and Cortisol

ACTH-Independent:

  • Adrenal adenoma and carcinoma: Low ACTH, High Cortisol
  • Iatrogenic/ steroid use: Low ACTH, Low Cortisol
25
Q

Clinical features of Cushing’s syndrome

A

Fat redistribution: Truncal obesity, moon face, buffalo hump, fat pads

Skin: Acne, Purple striae, excessive bruising, thin skin

Psychiatric: Depression, euphoria, frank psychosis

Sexual: impotence, Hirsutism, Oligo-/ Amenorrhea

MSS: Osteoporosis, Proximal myopathy

Endocrine: DM

Vascular: Hypertension

26
Q

Investigations for Cushing’s syndrome

(Basal, Screening and Diagnostic tests, imaging, sampling)

A

Basal studies:

  • 24h Urinary Free Cortisol, 17-ketosteroids
  • Plasma cortisol and ACTH (at 9am and midnight)

Screening tests:

  • Overnight dexamethasone suppression test (1mg oral dexamethasone at 9am and midnight, measure next day 9am)
  • Late night salivary free cortisol

Diagnostic test:

  • Dexamethasone suppression test
  • CRF Test

Imaging:

  • CXR
  • MRI pituitary
  • CT adrenal/ CT body scans

Sampling:

  • Venous sampling for peripheral blood ACTH
  • Inferior petrosal sinus sampling (for pituitary Cushing’s)
27
Q

Details of Diagnostic test for Cushing Syndrome

D/dx

A

Dexamethasone suppression test

  • Admin Dexamethasone and measure ACTH, Cortisol response
  • Normal response - ACTH, Cortisol suppression
  • Low dose: 0.5mg Q6H for 2 days - No suppression of Cortisol in Cushing’s Syndrome
  • High dose: 2mg Q6H for 2 days - No suppression in Ectopic ACTH, Primary Adrenal Hyperplasia/ Adenoma; Suppression in Pituitary Cushing’s

CRF Test

  • Differentiate Pituitary Cushing’s from ectopic ACTH production
  • 1ug/kg IV CRF given, sample ACTH and Cortisol
  • Pituitary Cushing’s - Exaggerated High ACTH and Cortisol
  • Ectopic ACTH production - No rise in ACTH or Cortisol
28
Q

Compare the diagnostic test results between Pituitary Cushing’s, Ectopic ACTH, Adrenal adenoma and carcinoma

A

Pituitary Cushing’s

  • Dexamethasone low-dose: No suppression
  • Dexamethasone high-dose: Suppression
  • ACTH level: High
  • CRF stimulus: Exaggerated rise

Ectopic ACTH

  • Dexamethasone low-dose: No suppression
  • Dexamethasone high-dose: +/- suppression
  • ACTH level: High
  • CRF stimulus: No change

Adrenal adenoma and carcinoma

  • Dexamethasone low-dose: No suppression
  • Dexamethasone high-dose: No Suppression
  • ACTH level: Low/ Zero
29
Q

How to localize cause of Cushing’s syndrome

A

Radiology:

  • CXR
  • MRI pituitary
  • CT adrenal (renal cause)
  • CT whole body (ectopic ACTH)

Sampling:

Venous sampling for peripheral ACTH
Inferior petrosal sinus sampling
e. g. Cushing’s disease - High petrosal sinus ACTH (pituitary output), low peripheral ACTH
e. g. Ectopic ACTH production - Low petrosal sinus ACTH, High peripheral ACTH

30
Q

How to localize cause of Cushing’s syndrome

A

Radiology:

  • CXR
  • MRI pituitary
  • CT adrenal (renal cause)
  • CT whole body (ectopic ACTH)

Sampling:

  • Venous sampling for peripheral ACTH
  • Inferior petrosal sinus sampling

e. g. Cushing’s disease - High petrosal sinus ACTH (pituitary output), low peripheral ACTH
e. g. Ectopic ACTH production - Low petrosal sinus ACTH, High peripheral ACTH

31
Q

Treatment of Cushing’s disease

A

Surgical:

  • Adrenal adenoma/ carcinoma - Surgical resection
  • Pituitary tumors - Transphenoidal surgery
  • Peri-operative: Control and correct BP, DM, HypoK
  • Prophylaxis against rapid cortisol drop: Steroid cover
  • Antibiotics cover

Medical:

  • Reduce hypercortisolism before surgery
  • Metyrapone: Block cortisol synthesis at 11 B-hydroxylase step in adrenal cortex
  • Ketoconazole: Inhibit cortisol and androgen secretion
32
Q

Production of adrenaline and noradrenaline

Anatomical structures involved

A

Catecholamine biosynthesis in Adrenal Medulla: Chromaffin cells and sympathetic nerve fibers, from neuroectoderm

Dual blood supply:

  • Portal blood in corticomedullary sinuses draining adrenal cortex
  • Medullary arteries

**PNMT in adrenal cortex convert Noradrenaline > Adrenaline

**PNMT is not in sympathetic nerve fiber > neurons can only make Noradrenaline

33
Q

List all circulating catecholamines and origins of production

A

Noradrenaline

  • Act on a1 and B1 receptors
  • Major circulating catecholamine under BASAL condition
  • 95% derived from sympathetic nerve endings, 5% from adrenal medulla

Adrenaline

  • Act on B1 and B2 receptors
  • 100% from adrenal medulla

Dopamine

  • Released during intense adrenal medullary activity
  • Mostly from kidneys
34
Q

Metabolism of circulating catecholamines

A

Extraneuron metabolism:

Catecholamine >> catalyze by Catecholamine-o-methyl transferase (COMT) in liver and kidney

>> Methylated catecholamine oxidized >> Vanillymandelic acid (VMA)

35
Q

Causes of adrenal medulla hyper-function

A

Tumors:

  • Pheochromocytoma
  • Ganglioneuroma
  • Symapthoblastoma
  • Neuroblastoma
36
Q

Pheochromocytoma

  • Cell of origin
  • Etiologies
  • Locations
  • S/S
A

Cell of origin - Chromaffin cell of adrenal medulla

Etiologies - spontaneous, familial (MENII, Neurofibromatosis)

Locations - Intra-adrenal (produce noradrenaline and adrenaline) or Extra-adrenal (20%, produce noradrenaline)

S/S:

  • Hypertension, Angina, Cardiac failure
  • Headache
  • Palpitations, Dizziness, anxiety
  • Hyperhydrosis
  • Pallor
  • Weight loss, pyrexia
  • Stroke
  • Glucose intolerance, DM
37
Q

Diagnosis of Pheochromocytoma

A

Basal test:

  • Urinary Vanillymandelic acid
  • Urinary catecholamines and metabolites - Metanephrine and normetanephrine
  • Plasma catecholamine

Radiological:

  • CT/MRI with contrast after adrenoceptor blockade (prevent pressor crisis)
  • Meta-iodo-benzyl guanidine (MIBG) scan - Chromaffin uptake of RAI
38
Q

Treatment of pheochromocytoma

A

Surgery

  • Full adrenoceptor blockage before
  • a blockade with Phenoxybenzamine first + B blockade with propranolol

Approaches:

  • Open approach adrenalectomy: anterior transabdominal, lateral extraperitoneal, or posterior lumbar
  • Minimal invasive laparoscopic adrenalectomy: Transabdominal, or Retroperitoneal
39
Q

Function of alpha and beta adrenoceptors

A
40
Q

Advantages of laparoscopic adrenalectomy

A
  1. Safe
  2. high efficacy
  3. Shorter hospital stay
  4. Reduce analgesic requirement
  5. Faster recovery
  6. Higher overall patient satisfaction
41
Q

Complications of adrenalectomy

A
  1. Intra-operative hemorrhage - damage adrenal capsule or vena cava
  2. Splenic injury
  3. Liver injury
  4. Pneumothorax
  5. Loss of adrenal tissue/ Acute adrenal insufficiency (Need glucocorticoid replacement post-op)
  6. Hypertensive crisis, electrolyte disturbance
42
Q

Conditions that require adrenal surgery

A

Conn’s syndrome

Cushing’s adenoma

Pheochromocytoma

Adrenal cortical carcinoma

Large adrenal incidentaloma

MBBS IV - Junior Clerkship WCS (131 decks)

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