Disease Profiles 2 Flashcards
Goitre
Enlarged palpable thyroid gland that moves on swallowing
Goitre: Pathophysiology
Reduced T3 and T4 production causes a rise in TSH that stimulates gland enlargement
Goitre: Aetiologies - Physiological
Puberty
Pregnancy
Goitre: Aetiologies - Autoimmune Disease (2)
Hashimoto’s Thyroiditis
Graves Disease
Goitre: Aetiologies - Endemic (2)
Iodine deficiency
Ingestion of Goitrogens - chemicals that exaggerate the effects of iodine deficiency
Goitre: Aetiologies - Inflammatory disease
Acute De Quervain’s Thyroiditis
Goitre: Pathophysiology - What develops if compensation fails?
Goitrous hypothyroidism state
Goitre: Pathophysiology - Histological findings (4)
Rupture of follicles
Haemorrhage
Scarring
Calcification
Diffuse Goitre: Clinical Presentation
Entire thyroid gland swells and is smooth to touch
Diffuse Goitre: Clinical Presentation - Mass effects (2)
Compression of the trachea - exertional dyspnoea, stridor and wheezing
Diffuse Goitre: Clinical Presentation - In children
Cretinism due to dyshormonogenesis
Diffuse Goitre: Investigations - Thyroid Function Tests
Normal T3 and T4
High TSH
Diffuse Goitre: Management -
Treat underlying cause
Multi-nodular Goitre: Pathophysiology
Recurrent hyperplasia and involution in response to external stimuli
Multi-nodular Goitre: Associated mutations
Mutations of the TSH signalling pathway
Multi-nodular Goitre: Clinical presentation
Irregular enlarged thyroid due to nodule formation that is bumpy on palpation
Multi-nodular Goitre: Investigations
TFT
US scan - demonstrates whether cystic or solid
FNA
Multi-nodular Goitre: Management - If toxic
Anti-thyroid drugs
Multi-nodular Goitre: Management - If significant thyroid problems
Radioactive Iodine
Multi-nodular Goitre: Management - If structural problem or significant retrosternal extension
Surgery
Hyperparathyroidism
Overactivity of the parathyroid glands with high levels of parathyroid hormone
Hyperparathyroidism: Primary Hyperparathyroidism
Uncontrolled parathyroid hormone produced directly from the tumour of the parathyroid glands
CAUSE - TUMOUR
Hyperparathyroidism: Management
Thyroidectomy
Hyperparathyroidism: Impact on calcium
Increased
Hyperparathyroidism: Secondary Hyperparathyroidism Pathophysiology
Insufficient vitamin D or chronic renal failure leading to low absorption of calcium from the intestines, kidneys and bones
CAUSE - LOW VITAMIN D OR CKD
Hyperparathyroidism: Impact on calcium
Hypocalcaemia
Hyperparathyroidism: Tertiary Hyperparathyroidism
Secondary hyperparathyroidism continues for a long time leading to hyperplasia of glands
CAUSE - HYPERPLASIA
Hyperparathyroidism: TFT for Primary Hyperparathyroidism
High PTH
High Calcium
Hyperparathyroidism: TFT for Secondary Hyperthyroidism
High PTH
Low or Normal Calcium
Hyperparathyroidism: TFT for Tertiary Hyperparathyroidism
High PTH
High Calcium
Hyperparathyroidism: Clinical presentation of primary hyperparathyroidism
Fatigue
Depression
Bone pain
Myalgia
Nausea
Thirst
Polyuria
Renal stones
Osteoporosis
Hyperparathyroidism: Pathophysiology - Function of PTH on Osteoclasts
Activates them to increase bone reabsorption and releases calcium
Hyperparathyroidism: Pathophysiology - Function of PTH on Renal tubules
Increased reabsorption of calcium by renal tubules
Hyperparathyroidism: Pathophysiology - Function of PTH on Phosphate
Increased urinary excretion of Phosphate
Hyperparathyroidism: Pathophysiology - Function of PTH on Vitamin D
Increased synthesis of active forms of Vitamin D
Hyperparathyroidism: Pathophysiology - How PTH regulated?
Increased serum calcium inhibits PTH secretion
Hyperparathyroidism: Pathophysiology - Fibrosa Cystica
Unchecked hyperparathyroidism results in the overproduction of PTH with continued osteoclasis - results in osteoporosis, brown tumours and osteitis
Hyperparathyroidism: Pathophysiology - Osteoclasis and Clinical Presentation (3)
Decreased bone mass - causes fractures, deformity and degenerative joint disease
Hyperparathyroidism: Pathophysiology - Osteoporosis location (3)
Phalanges
Vertebrae
Femur
Hyperparathyroidism: Pathophysiology - Osteoporosis where are the changes evident?
Cortical bone and medullary cancellous bone
Hyperparathyroidism: Pathophysiology - Osteoporosis what is present in the marrow spaces?
Fibrovascular tissue
Hyperparathyroidism: Pathophysiology - What are Brown Tumours?
Mass of reactive tissue
Hyperparathyroidism: Pathophysiology - Brown Tumours have what cells present?
Giant cells
Hyperparathyroidism: Pathophysiology - Brown Tumours have associated what?
Haemorrhages
Hyperparathyroidism: Pathophysiology - Brown Tumours Haemorrhages elicit what response? (20
Macrophage reactions
Processes of organisation and repair
Hyperparathyroidism: Pathophysiology - Brown Tumours present as what on X-ray?
Lytic lesion
Hyperparathyroidism: Primary Hyperparathyroidism Management
Surgical removal of the tumour
Hyperparathyroidism: Secondary Hyperparathyroidism Management
Correct Vitamin D deficiency or perform a renal transplant to treat renal failure
Hyperparathyroidism: Tertiary Hyperparathyroidism Management
Surgical removal of part of the parathyroid tissue to return PTH to normal
Hypercalcaemia
High levels of calcium within the blood
Hypercalcaemia: Aetiologies (6)
Excessive PTH secretion
Malignant disease
Genetic syndromes
Drugs
Granulomatous disease
High turnover states
Hypercalcaemia: Aetiologies - Causes of excessive PTH secretion (2)
Primary hyperparathyroidism - due to a single adenoma or diffuse hyperplasia of the parathyroid glands
Tertiary hyperparathyroidism
Hypercalcaemia: Aetiologies - Malignant Disease (3)
Metastatic bone destruction
PTH from solid tumours
Osteoclast activating-factors produced by tumours
Hypercalcaemia: Aetiologies - Genetic Syndromes (3)
MEN1 and 2
Familial isolated hyperparathyroidism
Familial Hypocalciuric Hypercalcaemia
Hypercalcaemia: Aetiologies - MEN1 and 2 presentation
Most will develop a parathyroid adenoma with hypercalcaemia at a young age
Hypercalcaemia: Aetiologies - Familial hypocalciuric hypercalcaemia Pathophysiology
Autosomal dominant deactivating mutation in the calcium sensing receptor resulting in decreased sensitivity of the receptor to the calcium
Hypercalcaemia: Aetiologies - Drug Examples (2)
Vitamin D
Thiazides
Hypercalcaemia: Aetiologies - Granulomatous disease (2)
Sarcoidosis
Tuberculosis
Hypercalcaemia: Clinical Presentation - Main 4 Symptoms (4)
Gallstones
Bone pain
Abdominal pain
Psychiatric Disturbances
STONE BONES GROANS AND PSYCHIC MOANS
Hypercalcaemia: Clinical Presentation - Acute (4)
Thirst
Dehydration
Confusion
Polyuria
Hypercalcaemia: Chronic Clinical Presentation - Musculoskeletal Symptoms (3)
Myopathy
Fractures
Osteopenia
Hypercalcaemia: Chronic Clinical Presentation - Cardiovascular
Hypertension
Hypercalcaemia: Chronic Clinical Presentation - Gastrointestinal (3)
Pancreatitis
Duodenal ulcers
Renal calculi
Hypercalcaemia: Diagnosis - Biochemistry (3)
Raised calcium
Serum PTH - elevated PTH
Serum Alkaline Phosphatase - raised with hypercalcaemia in malignancy
Hypercalcaemia: Diagnosis - Imaging required for malignancy (3)
X-ray
MRI
Isotope Bone Scan
Hypercalcaemia: Diagnosis - Familial Hypocalciuric Hypercalcaemia (2)
Bloods - increased calcium + Urine calcium excretion + PTH elevated
Genetic screening
Hypercalcaemia: Management of Acute Severe Hypercalcaemia - Fluids
Rehydrate with 0.9% saline 4-6 L in 24 hours
Hypercalcaemia: Management of Acute Severe Hypercalcaemia - Consider what medication once rehydrated?
Loop diuretics
Hypercalcaemia: Management of Acute Severe Hypercalcaemia - Avoid what medications?
Thiazides
Hypercalcaemia: Management of Acute Severe Hypercalcaemia - What drug is given to reduce Calcium?
Bisphosphonates - reduces Ca2+ over 2-3 days
Hypercalcaemia: Management of Acute Severe Hypercalcaemia - What drug is used if sarcoidosis is present?
Prednisolone 40-60 mg/day
Hypercalcaemia: Management of Primary Hyperparathyroidism - Indications for Surgery (4)
End organ damage
Calcium >2.85 mmol/L
Under 50
Reduced eGFR (<60 mL/min)
Hypercalcaemia: Management of Primary Hyperparathyroidism - Medication
Cinacalcet
Hypercalcaemia: Management of Primary Hyperparathyroidism - Cinacalcet Mode of Action
Calcium mimetic to reduce PTH
Hypocalcaemia: (4)
Congenital Absence - DiGeorge Syndrome
Destruction - Surgery, Radiotherapy and Malignancy
Autoimmune Disorders
Hypomagnesaemia
Hypocalcaemia: Clinical Presentation - Musculoskeletal symptoms (2)
Muscle weakness
Muscle cramps and tetany
Hypocalcaemia: Clinical Presentation - Nervous system symptoms
Paraesthesia - fingers, toes and perioral
Hypocalcaemia: Clinical Presentation - Respiratory
Bronchospasma or Laryngospasm
Hypocalcaemia: Signs - ECG
QT elongation
Hypocalcaemia: Signs - Chovsteks Sign
Tapping over the facial nerve causes twitch of the ipsilateral muscles
Hypocalcaemia: Signs - Trosseau Sign
Inflation of the sphygmomanometer cuff above systolic pressure for 3 minutes induces tetanic spasm of the fingers and wrist
Hypocalcaemia: Acute Management - Emergency
Infusion of IV Calcium Gluconate (10ml 10% over 10 minutes) in 50ml of saline or dextrose
Calcium infusion - 10ml 10% in 100ml infusate at 50ml per hour
Hypocalcaemia: Chronic Management (2)
Calcium supplement - 1-2g per day
Vitamin D supplement - 1 alpha-calcidol or depot injection of Cholecalciferol
Hypomagnesaemia
Low magnesium levels in the blood serum
Hypomagnesaemia: Aetiologies (4)
Alcohol
GI illness with diarrhoea
Pancreatitis
Malabsorption
Hypomagnesaemia: Examples of causative drugs (2)
Thiazide
Proton Pump Inhibitors
Hypomagnesaemia: Symptoms (4)
Anorexia
Nausea and vomiting
Muscle weakness
Fits
Hypomagnesaemia: Signs (3)
Cardiac Arrhythmias
Chovestek Sign
Trousseau Sign
Hypomagnesaemia: Diagnosis (2)
Low serum magnesium
Measure K+ and Ca2+
Hypomagnesaemia: Management
Magnesium and Calcium supplementation
Hypomagnesaemia: Main Complication
Secondary hypocalcaemia
Hypomagnesaemia: Complications - Pathophysiology of Secondary Hypocalcaemia
Calcium is released from cells is dependent - therefore in magnesium deficiency calcium is high
Hypomagnesaemia: Complications - Secondary hypocalcaemia has what impact on PTH?
Inhibited
Pseudohypoparathyroidism
Genetic defect associated with resistance to Parathyroid Hormone
Pseudohypoparathyroidism: Pathophysiology
Genetic mutation causing dysfunction of the Gs alpha subunit - GNAS-1 gene
Pseudohypoparathyroidism: Pathophysiology
End organ resistance to PTH due to mutation of the Gs alpha-protein that is coupled to the PTH receptor
Pseudohypoparathyroidism: Clinical Presentation (5)
McCune Albright - Bone abnormalities
Obesity
Subcutaneous calcification
Learning disability
Brachadactyly - shortened 4th metacarpal
Pseudohypoparathyroidism: Investigations (2)
Low Calcium
High PTH - due to resistance
Pseudohypoparathyroidism: Pseudo-pseudohypothyroidism
Phenotypic defects of pseudohypoparathyroidism without any abnormalities in calcium metabolism
Cushing’s Syndrome
Excess cortisol secretion
Cushing’s Disease
Benign Pituitary Adenoma that secretes excess ACTH
Cushing’s Disease: More common in what sex?
Females
Cushing’s Disease: Age
20-40 year olds
Cushing’s Syndrome: Aetiologies (2)
Therapeutic administration of synthetic steroids
Cushing’s Disease
Cushing’s Syndrome: Aetiologies - ACTH dependent (3)
Pituitary adenoma
Ectopic ACTH
Ectopic CRH
Cushing’s Syndrome: Aetiologies - ACTH independent (4)
Exogenous steroids
Adrenal adenoma or carcinoma
Adrenal cortical nodular hyperplasia
False positive - severe depression and alcoholism
Cushing’s Syndrome: Pathophysiology - ACTH independent
Over-production of cortisol by the adrenal gland due to neoplasia or nodular hyperplasia
Cushing’s Syndrome: Pathophysiology - ACTH-dependent adrenal enlargement is …
Diffuse
Cushing’s Syndrome: Pathophysiology - Cushing’s Disease
Pituitary secretes increased ACTH to increase cortisol production by the adrenal gland
Cushing’s Syndrome: Pathophysiology - ACTH-dependent Ectopic ACTH
Carcinoma secretes ACTH e.g. SCLC to increase cortisol production by the adrenal gland
Cushing’s Syndrome: Pathophysiology - ACTH-dependent Ectopic CRH
Carcinoma secretes CRH e.g. Medullary Thyroid Carcinoma to increase ACTH production by pituitary to increase cortisol by the adrenal gland
Cushing’s Syndrome: Consequences of Increased Cortisol Levels - Proteins
Reduction
Cushing’s Syndrome: Consequences of Increased Cortisol Levels - Proteins
Reduction
Cushing’s Syndrome: Consequences of Increased Cortisol Levels - Carbohydrates and Lipid
Metabolism changed
Cushing’s Syndrome: Consequences of Increased Cortisol Levels - Mineralocorticoid
Increased
Cushing’s Syndrome: Consequences of Increased Cortisol Levels - Androgens
Increased
Cushing’s Syndrome: Pathophysiology - Protein loss has what impact? (3)
Myopathy - muscular wasting
Osteoporosis - causes fractures
Thin skin - causes striae and bruising
Cushing’s Syndrome: Pathophysiology - Altered Carbohydrate and Lipid Metabolism has what consequence?
Diabetes Mellitus and Obesity
Cushing’s Syndrome: Pathophysiology - Excess mineralocorticoids consequence? (2)
Hypertension
Oedema
Cushing’s Syndrome: Pathophysiology - Excess Androgen results in (3)
Virulism - females with male characteristics
Hirsuitism - male hair pattern on women
Acne
Oligo- or Amenorrhoea
Cushing’s Syndrome: Clinical Presentation - Facial features (2)
Plethora - redness of the face
Moon face
Cushing’s Syndrome: Clinical Presentation - Cardiovascular (2)
Hypertension
Oedema
Cushing’s Syndrome: Clinical Presentation - Metabolic (4)
Central obesity
Glycosuria
Diabetes mellitus
Cushing’s Syndrome: Clinical Presentation - Back
Buffalo hump
Cushing’s Syndrome: Clinical Presentation - Skin (6)
Bruising
Striae - purple or red
Pigmentation
Thin skin
Hirsutism
Acne
Cushing’s Syndrome: Clinical Presentation - Musculoskeletal (2)
Proximal myopathy - wasting
Osteoporosis - fractures
Cushing’s Syndrome: Clinical Presentation - Reproductive
Oligo- or Amenorrhoea
Cushing’s Syndrome: Clinical Presentation - How is Cushing’s distinguished from Obesity? (5)
Thin Skin
Proximal myopathy
Frontal balding in women
Conjunctival oedema
Osteoporosis
Cushing’s Syndrome: Diagnosis - Main test
Dexamethasone suppression test
Cushing’s Syndrome: Diagnosis - Dexamethaone Suppression Test Description
1mg overnight dexamethasone - if the administration fails to suppress the cortisol Cushing’s Syndrome is present
Cushing’s Syndrome: Diagnosis - Dexamethasone Suppression Test Normal Result
Cortisol <50 nmol/L
Cushing’s Syndrome: Diagnosis - Dexamethasone Suppression Test Abnormal Result
Cortisol >130 nmol/L
Cushing’s Syndrome: Diagnosis - 24 hour urine cortisol test Normal Results (2)
Total Cortisol <250 nmol/L
Cortisol:Creatinine Ration <25 nmol/L
Cushing’s Syndrome: Diagnosis - Diurinal Cortisol Variation Procedure
Serum/Saliva/Urine Collection - if loss of diurnal variation at 8am and Midnight is present suspect Cushing’s
Cushing’s Syndrome: Diagnosis - If ACTH what is the likely origin?
Adrenal gland
Cushing’s Syndrome: Diagnosis - If ACTH is raised what is required next?
Distinguish Cushing’s Disease and Ectopic ACTH - CRF test with elevated ACTH and Cortisol indicates pituitary source
Cushing’s Syndrome: Management - Pituitary Source Options (2)
Hypopysectomy - transphenoidal route with external radiotherapy
Bilateral Adrenalectomy
Cushing’s Syndrome: Management - Adrenal source
Adrenalectomy
Cushing’s Syndrome: Management - Pharmacological Options (3)
Metyrapone
Ketoconazole
Pasiretoide LAR
Cushing’s Syndrome: Management - Side effect of Ketoconazole
Hepatotoxic
Cushing’s Syndrome: Management - Pasireotide LAR dose
10-20 mg monthly
Adrenal Adenoma
Benign neoplasma emerging from the cells of the adrenal cortex
Adrenal Adenoma: Appearance
Well-circumscribed encapsulated lesions that are small with bright yellow lipids buried within the gland
Adrenal Adenoma: Histological presence
Well-differentiated with small nuclei and made of cells resembling adrenocortical cells
Adrenal Adenoma: Clinical presentation if hyperfunctioning gland
Manifestations of Cushing’s or Conns Syndrome
Adrenal Adenoma: When is surgical excision required?
Functioning lesion
Large lesion - >3-5 cm
Adrenocortical Carcinoma
Malignancy of the adrenal cortex
Adrenocortical Carcinoma: In young patients this is associated with what?
Li-Fraumeni Syndrome
Adrenocortical Carcinoma: Histology - Size
Large - often >20cm
Adrenocortical Carcinoma: Histology - Mitosis
Frequent atypical mitoses present
Adrenocortical Carcinoma: Histology - There is a lack of what?
Clear cells
Adrenocortical Carcinoma: Histology - What are the two types of invasion?
Capsular or Vascular
Adrenocortical Carcinoma: Histology - What features may be present? (2)
Haemorrhage
Necrosis
Adrenocortical Carcinoma: Spread - Local invasion of what? (2)
Retroperitoneum
Kidney
Adrenocortical Carcinoma: Spread - Metastasis is often by what to where?
Haemogenous - Liver, Lung and Bone
Adrenocortical Carcinoma: Spread - Involves what? (2)
Peritoneum
Pleura
Adrenocortical Carcinoma: Clinical Presentation -(2)
Abdominal mass effects
Necrosis can cause a fever
Adrenocortical Carcinoma: Management
Resection with adjuvant therapy if no metastasis present
Primary Hyperaldostronism
Autonomous production of aldosterone independent of its regulators - Angiotensin II and Potassium
Primary Hyperaldostronism: Aetiologies (4)
Conn’s Syndrome
Bilateral Adrenal Hyperplasia
Genetic mutations
Unilateral hyperplasia
Conn’s Syndrome
Adrenal Adenoma
Primary Hyperaldostronism: Conn’s Syndrome - Genetic Pathophysiology
KCNJ5 channel mutation - leads to loss of ion selectivity for Na+ causing depolarisation ad therefore increased aldosterone production
Primary Hyperaldostronism: Main aetiology
Bilateral Adrenal Hyperplasia
Primary Hyperaldostronism: Examples of Genetic Mutations (5)
CLC-2
GIRK4
ATPase
Beta Catenin
Cav3.2/1.3 Channels
Primary Hyperaldostronism: Pathophysiology - Aldosterone impact on cardiac collagen
Increased
Primary Hyperaldostronism: Pathophysiology - Aldosterone impact on Sodium
Increases retention
Primary Hyperaldostronism: Pathophysiology - Aldosterone impact on Sympathetic Outflow
Increased
Primary Hyperaldostronism: Pathophysiology - Aldosterone increases the synthesis of what? (2)
Cytokines
ROS
Primary Hyperaldostronism: Pathophysiology - Aldosterone impact on endothelial function
Increased pressor response
Primary Hyperaldostronism: Clinical Presentation (3)
Hypertension
Hypokalaemia
Alkalosis
Primary Hyperaldostronism: Diagnosis - Initially required to confirm what?
Aldosterone excess
Primary Hyperaldostronism: Diagnosis - How is aldosterone excess confirmed?
Measure plasma aldosterone and renin - determine ratio
Primary Hyperaldostronism: Diagnosis - Raises Aldosterone:Renin ration requires further investigation with what?
Saline suppression test
Primary Hyperaldosteronism: Diagnosis - If saline suppression test fails to suppress ratio by >50% with 2 litres of saline shows what?
Confirms Primary Aldosteronism
Primary Hyperaldostronism: Diagnosis - How to confirm subtype?
Adrenal CT for adenoma
Or vein sampling
Primary Hyperaldostronism: Management - Adrenal Adenoma confirmed source with vein sampling
Unilateral Laparoscopic Adrenalectomy
Primary Hyperaldostronism: Management - Unilateral laparoscopic Adrenalectomy cures what? (2)
Hypokalaemia
Hypertension
Primary Hyperaldostronism: Management - Bilateral Adrenal Hyperplasia
MR Antagonists - Spironolactone or Eplerenone
Secondary Hyperaldosteronism
Increased adrenal production of aldosterone in response to extra adrenal stimuli
Secondary Hyperaldosteronism: Basic pathophysiology
Reduced renal flow leads to excess renin and hence angiotensin II
Secondary Hyperaldosteronism: Causes of reduced renal blood flow? (3)
Obstructive renal artery disease e.g. atheroma or stenosis
Renal vasoconstriction
Oedematous disorders e.g. heart failure or cirrhosis with ascites
Secondary Hyperaldosteronism: Most common aetiology
Renal artery stenosis - due to atheroma
Secondary Hyperaldosteronism: Can be caused by what in females?
Fibromuscular dysplasia
Secondary Hyperaldosteronism: Clinical presentation
Hypertension
Secondary Hyperaldosteronism: Diagnosis - Aldosterone:Renin Ratio
High aldosterone
High renin
Secondary Hyperaldosteronism: Diagnosis - How to detect Renal Artery Stenosis?
Doppler US
CT Angiogram
MRA
Secondary Hyperaldosteronism: Management
Aldosterone Antagonists e.g. Spironolactone
Secondary Hyperaldosteronism: Management of Renal Artery Stenosis
Percutaneous Renal Artery Angioplasty via the femoral artery
Addisons Disease
Primary adrenal insufficiency with decreased production of adrenocortical hormones - glucocorticoids, mineralocorticoids and adrenal androgens
Adrenocortical Insufficiency: Acute Aetiologies - Associated with drugs
Rapid withdrawal of steroid treatment
Adrenocortical Insufficiency: Acute Aetiologies - Crisis in what patients?
Patients with chronic adrenocortical insufficiency e.g. stress or infection
Adrenocortical Insufficiency: Acute Aetiologies - Involving the adrenal glands (4)
Adrenal haemorrhage
Adrenal tuberculosis
Adrenal malignancy
Congenital Adrenal Hyperplasia
Adrenocortical Insufficiency: Acute Aetiologies - Causes of massive adrenal haemorrhage (4)
Newborns
Anti-coagulant treatment
DIC - Disseminated Intravascular Coagulation
Septicaemic infection
Adrenocortical Insufficiency: Most common cause of Primary Adrenal Insufficiency?
Autoimmune adrenalitis
Adrenocortical Insufficiency: Acute Aetiologies - Septicaemic Infection may occur in what syndrome?
Waterhouse-Friderichsen Syndrome
Adrenocortical Insufficiency: Chronic Aetiologies - When does Addison’s Disease manifest?
Once >90% of the gland is destroyed
Adrenocortical Insufficiency: Addisons Disease - Aetiologies (3)
Autoimmune adrenalitis
Infections - TB, Histoplasma or HIV
Metastatic Malignancy - from lung or breast
Adrenocortical Insufficiency: Addisons Disease - Decreases Mineralocorticosteroids have what impacts? (4)
Hyperkalaemia
Hyponatraemia
Volume depletion
Hypotension
Adrenocortical Insufficiency: Addisons Disease - Decreased glucocorticoids have what impact?
Hypoglycaemia
Adrenocortical Insufficiency: Addisons Disease - In a crisis what is the presentation? (4)
Vomiting
Hypotension
Shock
Abdominal pain
Adrenocortical Insufficiency: Addisons Disease - Why is there excess pigmentation?
Excess ACTH due to low adrenocorticoids gets degraded to release MSH
Adrenocortical Insufficiency: Where do black spots present?
Buccal mucosa
Dark palmar creases
Dark finger spaces
Adrenocortical Insufficiency: Diagnosis - Biochemistry Results (3)
Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Adrenocortical Insufficiency: Diagnosis - Hormone markers
Increased renin
Decreased aldosterone
Adrenocortical Insufficiency: Diagnosis - What test should be conducted?
Short Synacthen Test
Adrenocortical Insufficiency: Diagnosis - Short Synacthen Test process and results
Measure plasma cortisol before and 30 minutes after injection of synthetic ACTH -
Normal Baseline - >250 nmol/L
Normal Post-ACTH - >550 nmol/L
Adrenocortical Insufficiency: Management - First line treatment
Hydrocortisone