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Endocrinology Flashcards

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1
Q

What are the 4 hormones involved in appetite regulation?

What do each of them do and detect?

A

INCREASE SATIETY AND REDUCE APPETITE
Leptin - detects lipids
Insulin - detects carbohydrates

REDUCE SATIETY AND INCREASES APPETITE
Ghrelin and GLP-1 (glucagon-like peptide 1)

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2
Q

Difference between Cushing’s syndrome and Cushing’s disease

A

Cushing’s syndrome: general term for chronic excessive and inappropriate elevated levels of circulating CORTISOL

Cushing’s disease: excessive cortisol resulting from inappropriate ACTH secretion due to pituitary tumour

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3
Q 
CUSHING'S BACKGROUND
What releases CRH? Full name?
What releases ACTH? Full name?
What releases cortisol?
Proportion in blood? Bound to?
Effects of cortisol (6)
A

Hypothalamus releases corticotrophin releasing hormone.

Pituitary gland releases adenocorticotrophic hormone.

Zona fasiculata releases cortisol.

95% cortisol binding globulin, 5% free

Increased gluconeogenesis, proteolysis, lipolysis. Increased BP. Anti-inflammatory. Mood and memory.

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4
Q

CUSHING’S SIGNS AND SYMPTOMS
Big 3?
Others?

A

MOON FACE, OBESITY, BUFFALO HUMP

Mood changes, infection?, thin skin, bruises, osteoporosis, purple striae, acne, increased BP

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5
Q

CUSHING’S DIFFERENTIAL DIAGNOSIS?

A

Pseudo-Cushing’s syndrome

Caused by alcohol excess - resolves with abstinence

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6
Q

CUSHING’S DIAGNOSIS?
Initial?
First line?
2nd line?

A

Initial - urine, blood, saliva cortisol
First line - dexamethasone suppression test
(overnight or 48hr)
Second line - ACTH test and dexamethasone injected
ACTH high - pituitary or ectopic
ACTH low - adrenal tumours
CT and MRIs to confirm

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7
Q

CUSHING’S CAUSES?

A

Exogenous - oral steroids (most common)
Endogenous -
ACTH dependent: pituitary or ectopic
ACTH independent: adrenal tumour

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8
Q

CUSHING’S TREATMENT?

A

Stops steroids
Surgery on tumours
Medications: inhibit cortisol synthesis, eg METYRAPONE, KETOCONAZOLE, FLUCONAZOLE

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9
Q

ACROMEGALY vs GIGANTISM?

A

Acromegaly - hormone disorder in adults as a result of excess growth hormone
Gigantism - excess growth hormone in childhood, leading to increased height

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10
Q

ACROMEGALY BACKGROUND
Feedback mechanisms on GH?
Two groupings for GH effects? Examples?

A

GHRH from hypothalamus stimulates
Somatostatin from muscle, liver, bones inhibits

Direct: 
increased metabolism and growth
increased bone thickness and muscle
growth
increased insulin resistance
increased glucose in blood

Indirect: via IGF-1
increased metabolism, increased cell division and differentiation, prevents cell death

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11
Q 
ACROMEGALY EPIDEMIOLOGY AND RISK FACTORS
How common?
Male vs Female?
Age?
Specific risk factor
A

Rare - 3 per million in the UK
Male = Female
Middle age
MEN-1 (multiple endocrine neoplasia)

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12
Q

ACROMEGALY CAUSES
Main?
3 others?

A

99% of cases: functional pituitary adenoma
also:
ectopic, hypothalamic tumour, MEN-1

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13
Q

ACROMEGALY SIGNS AND SYMPTOMS
List as many as possible.
Note on diagnosis?

A

Often takes years to diagnose

Headaches
increased size of extremities
sweating
snoring
decreased libido
amenorrhea
skin darkens
wide nose
deep voice
macroglossia
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14
Q

ACROMEGALY COMPLICATIONS

5 examples

A 
Impaired glucose tolerance (40%)
Leading to diabetes mellitus (15%)
Carpal tunnel syndrome
HTN, cardiac problems
Colon cancer
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15
Q

ACROMEGALY DIAGNOSIS

3 steps

A

Test for increased IGF-1 (diagnostic) and GH (non-diagnostic)
Oral glucose tolerance test (OGTT) - glucose should suppress GH
MRI for pituitary adenoma

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16
Q

ACROMEGALY TREATMENT
1st line?
2nd line?
3rd line?

A

1: Trans-sphenoidal surgery (+radiotherapy?)
2: Somatostatin analogues, eg octreotide or lanreotide
3: GH antagonist (pregvisomant)

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17
Q

ADRENAL INSUFFICIENCY CAUSES

2 categories? Examples?

A

Primary (ADDISON’S DISEASE)
autoimmune (80%)
TB, metastatic carcinoma, lymphoma, CMV in HIV, adrenal haemorrhage

Secondary
long term steroid use
hypothalamic-pituitary disease (ACTH)

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18
Q

ADRENAL INSUFFICIENCY EPIDEMIOLOGY
How common?
Can it be fatal? Expand on this

A

Rare - 0.3 per 100,000
Can be fatal - ADDISONIAN CRISIS
untreated w/ bad destruction, leads to dehydration, low BP, tachycardia: possibly death

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19
Q

ADRENAL INSUFFICIENCY SIGNS AND SYMPTOMS?

Split up into 3 categories

A
  1. Due to lack of aldosterone
    hyperkalaemia, hyponatraemia, hypovolemia, metabolic acidosis, craving salts, NAUSEA, fatigue
  2. Due to lack of cortisol
    glucose down, weakness, tiredness, BRONZE PIGMENTATION
  3. Due to lack of androgens
    women only: decreased libido and changes/decreases in body hair
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20
Q

ADRENAL INSUFFICIENCY DIAGNOSIS & TREATMENT
First line?
Second line?

A

1st Blood tests:
sodium, potassium, hormones, etc
2nd ACTH stimulation test:
synthetic ACTH given, measure the cortisol and aldosterone, should increase if healthy

Treatment: Replace hormones
HYDROCORTISONE/PREDNISOLONE (gluco-)
FLUDROCORTISONE (mineral-)

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21
Q

HYPERALDOSTERONISM BACKGROUND
What are the actions of aldosterone? On what cells?
Use these to show signs of hyperaldosteronism.

A 
Principle cell (Na+ and H20 in, K+ out)
Hypernatermia, Hypervolemia, Hypokalaemia

Alpha Intercalated Cell (H+ excretion)
Metabolic alkalosis

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22
Q

HYPERALDOSTERONISM EPIDEMIOLOGY AND RISK FACTORS
What is HYPERALDOSTERONISM a rare cause of? How much?
When to check for HYPERALDOSTERONISM?

A

Rare cause of HTN (less than 1%)

Check for patients with HTN under 35 with no family history

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23
Q

HYPERALDOSTERONISM CAUSES
2 categories?
2 (w/ numbers) x 2

A

Primary (pathology with adrenal gland)

  • adrenal adenoma (CONN’S SYNDROME) (2/3)
  • idiopathic bilateral hyperplasia (1/3)

Secondary (pathology elsewhere, increased Renin)

  • chronic low BP (heart failure)
  • reduced renal perfusion
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24
Q

HYPERALDOSTERONISM CLINICAL FEATURES?
Often?
5.

A

OFTEN ASYMPTOMATIC
Hypertension, Muscle weakness and paraesthesiae
Polydipsia, polyuria

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25
HYPERALDOSTERONISM DIAGNOSIS 1st tests 2nd tests
Blood tests: U and Es, Aldo, Renin (ARR) ECG: (hypokalaemia) 24hr aldosterone test (confirmatory) Adrenal CT scan
26
HYPERALDOSTERONISM TREATMENT Main principle: 3 leads from this principle. Specific medication?
= Treat the cause - Conn's (surgery) - Bilateral Hyperplasia (medication - oral spironolactone, potassium sparing diuretic) - Heart Failure (normal treatment)
27
How are pituitary tumours categorised? | 3 ways with examples
Size - microadenoma <1cm, macroadenoma >1cm Functional (less common - prolactinioma, Cushing's disease, main cause of Acromegaly) Non-functional (more common) Histology Chromophobe Acidophil - somatotrophs, lactrotrophs Basophil - corticotroph, thyrotrophs
28
3 key signs of a large pituitary tumour
Bilateral temporal hemianopia - starts at top Palsy of cranial nerves III, IV, VI (eye movement) CSF rhinorrhoea
29
What is a pituitary apoplexy? | When do it occur?
A rapid pituitary enlargement due to bleeding into the tumour Very serious - needs urgent treatment Can occur as a complication of a pituitary tumour
30
What is a prolactinoma? Symptoms? - M vs W How is it treated? Main example and other
Functional adenoma of lactotrophs that secrete prolactin. W: Amenorrhea and galactorrhea M: Low libido and gynecomastia Treated with BROMOCRIPTINE (main) or CABERGOLINE (dopamine agonists) Treated with surgery if macroadenoma
31
What is a craniopharngioma? Mostly occurs in? Symptoms?
Tumour orgininates from Rathke's pouch | Most commonly occurs in children - causes hypopituitarism symptoms and pituitary gland tumour symptoms
32
``` What is a neuroblastoma? Who does it occur in? Symptoms? 3 types? Dx and Management? ```
Tumour of neuroblasts - don't differentiate properly when forming the adrenal medulla Usually in infants (less than 5 years old) Fever, weight loss, sweating, BRUISING AROUND EYES Differentiated, undifferentiated, poorly differentiated. CT scan, adrenaline and noradrenaline metabolites (HMA and VMA) Surgery, chemotherapy, stem cell or bone marrow transplant
33
What is a pheochromocytoma? What is the base cell? Symptoms? Dx and management?
Rare adrenal gland tumour in the medulla - characterised by the darkening of cells Chromaffin cells PHEochromocytoma: palpitations, headaches, episodic sweating Test for catecholamines in blood Surgery
34
Causes for thyroid nodules?
``` Multinodular goitre Benign follicular adenoma Thyroid cysts (95% - benign) Thyroid cancers (5%) ```
35
Types of thyroid cancers? Which are the most common? Which are the most aggressive? Who do they normally occur in?
DIFFERENTIATED: papillary (70%) - from follicular cells, young follicular (20%) - from follicular cells, middle age medullary (5%) - from calcitonin C cells Anaplastic - (>5%) from follicular, aggressive, poor prognosis
36
Clinical presentation in thyroid tumours
Solitary, painless nodule (hard and immovable) | Later: dysphagia or hoarseness of voice from tumour, goitre?
37
How to diagnose thyroid tumours? 4 possible tests
Fine needle aspiration Blood tests - TSH, T4, T3, calcitonin Radioiodine scan (normally cold) Thyroid ultrascan
38
How to treat thyroid cancers?
Thyroidectomy (partial or full) Thyroid Hormone Replacement (TSH is a growth factor to cancer: will keep it down) Chemotherapy
39
What is goitre? Two types and causes of these types?
= enlarged thyroid gland ``` Diffuse = physiological, Grave's, Hasimoto's Nodular = multinodular, adenoma, cyst, carcinoma ```
40
Prevalence of hypothyroidism vs hyperthyroidism
``` HYPER = 2,5% HYPO = 5% ```
41
Summary of Grave's disease pathophysiology? | Antibody?
Autoimmune disease inducing excess production of thyroid hormone Main: TSH Receptor antibody (TSHR-Ab)
42
``` GRAVE'S DISEASE EPIDEMIOLOGY AND RISK FACTORS Fraction cause of hyperthyroid? Females vs Males? Age? Other risk factors? ```
2/3 cause of HYPERTHYROID Females >> Male (9:1) 40-60 years old Genetics, stress, smoking, other AI diseases
43
GRAVE'S DIAGNOSTIC TRIAD?
Hyperthyroidism: weight loss, despite appetite, goitre, heat intolerance, increased heart rate, sweating, anxiety, thin hair Grave's opthalmopathy: inflammation and sweating of eyes, lid lag, exopthalmos Grave's dermopathy: Pretibial myxoedema - waxy, orange, swelling on anterior of feet
44
MAJOR COMPLICATION OF HYPERTHYROIDISM? Name? Symptoms?
Thyroid storm - needs immediate treatment Heat intolerance into HIGH FEVER Tachycardia into CARDIAC ARRHYTHMIA
45
DIAGNOSTIC TESTS FOR THYROID DISORDERS?
Measure TSH, T3, T4 Antibodies (TPO-Ab, TSHR-Ab, Tg-Ab) Radioiodine scans FBC for anaemia?
46
4 POSSIBLE MANAGEMENT STRATEGIES FOR GRAVE'S?
Beta-blockers (propanolol) Anti-thyroid drugs (carbimazole) Radio-iodine therapy Thyroidectomy
47
Causes of hyperthyroidism? As many as possible
Grave's (main), toxic multinodular goitre, functional thyroid adenoma, thyroiditis, Jod-Basedow (iodine intake), drugs (amiodarone), neonatal, ectopic TSH pituitary tumour
48
Hyperthyroidism symptoms? As many as possible
Weight loss, heat intolerance, fast HR, sweating, anxiety, insomnia, tremor, irritance, diarrhoea, menstrual changes, thin hair, Grave's specific pathologies
49
What is Hashimoto's thyroiditis? | Antigens?
Thyroid gland is attacked by immune system? TPO-Ab (thyroid peroxidase antibody) TgAb (thyroglobulin antibody)
50
HASHIMOTO'S THYROIDITIS: symptoms, and risk factors, management?
Early: often asymptomatic Later: intial goitre, later shrinkage, goitre Women >> Men (7:1), other AI diseases, family history Levothyroxine treatment (thyroid replacement)
51
Causes of hypothyroidism? As many as possible
Iodine deficiency, Hashimoto's thyroiditis, atrophy, surgery, drug-induced (anti-thyroid, amiodarone) Tumour of anterior pituitary, hypothalamic damage
52
Hypothyroidism symptoms? As many as possible | BRADYCARDIC (signs)
``` Weight gain, cold sensitivity, decreased HR, mental slowness, tiredness, lethargy, low mood, constipation B Reflexes Ataxia Dry skin Yawning/Tiredness Cold sensitivity Ascites Round face/weight gain Depression Immobile Cystic fibrosis ```
53
MAJOR COMPLICATION OF HYPOTHYROIDISM? | Symptoms?
MYXOEDEMA COMA (severe) Exaggerated hypothyroidism symptoms: mental slowness, hypothermia, confusion
54
``` siADH BACKGROUND Other name for ADH? What receptor does ADH bind to? What does it cause in the kidney? What triggers release? Biggest cause of what? ```
Vasopessin V2 receptor Causes aquaporin 2 channels to merge with membrane, causing increased water retention in blood Triggered by high osmolarity or decrease in blood volume 25% cause of hyponatraemia
55
siADH AETIOLOGY | List some causes? Categories
Ectopic tumours - release ADH CNS - strokes, meningitis, trauma Pulmonary lesions Hypothyroidism, alcohol withdrawel, drugs
56
siADH SIGNS AND SYMPTOMS Mild and Severe: list as many as possible Signs
Mild: nausea, vomiting, lethargy Severe: muscle cramps, weakness, confusion, ataxia, tremors Signs: decreased level of consciousness, cognitive impairment, seizures, etc
57
``` siADH DIAGNOSIS What would serum and urine sodium be? Hence, plasma and urine osmolality? Which -volaemia? Why test with saline? ```
Serum sodium low Urine sodium high Plasma osmolality low Urine osmolality high Normally, euvolaemic Test with saline - may just be sodium deficient, especially elderly
58
siADH management Principle? Diet change? Two drugs?
Treat underlying cause Restrict fluid intake and increase sodium intake ORAL DEMECLOCYCLINE - induces nephrogenic DI ORAL TOLVAPTAN - V2 blocker, very expesnive
59
Diabetes Insipidus can be defined as... | Number?
Large volume of dilute urine produced, due to impaired water reabsorption >3L per day
60
Two categorical causes of DI with examples?
Cranial DI: decreased ADH idiopathic, congenital, hypothalamic disease, pituitary tumour, sarcoidosis Nephrogenic DI: can't bind or kidney damage CKD, metabolic disorders, gene mutations, drugs
61
Clinical presentation of DI? | Differential diagnosis?
Polyuria, nocturia, polydipsia, general dehydration NO GLYCOSURIA Rules out main ddx: diabetes mellitus Also: hypokalaemia and hypercalcaemia
62
Two diagnostic tests for DI?
Fluid Deprivation Test: Urine osmolality will stay low IM DESMOPRESSIN (ADH analogue) Cranial DI: will be fixed Nephrogenic DI: won't be fixed
63
How to treat cranial DI vs nephrogenic DI?
Cranial: give desmopressin, find cause, stop it Nephrogenic: find cause and stop it, high dose desmopressin, diet control, NSAIDs & Bendroflumethiazide (both inhibit ADH)
64
PARATHYROID BACKGROUND What cells produce parathyroid hormone (PTH)? What are the 4 actions of PTH?
Chief cells * Calcium absorption in stomach increased * Calcium reabsorption in kidney increased (phosphate decreases) * Calcium resorption in bone increased * Involved in activation of vitamin D (same actions as PTH)
65
What are the 5 main causes of hypercalcaemia?
* Hyperparathyroidism & parathyroid disorders * Hypercalcaemia of malignancy * Granulomatous lung diseases (tuberculosis and sarcoidosis) * Medications (diuretics) & dietary supplements * Dehydration
66
What is hypercalcaemia of malignancy? | Why does it occur? 3 reasons
Common metabolic abnormality seen in cancer patients Parathyroid hormone related protein is produced Local osteolysis Tumour production of calcitriol
67
Symptoms of hypercalcaemia? Name as many as possible
Polydipsia, polyuria, tiredness, headaches, nausea, muscle twitches, kidney stones, Note: can be asymptomatic
68
3 types of hyperparathyroidism? How is each treated? How is a diagnosis made?
Primary: increase in PTH due to parathyroid tumour (1: fluid intake, 2: parathyroidectomy) Secondary: insufficient vitamin D or renal failure leading to hypocalcaemia and hyperplasia to produce more PTH (treat cause) Tertiary: fixed secondary hypocalcaemia, but continued PTH secretion due to hyperplasia (1: fluid intake, 2: parathyroidectomy) Dx: calcium and PTH levels, scans - Sestamibi
69
2 types of parathyroid tumour? Which is more common?
Parathyroid adenoma: benign tumour, often functional causing primary hyperparathyroidism Parathyroid carcinoma: rare malignant neoplasm (>1% of parathyroid disease)
70
Cells in the islets of Langerhan: | Names, what they produce, percentage
Beta, insulin, 70% Alpha, glucagon, 20% Delta, somatostatin, 8% F?, polypeptide secreting cells
71
Mechanism of insulin secretion?
Glucose binds to beta cells Phosphorylation into glucose-6-phosphate and ATP formed from ADP K+ channels close, causing depolarisation Calcium channels open, and influx, causes insulin release
72
3 quantitative diagnostic factors for diabetes mellitus? What is used for borderline cases?
``` Random plasma glucose >11 mmol/L Fasting plasma glucose >7 mmol/L HbA1c >48 mmol/mol ``` Impaired glucose tolerance test for borderline cases
73
What is the stress effect on insulin and glucagon by cortisol?
Inhibits insulin Activates glucagon More glucose available to the body
74
What is the mechanism for type 1 DM? Associated with which HLA genes? Inhibited insulin secretion or insulin sensitivity
Beta cells express HLA antigens, auto-immune destruction, beta cell loss, impaired insulin secretion HLA-DR3, HLA-DR4 Impaired insulin secretion
75
Major symptoms of DM? Type 1 specific? Is type 2 normally symptomatic?
Polydipsia (thirst) Polyuria/Nocturia (excessive urine) Glycosuria (glucose in urine) T1 SPECIFIC: Weight loss despite polyphagia Fatigue and irritability
76
What is metabolic syndrome? Increased risk of...?
medical term for a combination of diabetes, high blood pressure (hypertension) and obesity Stroke and heart disease
77
``` KETOACIDOSIS: Who does it occur in? Basic mechanism? 3 ketones? Signs? Treatment? ```
T1 diabetics No insulin -> uncontrolled lipolysis -> FFA's oxidised into ketone bodies Acetoacetate, Acetone, Beta-hydroxybutyrate Signs: hypotension, tachycardia, Kussmaul breathing, ketone breath, dehydration Treatment: rehydration slowly, insulin, replacement of electrolytes
78
``` HHS: What does it stand for? Who does it occur in? Mechanism? Overlap with ketoacidosis? Treatment overlap? ```
Hyperosmolar hyperglycaemic state Occurs in T2 DM Dehydration with high glucose concentration in blood, acting as a solute Does overlap with ketoacidosis, same treatment: rehydration, insulin and replacement of electrolytes
79
How is T1 DM treated? | What are the complications of the major treatment?
Education, healthy diet, regular activity, BMI control, BP and hyperlipidaemia control INSULIN Complications of insulin therapy: Hypoglycaemia, lipohypertrophy of injection site, weight gain, insulin resistance, lifestyle issues
80
3 major risk factors for T2 DM?
Obesity, physical inactivity, family history
81
Complications of uncontrolled diabetes? | 2 categories and examples from each
Microvascular: diabetic retinopathy, diabetic nephropathy, diabetic peripheral neuropathy Macrovascular: CV disease and stroke
82
T2 diabetes control ladder?
Lifestyle change Metformin Metformin + Sulfonylurea Metf + Sulf + Insulin (increase as per severity)
83
T2 DM Medications: class, main example, mechanism, side effect, weight gain or loss? (4)
BIGUANIDE: metformin increases insulin sensitivity and inhibits gluconeogenesis, sickness and diarrhoea Weight loss SULPONHYLUREA: gliclazide stimulate insulin release by closing K+ pump on beta cells, hypoglycaemia Weight gain ``` DPP4 INHIBITORS: sitagliptin stimulate incretins (hormones released after eating, which stimulate insulin release) No weight change ``` GLITAZONES: pioglitazone enhance uptake of fatty acids and glucose (more fat made) Weight gain
84
4 other types of diabetes?
Maturity-onset diabetes of the young (MODY) Gestational diabetes Drug-induced diabetes Neonatal diabetes
85
Hypoglycaemia: Measurement in blood? Symptoms? Whipple's triad?
Roughly <3.9mmol/L Trembling, palpitations, sweating, anxiety, confusion, hunger Low blood glucose, symptomology, relief after treatment
86
What are carcinoid tumours? Where are the often found? Prognosis and signs? Treatment?
Slow growing tumours of neuroendocrine cells (enterochromaffin cells) Often found in GI tract, also: ovary, testes, bronchi Bad prognosis, heart failure and bronchoconstriction Can cause: CARLOAD CRISIS (mediators flood out) Treatment: octreotide (somatostatin analogue)
87
Two major puberty disorders?
Precocious puberty - secondary sexual characteristics appear before 8 y/o in girls and 9 y/o in boys (GNRH dependant or independent) Delayed puberty - lack of any pubertal signs by the age of 13 y/o in girls and 14 y/o in boys
88
Tanner stages: boys
1 - testicular size increases 2 - sparse pubic hair, increase in testicular size (>3ml) 3 - thicker hair, spreads to mon pubis, penis growth 4 - further enlargement, dark scrotal skin colour, not spreads to medial thighs 5 - adult size and shape, spread to medial surface of thighs
89
Tanner stages: girls
1 - no pubic hair, elevation of papilla 2 - breast bud, enlargement of areola, pubic hair 3 - darker, coarse hair, further enlargment 4 - thick adult hair, not spread to thighs, areola and papilla secondary mound 5 - adult size and shape, just papilla projected

Phase 2a (9 decks)

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