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ΩΩ 4 Bateman - Specialities + Endo + GI + Liver > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What peptide is used in making insulin?

A

C-peptide

Gliclazide functions by releasing vesicles stored within the pancreas containing insulin and C-peptide. This happens because insulin is derived from proinsulin and C-peptide is formed as a byproduct.

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2
Q

WHAT IS ACROMEGALY?

What is it caused by?

https://www.youtube.com/watch?v=54h3IUbvHDU

A

This is an abnormal enlargement of the extremities of the skeleton caused by hypersecretion of the pituitary growth hormone after epiphysial fusion

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3
Q

What does the hypothalamus release? What does this cause? In acromegaly

A

Release growth hormone releasing hormone

Stimulates pituitary to release growth hormone

Somatostatin (growth hormone inhibiting hormone)
Decrease growth hormone release from pituitary

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4
Q

What is the difference between gigantism and acromegaly?

A

Difference in when growth hormone is released

  1. Gigantism - Before the closure of the epiphyseal plates, end up very tall
  2. Acromegaly - After the closure of the epiphyseal plates
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5
Q

What is the cause of acromegaly?

A
  1. 95% of cases are due to a growth hormone secreting Pituitary adenoma
  2. Less than 3% of cases are due to ectopic GHRH production - carcinoid tumours especially bronchial, pancreatic islet tumours or adrenal tumours
  3. Less than 2% of cases result from ectopic GH secreting pancreatic islet tumours
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6
Q

What are the symptoms of acromegaly?

A
  1. Coarse facial appearance, spade-like hands, increase in shoe size
  2. Large tongue, prognathism, interdental spaces
  3. Excessive sweating and oily skin: caused by sweat gland hypertrophy
  4. Features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia
  5. Raised prolactin in 1/3 of cases → galactorrhoea
  6. 6% of patients have MEN-1
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7
Q

What are the signs of acromegaly?

A
  1. Skin darkening
    • Acanthosis nigricans
    • Face
  2. Big supraorbital ridge
    • Interdental separation
    • Macroglossia
    • Prognathism
    • Laryngeal dyspnoea
  3. Spade-like hands and feet
    • Tight rings
    • Carpal tunnel syndrome
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8
Q

How can you diagnose acromegaly?

A
  1. IGF-1 (somatomedin) tells tissues to grow
    • Elevated
  2. Glucose tolerance test
    • 75g or glucose
    • Wait 90 mins measure growth hormone levels
    • Will stay elevated! Should decrease
  3. Pituitary MRI
    • Could be no tumour, could be ectopic source

Growth hormone levels
Not usually used because pulsatile

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9
Q

What is the treatment of acromegaly?

A
  1. Trans-sphenoidal Surgery - FIRST LINE
  2. Medications to suppress GH
    • ​​Somatostatin analogue
      • Octreotide
    • Recombinant GH receptor antagonist
      • Pegvisomant
    • Dopamine agonist
      • Bromocriptine
  3. Radiation is sometimes used in older patinets or failed medicaitons
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10
Q

What are the complications of acromegaly?

A
  1. Hypertension
  2. Diabetes (>10%)
  3. Cardiomyopathy - MAIN CAUSE OF DEATH
  4. Colorectal cancer
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11
Q

WHAT IS CUSHING SYNDROME?

https://www.youtube.com/watch?v=ea1sXgd5ui8

A

Cushing’s syndrome refers to the set of clinical features resulting from persistently and inappropriately elevated levels of glucocorticoid. Usually the condition is iatrogenic

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12
Q

What is the electrolyte abnormality in cushing syndrome?

A

Hypokalaemic metabolic alkalosis

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13
Q

What does excess cortisol lead to?

Overload of what it normally reacts with

A
  1. Severe muscle, bone and skin breakdown
  2. Hypertension
  3. Inhibit gonadotropin releasing hormone from hypothalamus
  4. Dampens inflammatory response
  5. More susceptible to infections
  6. Impair normal brain function
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14
Q

What does elevated breakdown of muscle, bone and skin cause?

(What does this produce)

IN CUSHINGS

A

Elevated blood glucose

High insulin levels
Targets adipocytes in center of body
Activates lipoprotein lipase
Accumulate more fat molecules

Cause
Moon face
Buffalo neck hump

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15
Q

How is hypertension caused by excess cortisol?

A
  1. Amplifies effect of catecholamines on blood vessels
  2. Cortisol cross reacts with mineralcorticoid recptors
  3. Mineralcorticoids released from zona glomerulosa
  4. Triggers mineralcorticoid effect which is increasing blood pressure by retaining fluid - ALDOSTERONE
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16
Q

What are the causes of Cushing’s?

A
  1. ACTH dependent causes
    • Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
    • Ectopic ACTH production (5-10%): e.g. small cell lung cancer is the most common causes
  2. ACTH independent causes
    • Iatrogenic: steroids
    • adrenal adenoma (5-10%)
    • adrenal carcinoma (rare)
    • Carney complex: syndrome including cardiac myxoma
    • micronodular adrenal dysplasia (very rare)
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17
Q

What are the symptoms of Cushing’s?

A
  1. Muscle wasting and thin extemities
  2. Easy brusing
  3. Abdominal striae
  4. Fractues - osteoporisis
  5. Full moon shaped face
  6. Buffalo hump
  7. Truncal obesity
  8. Hypergylcemia
  9. Diabetes mellitius
  10. Hypertension
  11. Cardiovascular disease risk
  12. Increase vulnerability to infections
  13. Poor wound healing
  14. Amenorrhea
  15. Psychiatric
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18
Q

What is the diagnosis of Cushing’s?

A
  1. ENDOGENOUS / 24 urine sample
    • Measuring free cortisol - urine 3.5-4.5 microgram/day
  2. 1 mg Dexamethasone suppresion test
    • Low dose of dexamethasone (steroid)
    • Supressess ACTH production
    • Should cuase decrease cortisol levels <2
  3. 2mg Dexamethasone Supression Test
    • ACTH plasma levels checked
      • Low ACTH + Cotrisol gives diagnosis of
      • Adrenal adenomas and carcinoma
      • High ACTH + Cortisol gives diagnosis of
      • Cushing disease and ectopic ACTH production
  4. 8mg Dexamethasone Supression
    • Pituitary - Cortisol + ACTH suppressed
    • Ectopic - Cortisol + ACTH NOT suppressed
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19
Q

What types of imaging can be used for Cushing’s?

A
  1. MRI of pituitary
  2. CT of adrenals
  3. CT of chest abdomen or pelvis for ectopic
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20
Q

What is the treatment for Cushing’s?

A
  1. Exogenous
    • Drug is gradually stopped
    • Adrenal crisis if too fast
    • Adrenal glands might be atrophied
  2. Endogenous
    • Surgery
    • Adrenal steroid inhibitors - Ketoconazole and metyrapone
    • Most useful ectopic

ALL PATIENTS MUST UNDERGO LABROATORY EVALUATIONS SCREENING FOR HORMONE HYPERSECRETION AND HYPOPITUITARISM

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21
Q

What are you at risk of if you have your adrenals removed?

A

Nelson’s syndrome

Skin pigmentation increase

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22
Q

WHAT IS SYNDROME OF INAPPROPRIATE SECRETION OF ADH?

(Start with what it results in)

https://www.youtube.com/watch?v=0NHT8ERUBo0

A
  1. Hyponatremia and hypo-osmolality
  2. From inappropriate, continued secretion of ADH
  3. Despite normal or increased plasma volume
  4. Which results in impaired water excretion
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23
Q

What causes SIADH?

A

Drug-induced

  • Selective serotonin reuptake inhibitors
  • Carbamazepine
  • Tricyclic antidepressants

Neoplastic

  • Small cell lung cancer
  • Mesothelioma
  • GI tract malignancy

Pulmonary

  • Pneumonia - especially Legionella and Mycoplasma
  • Tuberculosis

CNS

  • Tumour
  • Meningitis, encephalitis
  • Head injury

Miscellaneous

  • Guillain–Barre syndrome
  • Multiple sclerosis
  • Acute intermittent porphyria
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24
Q

What are the symptoms caused by in SIADH?

A

Derived from decreased sodium in the blood

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25
Q

What are the symptoms of SIADH?

A

Stupor/coma

Anorexia (nausea and vomiting)

Lethargy

Tendon reflexes decreased

Limp muscles (weakness)

Orthostatic hypotension

Seizures/headache

Stomach cramping

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26
Q

What is the diagnosis of SIADH?

A

Sodium

  • Plasma sodium concentration <135 mmol/l
  • Urinary sodium concentration >30mmol/L

Osmolality

  • Plasma osmolality <280 mOsmol/kg
  • Urine osmolality > 100 mOsmol/kg

Other

  • Patient clinically euvolaemic
  • Absence of clinical or biochemical features of adrenal and thyroid dysfunction.
  • No diuretic use (recent or past)
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27
Q

What is the treatment for SIADH?

A

Treat underlying cause

Acute

Hypertonic (3%) saline given via continuous infusion
Intravenous furosemide 20 to 40 mg

Chronic

For most other cases of mild-to-moderate SIADH, fluid restriction represents the least toxic therapy, and has generally been the treatment of choice

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28
Q

WHAT IS PRIMARY AND SECONDARY HYPOTHYROIDISM?

A

Primary is a reduction in thyroxin (T4)

Secondary is a reduction in TSH

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29
Q

What are the causes of primary hypothyroidism?

A
  1. Primary atrophic hypothyroidism (No goitre)
  2. Hashimoto’s thyroiditis (Goitre)
  3. Iodine deficiency
  4. Post-thyroidectomy / radioiodine / antithyroid drugs
  5. Lithium / amiodarone
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30
Q

What are the causes of secondary hypothyroidism?

A

Hypopituitarism

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31
Q

What is the epidemology of hashimoto’s thyroiditis?

A

Older Women

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32
Q

What are the symptoms of hypothyroidism?

A

RS
Hoarse voice
GI
Constipation
Int
Cold intolerance
Endo
Weight gain
UG
Menorrhagia
MSK
Myalgia, weakness
Neuro / Psych
Tired, low mood, dementia

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33
Q

What are the signs of hypothyroidism?

A
  • *B**radycardic
  • *R**eflexes relax slowly
  • *A**taxia (cerebellar)
  • *D**ry, thin hair / skin
  • *Y**awning / drowsy / coma
  • *C**old hands +/- ↓T°C
  • *A**scites
  • *R**ound puffy face
  • *D**efeated demeanour
  • *I**mmobile +/- Ileus
  • *C**CF
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34
Q

What are the investigations for hypothyroidism?

A
  1. TFT
    • TSH RAISED
  2. Lipids/cholesterol
    • High
  3. FBC
    • Macrocytic anaemia
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35
Q

What are the disease associations of hypothyroidism?

A

AUTOIMMUNE

  1. VITILIGO
  2. Type 1 Diabetes Mellitus
  3. Addison’s disease
  4. Pernicious anaemia
  5. Primary biliary cirrhosis

INHERITED

  1. Turner’s syndrome
  2. Down’s syndrome
  3. Cystic fibrosis
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36
Q

What is the treatment of hypothyroidism?

A
  1. Levothyroxine (T4)
  2. Higher doses in the young
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37
Q

When should calcium be taken if patient is also taking levothyroxine?

A

Calcium 4 hours after levothyroxine

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38
Q

WHAT A HYPOTHYROID CRISIS?

A

Myxoedemic coma

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39
Q

What are the features of myxoedema coma?

A

Myxoedema coma typically presents with confusion and hypothermia

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40
Q

What is the treatment of a myxoedema coma?

A
  1. IV thyroid replacement
  2. IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)
  3. THEN IV fluid
  4. electrolyte imbalance correction
  5. sometimes rewarming
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41
Q

WHAT IS HASHIMOTO’s THYROIDITIS?

(inside hypothyroidism)

A

Autoimmune disease

T cell mediated attack

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42
Q

What are the symptoms of hasimoto’s thyroiditis?

A
  1. Goitre or hypothyroidism or both
  2. Enlargement is usually slow and painless but rarely, may be more rapid and painful
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43
Q

What are the investigations for hasmimoto’s thyroiditis?

A

The condition may be suspected clinically on the basis of the goitre with or without hypothyroidism.

  1. Serum TSH is usually raised
    • Measurement of antithyroid antibodies reveal:
      * *Thyroid peroxidase antibodies (TPO)** (previously known as thyroid microsomal antibodies) - HIGH titre
    • Thyroglobulin antibodies (TgAb) - HIGH titre
  2. Biopsy may be necessary to distinguish it from a carcinoma of the thyroid
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44
Q

What is the treatment of hasimoto’s thyroiditis?

A
  1. If the patient is hypothyroid then oral thyroxine may keep the patient euthyroid and lead to resolution of the goitre.
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45
Q

WHAT IS TOXIC MULTINODULAR GOITRE?

A

Toxic multinodular goitre describes a thyroid gland that contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism

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46
Q

What is the treatment for toxic multinodular goitre?

A
  1. Radioactive iodine
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47
Q

WHAT IS HYPERTHYROIDISM?

A

Too much thyroid hormones

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48
Q

What are the causes of hyperthyroidism?

A
  1. GRAVES’ DISEASE
  2. TOXIC MULTINODULAR GOITRE
  3. EXOGENOUS (Iodine / T4 excess)
  4. DE QUERVAIN’S THYROIDITIS (post-viral)
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49
Q

What are the symptoms of hyperthyroidism?

A

CVS
Palpitations
GI
Diarrhoea
Int
Heat intolerance
Endo
↓Weight, ↑appetite
UG
Oligomenorrhoea +/- infertility
Neuro / Psych
Tremor, irritability, labile emotions

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50
Q

What are the signs of hyperthyroidism?

A

HANDS
Palmar erythema; warm, moist skin; fine tremor

PULSE
Tachycardia; SVT; AF

FACE
Thin hair; lid lag / retraction

NECK
Goitre; nodules; bruit

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51
Q

What are the investigations for hyperthyroidism?

A
  1. TFT
    • Increase T4 and T4
  2. FBC
    • Normocytic anaemia
  3. ESR (↑)
  4. Calcium (↑)
  5. LFT (↑)
  6. Thyroid autoantibodies
  7. Visual fields, acuity, eye movements
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52
Q

What is the treatment for hyperthyroidism?

A

Depends on underlying cause

  1. β-blockers
    • Propanolol(rapid control of symptoms)
  2. Antithyroid medication
    • Carbimazole SE = AGRANULOCYTOSIS
    • Block and replace (carbimazole + thyroxine)
    • Propythiouracil
  3. Radioiodine (131I)
  4. Thyroidectomy
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53
Q

WHAT HAPPENS IN GRAVES DISEASE?

What are the triggers?

A

Autoimmune

IgG autoantibodies bind to and stimulate TSH receptors

Infection, stress, childbirth

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54
Q

What is a risk factor for grave’s?

A

Smoking

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55
Q

What are the symptoms of graves disease?

A
  1. Hyperthyroidism
  2. Diffuse goitre
  3. Extrathyroid features:
    • Thyroid acropachy, a triad of:
      Digital clubbing
      Soft tissue swelling of the hands and feet
      Periosteal new bone formation
    • Graves’ ophthalmology - 40% of cases
    • Pretibial myxoedema - 5% of cases
    • Thyroid acropachy - rare
    • Onycholysis - not specific to Grave’s!!
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56
Q

What are the investigations for Grave’s disease?

A
  1. Thyroid peroxidase antibodies
  2. TSH receptor stimulating antibodies
  3. Radioactive iodine uptake and scan
    • Diffuse, homogenous, increase uptake of radioactive idodine
  4. Thyroid ultrasound scan
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57
Q

What is the treatment of Grave’s disease?

A
  1. Propanolol
    • Use to help block the adrengergic effects
  2. Carbimazole - first-line
  3. Radioactive idodine
  4. Thyroidectomy
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58
Q

What are some causes of goitre?

A
  1. Physiological
  2. Graves’ disease
  3. Hashimoto’s thyroiditis
  4. De Quervain’s - TENDER GOITRE
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59
Q

WHAT IS A THYROID STORM?

A

Thyroid storm is a rare but life-threatening complication of thyrotoxicosis. It is typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature. Iatrogenic thyroxine excess does not usually result in thyroid storm.

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60
Q

What are the precipitating events to a thyroid storm?

A
  1. thyroid or non-thyroidal surgery
  2. trauma
  3. infection
  4. acute iodine load e.g. CT contrast media
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61
Q

What are the clinical features of a thyroid storm?

A
  1. fever > 38.5ºC
  2. tachycardia
  3. confusion and agitation
  4. nausea and vomiting
  5. hypertension
  6. heart failure
  7. abnormal liver function test - jaundice may be seen clinically
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62
Q

What is the management of a thyroid storm?

A
  1. Symptomatic treatment e.g. paracetamol
  2. Treatment of underlying precipitating event
  3. Beta-blockers: typically IV propranolol
  4. Anti-thyroid drugs: e.g. methimazole or propylthiouracil
  5. Lugol’s iodine
  6. Dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3
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63
Q

WHAT ARE THE MOST LIKELY THYROID CELL TYPE CANCERS?

A
  1. Papillary (60%)
  2. Follicular (≤25%)
  3. Medullary (5%)
  4. Lymphoma (5%)
  5. Anaplastic
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64
Q

What are some causes of thyroid cancer?

A
  1. Low dose radiation
  2. Radioiodine
  3. A history of radiation exposure to the neck area is associated with increased risk of thyroid cancer
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65
Q

What are the symptoms of thyroid cancer?

A

A rapidly growing hard thyroid mass with lymphadenopathy and indicators of extrathyroidal invasion

e.g. hoarseness, dysphagia is suggestive of maligancy.

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66
Q

What are the investigations for thyroid cancer?

A

Fine needle biopsy - the most effective method of distinguishing benign from malignant nodules.

Tumour products - basal and pentagastrin-stimulated serum calcitonin distinguishes medullary carcinoma.

Ultrasound - not useful as a primary test but may help to distinguish cystic lesions

Thyroid scanning with radioiodine - thyroid cancer is characteristically

Chest X-ray - lung secondaries

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67
Q

What is the treatment for thyroid cancer?

A

Most thyroid tumours are treated surgically with follow up radioiodine ablation

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68
Q

What is used to yearly to detect for early thyroid cancer reoccurance?

A
  1. Thyroglobulin levels
  2. Except in medullary - calcitonin
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69
Q

WHAT IS PRIMARY ADRENAL INSUFFIENCY?

https://www.youtube.com/watch?v=V6XcBp8EV7Q

A

The adrenal glands can’t produce enough hormones

Aldosterone and cortisol

Primary refers to the adrenal glands themselves

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70
Q

What are the different layers of the adrenal glands?

A

Cortex
Zona glomerulosa
Zona fasiculata
Zona reticularis

Medulla

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71
Q

What does each layer of the adrenal cortex produce?

A
  1. Zona glomerulosa - Aldosterone
  2. Zona fasiculata - Cortisol and glucocorticoids
  3. Zona reticularis - Make androgens E.g. deyhydroepiandosterone, Precursor to testosterone
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72
Q

What does the renin, angiotensin aldosterone system do?

A

Decrease potassium

Increase sodium

Increase blood volume and pressure

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73
Q

What are the causes of primary adrenal insuffiency?

A
  1. Autoimmune destruction
  2. Tuberculosis
  3. Metastases (e.g. bronchial carcinoma)
  4. Meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
  5. HIV
  6. Antiphospholipid syndrom
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74
Q

What happens if the zona glomerulosa is destroyed?

A
  1. Aldosterone levels fall
  2. Leads to high potassium levels in the blood
  3. Low sodium - hyponatremia
  4. Low sodium water moves out of the blood vessels
  5. Hypovolemia
  6. High protons in blood
  7. Metabolic acidosis since it’s caused by the kidneys
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75
Q

What are the symptoms if the zona glomerulosa is affected?

A

Cravings for salty foods

Nausea and vomiting

Fatigue

Dizzyness

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76
Q

What are the symptoms if the zona fasiculata is destroyed?

A

Fatigue in times of stress

Hyperpigmentation on knuckles and joints

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77
Q

What happens if the zona reticularis is destroyed?

A

Men not affected

Testes major source of male androgens

Females
Loss of pubic hair
decreased sex drive

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78
Q

What does primary adrenal insuffiency usually need to cause symptoms?

A

Symptoms often slow,

Major stressor comes along
Injury, surgery or infection
Cause symptoms to appear

Sudden need for aldosterone and cortisol

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79
Q

How can you diagnose addison’s disease?

A
  1. ACTH hormone test
    • Small amount of synthetic ACTH injected
    • Measure cortisol and aldosterone produced
    • Both will be low
  2. Serum cortisol
  3. Bloods
    • FBC(anaemia, eosinophilia)
    • U&E(↓Na+, ↑K+, ↑Ca2+, ↑Urea)
    • BM(↓)
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80
Q

What is the treatment for addison’s disease?

A
  1. Cortisol - hydrocortisone
  2. Aldosterone - Fludrocortisone
  3. Dehydroepiandrosterone (DHEA)
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81
Q

If a patient with Addison’s disease becomes acutely unwell what is needed to be done to their medications?

A
  1. Double the glucocorticoid
  2. Keep the fludrocortisone dose the same
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82
Q

What is it called when the body suddenly needs aldosterone or cortisol and the body can’t deliver?

A

Addisonian crisis (acute primary adrenal insufficiency)

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83
Q

What syndrome can cause an addisonian crisis?

A

Waterhouse-friderichsen syndrome

Causes blood vessels in adrenal glands to rupture

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84
Q

What are the symptoms of addisonian crisis?

A
  1. Pain in back abdomen or legs
  2. Vomiting and diarrhoea leading to dehydration
  3. Low blood pressure leading to loss of consciousness
  4. Death
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85
Q

What is the treatment of an Addisonian crisis?

A
  1. Hydrocortisone 100 mg im or iv
  2. 1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
  3. Continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
  4. Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
86
Q

WHAT IS SECONDARY ADRENAL INSUFFICIENCY?

A

Lack of ACTH

and therefore cortisol

87
Q

What are the causes for secondary adrenal insufficiency?

A
  1. Pituitary mass or infection
    • The basic failure is in the elaboration of ACTH
88
Q

Why is aldosterone unaffected in secondary adrenal insufficiency?

A

Aldosterone secretion independent of ACTH

89
Q

What are the symptoms of secondary adrenal insufficiency?

A

Features common to both primary and secondary hypoadrenalism include:

  1. Lassitude and muscle weakness and pain
  2. Hypotension
  3. Gastro-intestinal symptoms - anorexia, weight loss, nausea and vomiting, intermittent abdominal pain, salt craving
  4. Decrease in axillary and pubic hair - common in women
  5. Depression

Pigmentation only occurs in primary hypoadrenalism, due to high ACTH

90
Q

What is the diagnosis of secondary adrenal insufficiency?

A

Bloods
Low cortisol

91
Q

What is the treatment for secondary adrenal insufficiency?

A
  1. Glucocorticoid analogues - hydrocortisone
    • 10mg in morning
    • 5 mg at midday
    • 5mg in evening
  2. Fludrocortisone
    • ​​One dose

​​

92
Q

What is the cause of tertiary adrenal insufficiency?

A

Chronic administration of high doses of glucocorticoids

93
Q

WHAT IS CONN’S SYNDROME?

https://www.youtube.com/watch?v=JBfkGNr01V8&t=1s

A

Hyperaldosteronism

94
Q

What is the cause of Conn’s syndrome?

A
  1. Bilteral adrenal nodular hyperplasia - MOST COMMON
  2. Adrenal adenoma
95
Q

If there is high aldosterone levels, what will the ion levels be in the blood?

A

Potassium low

Sodium high

Less protons

96
Q

What do the ions in the blood in conn’s syndrome cause?

A

Hypertension

Metabolic alkolosis

97
Q

What are the symptoms of Conn’s syndrome?

A

Headaches and flushing

Constipation
Weakness
Heart rhythm changes

98
Q

What is the diagnosis of Conn’s syndrome?

A

Preliminary investigations

  1. Hypokalaemia*- ensuring absence of diuretics, steroids, laxatives
  2. ​Hypernatraemia - sodium may be mildly elevated or normal
  3. Hypertension
  4. Metabolic alkalosis

Special investigations

  1. Bloods - aldosterone/renin ratio
    • High levels of aldosterone
    • Low levels of renin
  2. 24 hour urinary aldosterone - raised in primary disease

Differentiate between adenoma and hyperplasia

  1. CT
  2. Adrenal vein sampling
  3. Measure plasma aldosterone 9am after overnight recumbency
99
Q

What is the treatment for Conn’s syndrome?

A
  1. Identification of underlying cause
  2. If due to adenoma
    • Surgery after 4 to 6 weeks of spironolactone therapy
  3. if due to adrenal hyperplasia
    • Spironolactone or amiloride is generally sufficient
100
Q

WHAT DIABETES MELLITUS?

A

Trouble moving glucose from blood into cells

High level in blood

Not alot in cells

101
Q

What are the different types of diabetes?

A

Type 1
10%

Type 2
90%

102
Q

What is the cause of type 1 diabetes?

A

Bodies own cells attack the pancreas

Type 4 hypersensitivty reaction
Cell-mediated response

103
Q

What are the symptoms of type 1 diabetes?

A
  1. Polydipsia
  2. Polyuria, with associated nocturia or enuresis
  3. Glycosuria
  4. Weight loss due to dehydration and catabolism
  5. Polyurea, polydipsia (due to osmotic diuresis), polyphagia,
  6. Constipation
  7. Fatigue
  8. Cramps
  9. Blurred vision
  10. Bacterial and fungal infections e.g. - candidiasis
104
Q

What are some complications of diabetics with bad control?

A

Vascular disease

Nephropathy

Neuropathy

Diabetic foot

Retinopathy

105
Q

What are the investigations for type 1 diabetes?

A

Diabetes is diagnosed on the basis of history (ie polyuria, polydipsia and unexplained weight loss) PLUS

  1. A random venous plasma glucose concentration >= 11.1 mmol/l
  2. OR a fasting plasma glucose concentration >= 7.0 mmol/l (whole blood >= 6.1 mmol/l)
  3. OR 2 hour plasma glucose concentration >= 11.1 mmol/l 2 hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT)
  4. an HbA1c of 6.5% (48 mmol/mol) is recommended as the cut point for diagnosing diabetes (i.e. HbA1c >= 6.5% (48 mmol/mol) is sufficient for the diagnosis of diabetes)
106
Q

What is the treatment for type 1 diabetes?

A

Lifelong insulin injections

Education

107
Q

What are the diabetic emergencies?

A
  1. Hypoglycaemia
  2. Hyperglycaemia
  3. Diabetic ketoacidosis
  4. Hyperosmolar non-ketotic hyperglycemia
108
Q

What are the sick day rules for diabetes mellitus?

A
  1. Increase frequency of blood glucose monitoring to four hourly or more frequently
  2. Encourage fluid intake aiming for at least 3 litres in 24hrs
  3. If unable to take struggling to eat may need sugary drinks to maintain carbohydrate intake
  4. It is useful to educate patients so that they have a box of ‘sick day supplies’ that they can access if they become unwell
  5. Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis
109
Q

What is it important not to stop when a diabetic patient is sick?

A

Their normal medication

Keep taking insulin

110
Q

What is the first line antihypertensive for a diabetes type 2 patient?

A
  1. ACE inhibitor
  2. ARB if black african
111
Q

When do diabetic patients need to inform the DVLA and surrender their license?

A

After more than one hypoglycaemic episode requiring help

112
Q

How often should diabetic patients measure their blood glucose?

A

At least 4 times a day, including before each meal and before bed

113
Q

Which condition is important to factor in when measuring HbA1c in diabetic patients?

A

Hereditary spherocytosis

Sickle cell

Anytnhing that makes red blood cells live longer

114
Q

What is the treatment of a peripheral neuropathy e.g. diabetic?

A
  1. First-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin
  2. If the first-line drug treatment does not work try one of the other 3 drugs
  3. Tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
  4. Topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
  5. Pain management clinics may be useful in patients with resistant problems
115
Q

What are the rules for driving a HGV with diabetes?

A
  1. Can drive a HGV
  2. Must meet hypoglycaemic control standards
116
Q

WHAT IS DIABETIC KETOACIDOSIS?

A

Biochemical triad of

  1. Ketonaemia
  2. Hyperglycaemia
  3. Acidaemia
117
Q

What can ketones do to the blood?

A

Make the blood acidic

Kussmaul respiration

Deep/labored breathing
To reduce CO2
Reduce acidity

118
Q

How can a diabetic ketoacidosis happen in somebody who already has insulin treatment?

A
  1. A stress e.g. infection
  2. Release of epinephrine
  3. Release of glucagon
  4. More glucose in blood
  5. Loss of glucose in urine
  6. Loss of water
  7. Dehydration

Need for alternative energy
Generation of ketone bodies

119
Q

What are the symptoms of diabetic ketoacidosis?

A
  1. Polyuria with polydipsia – commonest presenting symptom
  2. Vomiting
  3. Preceding febrile illness
  4. Abdominal pain
  5. Kussmaul respirations
  6. Acetone breath
120
Q

What do the ketone bodies break down into? What does this cause to the breath?

A

Acetone

Fruity smell

121
Q

What are the investigations for DKA?

A
  1. Serum glucose level
    • Usually greater than 250 mg/dL (13.9 mmol/L)
  2. Arterial blood gas measurement
    • pH varies from 7.00 to 7.30
  3. Serum electrolytes
    • Bicarbonate level - <18 mmol/L (18 mEq/L)
    • Serum sodium level - usually low
    • Serum potassium - may be low, normal, or elevated
    • Magnesium – usually low but can be normal
  4. Blood urea nitrogen, creatinine levels
  5. Serum ketone level
  6. Urinalysis
    • Confirms the presence of glucose and ketones
    • Positive for leukocytes and nitrites in the presence of infection
122
Q

What is the diagnostic criteria of DKA?

A
  1. Glucose > 11 mmol/l or known diabetes mellitus
  2. pH < 7.3
  3. Bicarbonate < 15 mmol/l
  4. Ketones > 3 mmol/l or urine ketones ++ on dipstick
123
Q

What is the treatment for diabetic ketoacidosis?

A
  1. Fluids for dehydration
    • 0.9% sodium chloride
  2. Insulin to lower blood glucose
    • 0.1 units/kg/hour
  3. When blood glucose falls below 15 mmol/l
    • 5% dextrose
  4. Electrolytes (K+)
  5. Long-acting insulin continued should be continued, short-acting insulin should be stopped
124
Q

What is definied as DKA resolution?

A
  1. pH >7.3 and
  2. Blood ketones < 0.6 mmol/L and
  3. Bicarbonate > 15.0mmol/L
125
Q

What are the complication of DKA?

A
  1. Gastric stasis
  2. Thromboembolism
  3. Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
  4. Iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
  5. Acute respiratory distress syndrome
  6. Acute kidney injury
126
Q

What is the difference between diabetic and alcoholic ketoacidosis?

A
  1. Normal or low glucose in alcoholic ketoacidosis
127
Q

What is the first-line treatment for newly diagnosed diabetic patients after a DKA?

A

Basal-bolus insulin regimen with twice-daily insulin detemir

128
Q

WHAT IS TYPE 2 DIABETES MELLITUS?

A

Body makes insulin but the cells don’t respond

Not fully understood

129
Q

What are the risk factors for type 2 diabetes?

A

Obesity

Lack of exercise

Hypertension

130
Q

What is normoglycemia?

A

Insulin levels high when cells don’t respond to insulin

Blood glucose levels remain normal

131
Q

What are the symptoms of type 2 diabetes mellitus?

A
  1. Polydipsia
  2. Polyuria, with associated nocturia or enuresis
  3. Glycosuria
132
Q

What is the test for diabetes type 2?

A

Fasting glucose
No food or drink for 8 hours
7 mmol/l or over indicates diabetes

Non-fasting or random glucose
Over 11.1 mmol/l

Oral glucose tolerance
Over 11.1 mmol/l at 2 hours

HbA1C
Percentage or red blood cells with glucose on
48 or higher

133
Q

What are the investigations for diabetic nephropathy?

A
  1. all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
  2. should be an early morning specimen
  3. ACR > 2.5 = microalbuminuria

Start with a spot urine sample

If abnormal then do first-pass morning urine specimin

134
Q

What do asymptomatic diabetic patients with a high HbA1c need?

A

Another HbA1c to confirm

135
Q

What is the management of diabetes type 2?

A
  1. Metformin
  2. SU - e.g. Gliclazide - HYPOHLYCAEMIA - HNF-1 alpha
  3. DPP-4i - GLIPTINS
  4. Pioglitazone
  5. SGLT-2i - GLIFLOZINS - Genitalia (fournier’s gangrene)
136
Q

What systemic problems can diabetes cause?

A

Retinopathy

Kidneys
Nephrotic syndrome

Nerves
Decrease in sensation
Stocking-glove distribution

137
Q

How does metformin work?

A

Improves insulin sensitivity by

  1. Actions upon the liver:
    reducing hepatic gluconeogenesis and glycogen breakdown
  2. Actions upon skeletal muscle and adipose tissue:
    increasing insulin-stimulated glucose uptake and oxidation and, in muscle, increasing glycogen formation
138
Q

How do sulphoylureas work? SE?

A

Augmentation of secretion of insulin from pancreatic beta-cells.

Sulphonylureas may also cause a reduction in serum glucagon and potentiate the action of insulin at the extrapancreatic tissues

WEIGHT GAIN

139
Q

How do DDP-4i work?

A
  1. In response to a meal, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are released (these hormones are termed incretin hormones)
  2. These incretin hormones stimulate insulin and suppress glucagon release (both in a glucose-dependent manner), delay gastric emptying, and increase satiety
  3. Incretins are rapidly degraded by dipeptidyl peptidase-4 (DPP-4)
  4. DPP-4 inhibitors are a class of oral antihyperglycemic agents that work via slowing incretin degradation
  5. DPP-4 inhibitors enhance meal-stimulated active GLP-1 and GIP levels by two- to threefold
140
Q

What is the difference between diabetes type 1 and diabetes type 2?

A

Factors favouring type 1

  1. Rapid onset of osmotic symptoms
  2. Normal or low body weight or rapid weight loss
  3. Ketonaemia >=3mmol/l on capillary testing or ketonuria
  4. Family or personal history of other autoimmnune conditions
  5. Failure to respond to oral therapy
  6. Positive antibody test (anti-GAD, insulin autoantibodies (IAA) and islet cell antibodies (ICA) most commonly used)
  7. Urine C-peptide:creatinine ratio less than 0.5nmol/l
141
Q

What is needed for impaired fasting glucose?

A

Two readings 6.1-7 mmol/l

142
Q

WHAT IS HYPERGLYCEMIC HYPEROSMOLAR STATE?

A

Extreme elevations in serum glucose concentrations, hyperosmolality and dehydration without significant ketosis

143
Q

What are the clinical features of HHS?

A
  1. General
    • ​​Fatigue, lethargy, nausea and vomiting
  2. Neurological
    • Altered level of consciousness, headaches, papilloedema, weakness
  3. Haematological
    • Hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
  4. Cardiovascular
    • Dehydration, hypotension, tachycardia
144
Q

What is the diagnostic criteria for HHS?

A
  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity (> 320 mosmol/kg)

Also useful is:

  1. Arterial pH
  2. Serum bicarbonate >15 mmol/L
  3. Small ketonuria, absent to small ketonemia
  4. Obtundation, combativeness, or seizures (in approximately 50%)
145
Q

What is the management of HHS?

A

The goals of management of HHS can be summarised as follows:

  1. Normalise the osmolality (gradually)
    • the serum osmolality is the key parameter to monitor
    • if not available it can be estimated by 2 * Na+ + glucose + urea
  2. Replace fluid and electrolyte losses
    • 0.9% saline 3-6 litres by 12 hours
    • Potassium added or omitted as required
  3. Normalise blood glucose (gradually)
146
Q

What are the complications of HHS?

A
  1. Myocardial infarction
  2. Stroke
  3. Peripheral arterial thrombosis
  4. Seizures
  5. Cerebral oedema
  6. Central pontine myelinolysis (CPM)
147
Q

WHAT IS CARCINOID SYNDROME?

What three symptoms are under the syndrome?

A

Specific type of tumour

Causes neuroendocrine cells to secrete hormones

  • *Syndrome**
  • *D**iarrhoea
  • *F**lushing
  • *S**OB
148
Q

Where are neuroendocrine cells found?

A

Epithelial layer of GI organs and lungs

Kulchitsky cells

Mid-gut

Hind-gut

149
Q

How are neuroendocrine cells activated and what can they release?

A

Nerves

  1. Serotonin
  2. Histamine
  3. Bradykinin
  4. Prostaglandins
150
Q

What are symptoms of carcinoid syndrome worsened by?

A
  1. Paroxysmal flushing - for example, following coffee, alcohol, certain foods and drugs
  2. Bronchoconstrictive episodes, similar to asthma
  3. Right-sided heart failure
  4. Episodes of explosive watery diarrhoea
  5. Abdominal pain
  6. Pellagra-like lesions of the skin and oral mucosa
151
Q

What are the investigations for carcinoid syndrome?

A
  1. Urinalysis - FIRST LINE
    • 5-hydroxyindoleacetic acid (5-HIAA)
  2. Plasma Chromogranin A (CgA) - SECOND LINE
  3. Octreoscan
    • Inject radioactive labelled octreotide
    • Binds to increase number of somatostatin
  4. Blood tests
    • Niacin deficiency
152
Q

What is the treatment for cacinoid syndrome?

A
  1. Somatostatin analogues
    • Octreotide
  2. Carcinoid tumour
    • Surgery
    • Chemo
153
Q

WHAT IS DIABETES INSIPIDUS?

A

Lack of ADH

154
Q

What happens from a lack of ADH?

A

Water not sufficiently reabsorbed from collecting duct

Large amounts of undilute urine

155
Q

What are the symptoms of diabetes insipidus?

A
  1. Polydipsia
  2. Polyuria
  3. Dehydration
  4. Hypernatremia
156
Q

What is central and nephrotic diabetes insipidus?

A
  1. Central problem with hypothamus and pituitary
    • ADH low
  2. Nephrotic problem with kidneys
    • ADH high
157
Q

What are the causes of central diabetes insipidus?

A
  1. Tumour
  2. Lack of blood supply (inc Sheehan’s)
  3. Impact/fracture
  4. Surgical
  5. Autoimmune
  6. Haemochromatosis
158
Q

What are the nephrogenic causes of diabetes insipidus?

A
  1. Lithium toxicity
  2. Release of obstruction
  3. Hypercalcemia
  4. Hypokalaemia
159
Q

What are the investigations for diabetes insipidus?

A
  1. High plasma osmolality, low urine osmolality
  2. A urine osmolality of >700 mOsm/kg excludes diabetes insipidus
  3. Urine osmolality is AUTOMATICALLY LOW ANYWAY
  4. Nephrogenic DI
    • Water deprivation test
      • Low urine osmolality
    • Desmopressin
      • Low urine osmolality
  5. Cranial DI
    • ​​Water deprivation test
      • Low urine osmolality
    • Desmopressin
      • High
160
Q

How can you determine the cause of diabetes insipidus?

A
  1. Give desmopressin
  2. If urine output falls, osmolality increases
  3. Suggests central
161
Q

What is the treatment of diabetes insipidus?

A
  1. Central
    • Desomopressin 5-40mg intranasally
  2. Diuretics
    • Hydrocholorothiazide
    • Low salt/protein diet
162
Q

Why do you give a patients diuretics with nephrotic diabetes insipidus?

A

Promote water AND SALT LOSS

Activate RAAS!!

163
Q

WHAT IS THE DIFFERENCE BETWEEN DIABETES INSIPIDUS VS SIADH?

164
Q

WHAT DOES THE PARATHYROID DO?

What does this hormone do?

A

Release parathyroid hormone

  1. Increases bone resorption
  2. Increases calcium absorption in kidneys
  3. Increases Vit D synthesis in kidney
    • Vit D increases GI absorption
165
Q

What does the thyroid release in high levels of calcium?

What does this do?

A

Calcitoin

Increase bone deposition

Decrease kidney absorption of calcium

166
Q

WHAT IS HYPERPARATHYROIDISM?

A

Increase in parathyroid hormone

167
Q

What are the different causes of hyperparathyroidism?

A
  1. Primary
    • Solitary Adenoma - normal parathyroid
    • Hyperplasia
  2. Secondary
    • PTH is high to attempt to correct persistently low calcium levels
    • CKD
    • Malabsorption and vitmain D deficiency
  3. Tertiary
    • After many years of uncorrected secondary hyperparathyroidism
168
Q

What are the symptoms of hyperparathyroidsm?

A

STONES, BONES and GROANS

Increased Ca2+
Weak, tired, depressed, thirsty, renal stones, abdopain.

Bone resorption
Pain, fractures, osteopenia/porosis.

Increased BP
Check Ca2+ in hypertension.

169
Q

What are the tests for primary hyperparathyroidism?

A

PTH
High

Calcium
High

Phosphate
Low

Phosphatase
High

170
Q

What is the treatment for primary hyperparathyroidism?

A
  1. Parathyroidectomy - first choice if symptomatic
  2. Medical management
    • Bisphosphonates
171
Q

What are the tests for secondary hyperparathyroidism?

A

PTH
High

Calcium
Low

Phosphate
High

Phosphatase
High

172
Q

What is the treatment for secondary hyperparathyroidism?

A

Treat underlying cause

Bisphosphonates

173
Q

WHAT IS HYPOPARATHYROIDISM?

A

Low levels of parathyroid hormone

174
Q

What are the causes of hypoparathyroidism?

A
  1. Primary
    • AI
    • Congenital (Di George syndrome)
  2. Secondary
    • Radiation
    • Surgery
    • Hypomagnesaemia
175
Q

What are the features of hypoparathyroidism?

A

Hypocalcaemia

SPASMODIC

  1. Spasms
  2. Trousseau’s on inflation of cuff
  3. Anxious
  4. Seixures
  5. Chvostek’s – tap facial nerve over parotid – corner of mouth twitches.
176
Q

What are the investigations for hypoparathyroidism?

A
  1. Low serum calcium
  2. Increased plasma phosphate - low in hypocalcaemia due to intestinal malabsorption or vitamin D deficiency
  3. Normal alkaline phosphatase - raised in hypocalcaemia due to chronic renal failure
  4. Skull radiology may reveal basal ganglia calcification
  5. PTH: low plasma levels
  6. urinary cAMP excretion rises following administration of PTH
177
Q

What is the treatment of hypoparathyroidism?

A
  1. Acute symptomatic hypocalcaemia
    • IV correction wioth calcium
  2. Vitamin D
  3. Ca2+ supplements
    • if diet is lacking
  4. Calcitriol (prevents hypercalciuria)
178
Q

What is the treatment for postmenopausal woman who have a fracture?

A

Risedronate and calcium supplements

179
Q

WHAT IS PHAEOCHROMOCYTOMA?

A

Catecholamine secreting tumour

180
Q

What are the clinical features of phaeochromocytoma?

A
  1. hypertension (around 90% of cases, may be sustained)
  2. headaches
  3. palpitations
  4. sweating
  5. anxiety
181
Q

What are the investigations for phaeochromocytoma?

A
  1. 24 hr urinary collection of metanephrines
    • This replaced 24hr collection of catecholamines
182
Q

What is the management for phaeochromocytoma?

A
  1. Surgery is definitive
  2. Alpha-blocker (e.g. phenoxybenzamine) before
  3. Beta-blocker (e.g. propranolol)
183
Q

WHAT HORMONES ARE INCREASED AFTER SURGERY?

A
  1. Growth hormone
  2. Cortisol
  3. Renin
  4. Adrenocorticotrophic hormone (ACTH)
  5. Aldosterone
  6. Prolactin
  7. Antidiuretic hormone
  8. Glucagon
184
Q

What hormones are decreased following surgery?

A
  1. Insulin
  2. Testosterone
  3. Oestrogen
185
Q

What hormones have no change after surgery?

A
  1. Thyroid stimulating hormone
  2. Luteinizing hormone
  3. Follicle stimulating hormone
186
Q

WHAT IS SICK EUTHYROID SYNDROME?

A
  1. In sick euthyroid syndrome (now referred to as non-thyroidal illness) it is often said that everything (TSH, thyroxine and T3) is low.
  2. In the majority of cases however the TSH level is within the >normal range
187
Q

What is the treatment for sick euthyroid syndrome?

A

Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed

188
Q

WHAT ARE THE SIDE EFFECTS OF STEROIDS?

A
  1. endocrine: impaired glucose regulation, increased appetite/weight gain, hirsutism, hyperlipidaemia
  2. Cushing’s syndrome: moon face, buffalo hump, striae
  3. musculoskeletal: osteoporosis, proximal myopathy, avascular necrosis of the femoral head
  4. immunosuppression: increased susceptibility to severe infection, reactivation of tuberculosis
  5. psychiatric: insomnia, mania, depression, psychosis
  6. gastrointestinal: peptic ulceration, acute pancreatitis
  7. ophthalmic: glaucoma, cataracts
  8. dermatological: acne
  9. suppression of growth in children
  10. intracranial hypertension
  11. neutrophilia
189
Q

WHAT IS A PROLACTINOMA?

A

Prolactinomas are a type of pituitary adenoma, a benign tumour of the pituitary gland

190
Q

What are pituitary adenomas classified by?

A
  1. Size (a microadenoma is <1cm and a macroadenoma is >1cm)
  2. Hormonal status (a secretory/functioning adenoma produces and excess of a particular hormone and a non-secretory/functioning adenoma does not produce a hormone to excess)
191
Q

What are the features of prolactinomas?

A
  1. Excess prolactin in women
    • amenorrhoea
    • infertility
    • galactorrhoea
    • osteoporosis
  2. Excess prolactin in men
    • impotence
    • loss of libido
    • galactorrhoea
  3. Other symptoms may be seen with macroadenomas
    • headache.
    • visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia)
    • symptoms and signs of hypopituitarism
192
Q

How is a prolactinoma diagnosed?

193
Q

What is the management of a prolactinoma?

A
  1. In the majority of cases, symptomatic patients are treated medically with dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland
  2. Surgery is performed for patients who cannot tolerate or fail to respond to medical therapy. A trans-sphenoidal approach is generally preferred unless there is a significant extra-pituitary extension
194
Q

WHAT ARE THE MANAGEMENT OPTIONS FOR OBESITY?

A
  1. Conservative: diet, exercise
  2. Medical
  3. Surgical
195
Q

What is orlistat?

A

Pancreatic lipase inhibitor

196
Q

WHAT IS CONGENITAL ADRENAL HYPERPLASIA?

A
  1. Group of autosomal recessive disorders
  2. Affect adrenal steroid biosynthesis
  3. In response to resultant low cortisol levels the anterior pituitary secretes high levels of ACTH
  4. ACTH stimulates the production of adrenal androgens that may virilize a female infant
197
Q

What are the causes of congenital adrenal hyperplasia?

A
  1. 21-hydroxylase deficiency (90%)
  2. 11-beta hydroxylase deficiency (5%)
  3. 17-hydroxylase deficiency (very rare)
198
Q

WHAT IS PEUTZ-JEGHERS SYNDROME?

A

Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles. Although the polyps themselves don’t have malignant potential, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.

199
Q

What are the features of peutzs-jeghers syndrome?

A
  1. hamartomatous polyps in GI tract (mainly small bowel)
  2. pigmented lesions on lips, oral mucosa, face, palms and soles
  3. intestinal obstruction e.g. intussusception
  4. gastrointestinal bleeding
200
Q

WHAT IS KLINEFELTER’S SYNDROME?

A

Klinefelter’s syndrome is associated with karyotype 47, XXY.

201
Q

What are the features of Klinefelter’s syndrome?

A
  1. often taller than average
  2. lack of secondary sexual characteristics
  3. small, firm testes
  4. infertile
  5. gynaecomastia - increased incidence of breast cancer
  6. elevated gonadotrophin levels but low testosterone
202
Q

How do you diagnose klinefelter’s syndrome?

203
Q

WHAT IS WATERHOUSE-FRIDERICHSEN SYNDROME?

A
  1. Adrenal gland haemorrhage
  2. Profound sepsis
  3. Coagulopathy
204
Q

WHAT IS MATURITY-ONSET DIABETES?

A
  1. Maturity-onset diabetes of the young (MODY) is characterised by the development of type 2 diabetes mellitus in patients < 25 years old.
  2. It is typically inherited as an autosomal dominant condition.
  3. Over six different genetic mutations have so far been identified as leading to MODY.
205
Q

WHAT IS THE TREATMENT OF HYPERTHYROID IN PREGNANCY?

A

Propylthiouracil

206
Q

WHAT IS BARTONELLA INFECTION?

A

Bartonella infection may occur following a cat scratch. The organism is intracellular. Generalised systemic symptoms may occur for a week or so prior to clinical presentation.

207
Q

WHAT ARE THE CAUSES OF HYPOPITUITARISM?

A
  1. compression of the pituitary gland by non-secretory pituitary macroadenoma (most common)
  2. pituitary apoplexy
  3. Sheehan’s syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage
  4. hypothalamic tumours e.g. craniopharyngioma
  5. trauma
  6. iatrogenic irradiation
  7. infiltrative e.g. hemochromatosis, sarcoidosis
208
Q

What are the symptoms of hypopituitism?

A
  1. low ACTH
    • tiredness
    • postural hypotension
  2. low FSH/LH
    • amenorrhoea
    • infertility
    • loss of libido
  3. low TSH
    • feeling cold
    • constipation
  4. low GH
    • if occurs during childhood then short stature
  5. low prolactin
    • problems with lactation
  6. there may also be features suggestive of the underlying causes
    • pituriary macroadenoma → bitemporal hemianopia
    • pituitary apoplexy → sudden, severe headache
209
Q

What are the investigations for hypopituitism?

A
  1. hormone profile testing
  2. imaging
210
Q

What is the management of hypopituitarism?

A
  1. treatment of any underlying cause (e.g. surgical removal of pituitary macroadenoma)
  2. replacement of deficient hormones

ΩΩ 4 Bateman - Specialities + Endo + GI + Liver (6 decks)

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