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Conditions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Define Adrenal Insufficiency

A

Destruction of adrenal cortex with reduced adrenal output

Can be Primary (Addison’s) or Secondary

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2
Q

Causes of Adrenal Insufficiency

A

AI most common in developed countries
TB most common in rest of world

Primary: Addisons, Adrenectomy, Trauma, Infection, Haemorrhage, infarction, neoplasm
Secondary: Congenital, Trauma, CAH
Other: Suppression of axis, AIDS patients, Critically ill

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3
Q

Symptoms of adrenal insufficiency

A 
Hypotension
Hypovolaemic shock
Fever
Vomiting
Fatigue
Weakness
Anorexia
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4
Q

Signs of adrenal insuffciency

A

Hyperpigmentation
Hypotension
Postural hypotension

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5
Q

What things would make you consider addisons?

A

Hypothyroidism / Women on thyroxine
Unexplained hypotension in T1DM
Presence of other AI conditions
Low Na+ and Low K+

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6
Q

Investigations for Adrenal insufficiency

A 
Electrolytes (Low Na+, Raised K+)
FBC ( Anaemia, mild eosinophilia, WBC)
Glucose (Low)
LFTs (Raised)
ACTH (Raised in Primary, low/normal in secondary)
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7
Q

Management for Adrenal insufficiency

A

Medical emergency bracelet
Steroids (Hydrocortisone + Fludrocortisone in prmiary disease)
Double dose of hydrocortisone for surgery, infections

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8
Q

Manage acute Adrenal insufficiency

A

ICU
High dose Hydrocortisone Paternally
IV Fluid

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9
Q

Complications of Adrenal insufficiency

A

Adrenal crisis
Osteoporosis
Reduced QOL

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10
Q

Prognosis of Adrenal insuffciency

A

If untreated = fatal

Lifelong treatment but normal life

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11
Q

What is Acromegaly?

A

Growth hormone stimulates production of IGF-1. This is produced in liver and many other tissues.

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12
Q

What causes Acromegaly?

A

Usually caused by a pituitary tumour (1:3 microadenoma to macroadenoma)
Rarely, ectopic GH from non-endocrine tumours e.g. Lung cancer, cancer of the pancreas
Insidious onset and slow progression
Several familial causes (MEN1, Mccube-albright’s syndrome or familial isolated pituitary adenoma)

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13
Q

What are the risk factors for acromegaly?

A 
GPR101 over-expression
MEN1
Isolated familial acromegaly
McCune-albright's syndrome
Carney's complex
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14
Q

What are the signs and symptoms of Acromegaly?

A 
Coarsening of facial features
Soft-tissue and skin changes
Carpal tunnel syndrome
Joint pain and dysfunction
Snoring (macroglossia)
Alterations in sexual functioning
History or family history of inherited syndromes
Fatigue
Hypertension, arrhythmias
Organomegaly
Increased appetite, polyuria/polydipsia
Headaches
Visual field defects
Signs and symptoms of hypopituitarism
Cranal nerve palsies (ophthalmoplegia)
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15
Q

What investigations are done for Acromegaly?

A 
Serum IGF-1 (elevated)
Oral glucose tolerance test (GH value >1 microgram/L)
Random serum GH
Pituitary MRI or CT scan (Adenoma)
Plasma cortisol (May be low)
TSH and free T4 (abnormal)
Estradiol or testosterone
Visual field testing
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16
Q

How do you manage Acromegaly?

A 
Somatostatin analogues (Octreotice)
Dopamine agonists (Bromocriptine, cabergoline and quiagolide)
Pegyisomant (PEG)
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17
Q

How do you manage Acromegaly in pregnancy?

A

Medical therapy withheld during pregnancy
Short-acting octreotide used as needed when attempting to conceive
Patients with macroadenomas monitored for headaches and visual symptoms
Cabergoline safe to the foetus

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18
Q

What are complications of acromegaly?

A 
Cardiac complications
Sleep apnoea
Osteoarticular complications
Impaired glucose tolerance and diabetes
Pre-cancerous polyps
Carpal tunnel syndrome
Hypopituitarism
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19
Q

What is Carcinoid syndrome?

A

Constellation of symptoms caused by systemic release of humoral factors from carcinoid tumours (tumour of neuroendocrine cells)

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20
Q

What causes carcinoid syndrome?

A

Slow-growing neuroendocrine tumours
Mostly derived from serotonin-producing enterochromaffin cells (Neural crest origin)
Common sites: Appendic, ileum, Rectum
Produce secretory products: Serotonin, Histamin, Tachykinins, kallikrein and prostaglandins
75-80% with it have small bowel carcinoids

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21
Q

What is important to know about Carcinoid syndrome in the bowel?

A

Hormones released into the portal circulation will be metabolised by the liver so symptoms dont appear untill there are hepatic metastases

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22
Q

What are the Risk factors for carcinoid syndrome?

A

None

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23
Q

What are the Symptoms of Carcinoid syndrome?

A 
Paroxysmal flushing
Diarrhoea
Crampy abdominal pain
Wheeze
Sweating 
Palpitations
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24
Q

What are the signs of carcinoid syndrome?

A

Telangiectsia
Congestive cardiac failure (Due to tricuspid incompetence/pulmonary stenosis from serotnonin induced fibrosis)
Right-sided murmurs
Nodular hepatomegaly
Carcinoid crisis (When mediators flood out - often during surgery) [Profound flushing, Bronchospasm, Tachycardia, Fluctuating blood pressure]

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25
Q

What are the investigations for Carcinoid syndrome?

A

24hr urine collection (Check 5-HIAA levels)
Blood (Plasma chromogranin A and B, Octreoscan, fasting gut hormones)
CT/MRI scan (Localise tumour)
Radioisotope scan (Radiolabelled somatostatin analogue (octreotide) localises the tumour)
Investigations for MEN-1
Echo and BNP investigates carcinoid heart disease

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26
Q

What is Cushing’s syndrome?

A

Clinical manifestation of pathological hypercortisolism from any cause.

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27
Q

What is caused by Cushing’s syndrome?

A

Exogenous corticosteroid exposure is most common cause of cushing’s syndrome
Majority caused by ACTH-secreting pituitary adenomas
10-15% of pituitary tumours secrete ACTH
New gene ubiquitin-specific protease 8, mutated in Cushing’s disease
Adrenal overproduction of cortisol in 30-40% of carcinomas, resulting in ACTH-independent cushing syndrome

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28
Q

What are the Risk Factors for Cushing’s syndrome?

A 
Exogenous corticosteroid use
Female 
20-45
Pituitary adenoma
Adrenal adenoma
Adrenal carcinoma
Neuroendocrin tumours
Thoracic or bronchogenic carcinoma
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29
Q

What are the signs and symptoms of Cushing’s syndrome?

A 
Truncal obesity
Buffalo hump
Supraclavicular fat pads
Weight gain
Facial fullness
Moon facies 
Facial plethora
Proximal muscle wasting and weakness
Diabetes or impaired glucose tolerance
Skin atrophy
Purple striae
Easy bruising
Hirsutism
Acne
Pigmentation 
Oedema
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30
Q

What are the investigations for Cushing’s syndrome?

A

Pregnancy test (Negative)
Serum Glucose (Raised)
Late-night salivary cortisol (Raised)
1mg overnight dexamethasone suppression test (morning cortisol >50)
24-hour urinary free cortisol (>50)
48-hour 2mg dexamethasone suppression test

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31
Q

How do you manage Cushing’s syndrome?

A 
Tumour resection (Trans-sphenoidal microsurgery or Bilateral adrenelectomy)
Medications for those who are unfit for surgery or with an unknown tumours
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32
Q

What medications are used for Cushing’s syndrome?

A

Drugs (Metyrapone, Ketoconaxole and mitotane)

Pituitary radiotherapy

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33
Q

What are the complications of Cushing’s syndrome?

A

Adrenal insufficiency secondary to adrenal suppression
CVS Disease
HTN
DIabetes mellitus
OSteoporisus
Nephrolithiasis
Nelson’s syndrome
Treatment- related central hypothyroidism/GH deficiencies
Treatment related adrenal insufficiency/hypogonadism/DI

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34
Q

What is Cushing’s disease?

A

Cushing’s syndrome caused by a pituitary adenoma specifically

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35
Q

What is Diabetes Insipidus?

A

Diabetes insipidus is caused by hyposecretion of, or insensitivity to the effects of ADH aka AVP.
Its failure to act causes an inability to concentrate urine in the distal renal tubule, leading to passage of a lot of urine
Passes >3 litres of urine in 24hrs with low osmolality (<300mOsml/kg)

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36
Q

What are the 2 major forms of Diabetes insipidus?

A

Cranial

Nephrogenic

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37
Q

What is Cranial DI?

A

Decreased ADH secretion, reducing the ability to concentrate urine and so causes polyuria and polydipsia

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38
Q

What is Nephrogenic DI?

A

Decreased ability to concentrate urine because of resistance to ADH in the Kidney

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39
Q

What are the 2 other forms of DI?

A

Gestational

Primary polydipsia

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40
Q

What is Gestational DI?

A

Degaradtion of Vasopressin by a placental vasopressinase. associated with increased complications of pregnancy

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41
Q

What is primary polydispia?

A

AKA Dipsogenic DI - caused by a primary defect in osmoregulation of thirst. Reported in TB meningitis, MS and Neurosarcoidosis

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42
Q

What causes cranial DI?

A

Acquired
- Idiopathic
- Tumours
- Intracranial surgery
- Head injury
- Granulomata (sarcoidosis, TB, Wegner’s granulomatosis)
- Infections (Encephalitis, Meningitis, cerebral abscess)
- Vascular disorders (Haemorrhage/thrombosis, aneurysms, SCD, sheehan’s syndrome)
- Post Radiotherapy
Inherited
- Autosomal recessive (Wolfram’s syndrome)
- AD mutations of vasopressin gene

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43
Q

What causes Nephrogenic DI?

A 
Acquired
- Idiopathic
- Hypokalaemia
- Hypercalcaemia
- CKD
- Other metabolic derangements
- Drugs (Ofloxacin, orlistat, lithium)
- Renal tubular acidosis
- Pregnancy
- Post obstructive uropathy
Congenital/genetic nephrogenic DI
- X linked mutations in V2 ADH-receptor gene
- Autosomal recessive defect in aquaporin 2 (AQP2) gene - water channel in distal renal tubule
- Sporadic nephrogenic DI with general learing disability and intracerebral calcificaiton (very rare)
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44
Q

What are the risk factors for Diabetes insipidus?

A 
Pituitary surgery
Craniopharyngioma
Pituitary stalk lesions
Traumatic brain injury
Congenital pituitary abnormalities
Medication
AI disease
Family history/genetic mutations
Pregnancy
Subarachnoid haemorrhage
Renal sarcoidosis/amyloidosis
Hypercalcaemia or hypokalaemia
Release of obstructive uropathy
Previous CNS infection
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45
Q

What are the symptoms of Diabetes insipidus?

A 
Polyuria
Nocturia
Polydipsia
In children: Enuresis (bed wetting), Sleep disturbance 
Sensorineural deafness and visual failure
Visual field defects
Motor deficits
Skin lesions
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46
Q

What are the signs of Diabetes Insipidus?

A

Urine output >3L/day
Fluid intake < fluid output, signs of dehydration (tachycardia, reduced tissue trigor, postural hypotension)
Signs related to teh cause

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47
Q

What are the investigations for Diabetes Insipidus?

A

Plasma glucose
U&Es
Urine specific gravity
Simultaneous plasma and urine osmolality
MRI of pituitary, hypothalamus and surrounding tissues, including the pineal gland
Fluid deprivation test with response to desmopressin!

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48
Q

What results are seen in the fluid deprivation test?

A

Normally:

  • Increased plasma osmolality
  • Increased ADH secretion
  • Increased water reabsorption
  • Increase in urine osmolality (Urine >600 mosmol/kg)

In psychogenic polydipsia:
- Urine osmolality is slightly lower than a normal person

In Diabetes insipidus:

  • Lack of ADH means that urine cannot be concentrated
  • Urine osmolality is LOW (<400 mosmol/kg)

Cranial - urine osmolality rises >50% following administration of desmopressin; Nephrogenic has a rise of <45% after desmopressin

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49
Q

What is the management of Diabetes insipidus?

A

Treat Cause!
Cranial DI - MRI to find cause, give desmopressin, if mild: chlorpropamide/carbamezapine to potentiate residual effects of any residual vasopressin
Nephrogenic diabetes insipidus - Sodium and/or protein restriction helps with polyuria, thiazide diuretics e.g. bendroflumethiazide

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50
Q

What are the complications of DI?

A

Desmopressin worsens MI in susceptible patients, may be a need for nitrates/other anginal methods
Need careful management of fluid balance and therapy following surgery
Patients with genetic causes of Nephrogenic DI are prone to bladder dysfunction and hydroureter/hydronephrosis
Hypernatraemic dehydration
Thrombosis
Bladder and Renal dysfunction
Iatrogenic hyponatraemia

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51
Q

What is Diabetes Mellitus?

A

Lack of effective endogenous insulin
Leading to serious microvascular (Retinopathy, Neuropathy and Nephropathy) or Macrovascular (stroke, renovascular disease, limb ischaemia, heart disease) problems

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52
Q

What is Type 1 diabetes mellitus?

A 
Immune destruction of the pancreas
Insulin dependent diabetes
Usually young
Diabetic ketoacidosis
Quite high glucose
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53
Q

What is Type 2 diabetes mellitus?

A 
Resistance to action of insulin
Non-insulin dependent diabetes
Maturity onset diabetes (30-70 years old)
Often overweight
Very high glucose
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54
Q

What is the cause of T1DM?

A

Destruction of pancreatic beta cells
AI process
Associated with other AI conditions
90% carry HLA DR3 +/- DR4
Latent autoimmune diabetes of adults is a form of T1DM with slower progression to insulin dependence
T1DM prone to ketoacidosis have sufficient insulin to suppress ketone body
Auto antigens: GAD, Insulin, Insulinoma-associated protein 2, Cation efflux zinc transporter

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55
Q

What are the risk factors for T1DM

A

Geographical region
Genetic predisposition
Infectious agents
Dietary factors

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56
Q

What are the symptoms of T1DM?

A 
Polyuria
Nocturia
Tiredness
Weight loss
DKA symptoms ( Caused by: Surgery, UTI, MI, pancreatitis, chemo, psychotics, wrong dose)
- Drowsiness
- Confusion
- Kussmaul breathing
- Ketotic breath
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57
Q

What are the signs of T1DM?

A

Diabetic retinopathy
Neuropathy
Monitor BP
Associated with AI conditions: Vitiligo, Addison’s disease, AI thyroid disease

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58
Q

What are the investigations for Diabetes mellitus?

A 
Urinalysis > Random glucose (>7.1) > Fasting glucose (>11.1) > OGTT > HbA1c
U&amp;Es - Nephropathy and hyperkalaemia
Lipid profile
Urine A:CR - detect microalbuminaemia
Urine - glycosuria, ketonuria, MSU
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59
Q

What investigations are done for Ketoacidosis?

A

Capillary blood glucose > Urine dipstick > ABG (metabolic acidosis)> Plasma osmolality
FBC (leucocytosis)
Fasting C-peptide (Low)
AI markers (Positive)

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60
Q

What is the management of T1DM?

A

Patient education
- Short acting insulin 3x daily or long acting insulin once daily
Insulin pumps
Monitor: Capillary blood glucose, HbA1c every 3-6 months.
Screen and manage complications

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61
Q

How do you manage DKA?

A 
If Systolic BP <90 give 500ml saline
50U soluble insulin
Continue untill:
Ketones <0.3
Venous pH >7.30
Venous bicarbonate >18
Potassium replacement
Thromboprophylaxis
Broad spectrum ABx
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62
Q

What are the complications of T1DM?

A 
Diabetic Ketoacidosis
Hypoglycaemia
Retinopathy
Diabetic kidney disease
Peripheral or autonomic neuropathy
Cardiovascular disease
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63
Q

What are the macrovascular complications of T1DM?

A

Retinopathy
Neuropathy
Nephropathy

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64
Q

What are the complications of T1DM treatment?

A 
Weight gain
Fat hypertrophy at insulin injection sites
Hypoglycemia
- Personality changes
- Fits
- Confusion
- Coma
- Pallor
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65
Q

What is T2DM?

A

Increased peripheral resistance to insulin action, impaired insulin secretion and increased hepatic glucose output. Associated with Obesity, lack of exercise, calorie and alcohol excess

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66
Q

What causes T2DM?

A 
Genetic predisposition characterised by insulin resistance 
Causes:
Obesity
Genetics
Pancreatic disease
Endocrine disease
Drugs
Circulating autoantibodies
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67
Q

What are the Risk factors for T2DM?

A 
Metabolic syndrome
Obesity
Asian ethnicity
TB drugs
SSRIs
Pregnancy
Acromegaly
Renal failure
Cystic fibrosis
PCOS
Werner's syndrome
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68
Q

What are the symptoms of T2DM?

A

May be incidental
Polyuria
Polydipsia
Tiredness
Present with hyperosmolar hyperglycaemic state
Infections
Assess cardiovascular RFs (HTN, Hyperlipidaemia, Smoking)

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69
Q

What are the signs of T2DM?

A 
Calculate BMI
Waist circumference
Blood pressure
Diabetic foot (Dry skin, reduced SC tissue, Ulcerations, Gangrene, Charcot's arthropathy, Weak foot pulses)
Skin changes 
- Necrobiosis lipoidica diabeticorum
- Granuloma annulare
- Diabetic dermopathy
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70
Q

What are the investigations for T2DM?

A

Urinalysis > Random glucose > Fasting glucose > OGTT > HbA1c
Diagnosed with: Plasma glucose (>7.1), Plasma glucose (>11.1)
Monitor: HbA1c, U&Es, Lipid profile, eGFR,Urine A:CR
Ankle-brachial index (= 0.9)

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71
Q

What is the management of T2DM?

A

Glycaemic control
Initial:
- Lifestyle advice (smoking cessation, diet, exercise)
- Metformin [a Biguanide] increases insulin sensitivity
HbA1c >53 add sulphonylurea [gliclazide]
HbA1c >57 at 6 months consider: Insulin, Glitazone, sulphonylurea, GLP analogues and DPP4 inhibitors, A-glucosidase inhibitors)
Screen for complications, pregnancy, hyperosmolar hyperglycaemic state

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72
Q

What are the complications of T2DM?

A 
Diabetic kidney disease
Impaired vision
Lower extremity amputation
Cardiovascular disease
Congestive heart failure
Stroke
Infection
Peridontal disease
Treatment-related hypoglycaemia
Depression
Obstructive sleep apnoea
Diabetic ketoacidosis
Non-ketotic hyperosmolar state
Autonomic or peripheral neuropathy
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73
Q

What is Diabetic Ketoacidosis?

A

Medical emergency with a significant morbidity and mortality

Characterised by hyperglycaemia, acidosis and ketonaemia

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74
Q

What are the precipitating conditions?

A

Infection
Discontinuation of insulin
Inadequate insulin
CVS disease
Drug treatments (Steroids, thiazide-like diuretics or SGLT2 inhibitors)
Menstruation
Physiological stress (pregnancy, trauma and/or stress)

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75
Q

What is Graves’ disease?

A

AI thyroid condition associated with hyperthyroidism. Associated orbitopathy occurs in 25% of cases and is usually mild

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76
Q

What causes Graves’ disease?

A

AI condition, caused by TSH receptor antibodies

80% genetic, 20% environmental

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77
Q

What are the Risk Factors for Graves’ disease?

A 
Family history of AI thyroid disease
Female sex
Tobacco use
High iodine uptake
Lithium therapy
Biological agent and cytokine therapies
Radiation
Radioiodinetherapy for benign nodular goitres
Stress
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78
Q

What are the signs and symptoms of Graves’ disease?

A 
Heat intolerance
Sweating
Palmar erythema
Weight loss
Palpitations
Tremor
Tachycardia (may be AF)
Urticaria/pruritis
Diffuse goitre
Orbitopathy
Lid lag
Pretibial myxoedema
Proptosis
Onycholysis (detachment of nail from nail bed)
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79
Q

What are the investigations for Graves’ disease?

A

TSH (suppressed/low)
Serum free or total T4 (Raised)
Serum free or total T3 (elevated)
Total T3/T4 or fT4/fT3 (high compared to thyroiditis)

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80
Q

What is Hyperparathyroidism?

A

An endocrine disorder in which autonomous overproduction of PTH results in derangement of calcium metabolism. In approximately 80% of cases, over-producton of PTH is due to a single parathyroid adenoma, and less commonly, multi-gland involvement may occur

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81
Q

What are the types of hyperparathyroidism?

A

Primary
Secondary
Tertiary

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82
Q

What is Primary Hyperparathyroidism?

A 
Parathyroid adenoma most common and familial forms are well defined 
May be due to external radiation - lithium therapy
Familial causes (MEN1/2a), HPT-JT or familal isolated hyperparathyroidism
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83
Q

What are the risk factors for primary hyperparathyroidism?

A 
Female sex
Age >50-60 years
Family history
MEN (1,2a or 4)
Current or history of lithium treatment
HPT-JT
History of head and neck irradiation
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84
Q

What are the signs and symptoms for Primary hyperparathyroidism?

A 
History of Osteoporosis/Osteopenia
Family history
Nephrolithiasis
Bone pain
Poor sleep
Fatigue
Anxiety 
Depression
Memory loss 
Myalgia
Paraesthesia 
Muscle cramp
Constipation 
Overt neuromuscular dysfunction
Abdominal pain
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85
Q

What are the investigations for primary hyperparathyroidism?

A

Serum Calcium (raised)
Serum intact PTH with immunoradiometric or immunochemical assay
Serum ALP
Serum phosphorous
24 hour urinary calcium
Tc99m sestamibi scanning and ultrasonography
MRI neck

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86
Q

What is the management of primary hyperparathyroidism?

A 
Mild, asymptomatic disease:
- Elevated calcium
- 1/3 will have features of HPT
-Avoid dehydration
-Avoid thiazide diuretics
Surgical treatment: parathyroid surgery to remove abnormal glands 
Surgical treatment
Medical treatment
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87
Q

What are the guidelines for surgical treatment?

A 
Age under 50
Creatinine clearance <60
Nephrolithiasis
DXA of less than -2.5
Vertebral fracture
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88
Q

What is the medical treatment for primary hyperparathyroidism?

A

HRT and Raloxifene in post menopausal women

Cincalcet reduces serum Calcium and PTH levels and raises serum phosphorous

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89
Q

What are the complications for primary hyperparathyroidism?

A 
Neck haematoma following surgery
Recurrent and superior laryngeal nerve injury
Hypocalcaemia post-surgery
Pneumothorax post-surgery
Osteoporosis
Bone fractures
Nephrolithiasis
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90
Q

What is Secondary hyperparathyroidism?

A

Most commonly in CKD
Parathyroid glands become hyperplastic after long-term stimulation on response to chronic hypocalcaemia
Seen in all patients with dialysis-dependent CKD
Occur in any condition with chronic hypocalcaemia

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91
Q

What are the risk factors for secondary hyperparathyroidism?

A 
Ageing
Chronic renal failure
Absence of dairy and fish
Malabsorption
Hepatic dysfunction
Genetic disorder
Obesity
Medication use
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92
Q

What are the signs and symptoms of secondary hyperparathyroidism?

A

Features of chronic renal failure
Features of underlying malabsorption syndrome
Muscle cramps and bone pain
Perioral tingling or paraesthesia in fingers or toes
Chvostek’s/trousseau’s sign
Bowed legs or knocked knees
Fractures

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93
Q

What investigations are done for Secondary hyperparathyroidism?

A

Serum Calcium (Decreased)
Serum Intact PTH (Raised)
Serum creatinine (Raised)
Serum Urea Nitrogen (Raised)

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94
Q

What is the management of secondary hyperparathyroidism?

A

Mostly medical - treat underlying conditions
In CKD (calcium supplementation, correct Vit. D analogues, calchimimetics [cincalet])
Parathyroidectomy

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95
Q

What are the complications of secondary hyperparathyroidism?

A

Osteodystrophy
Osteoporosis
Uraemia
Calchiphylaxis

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96
Q

What causes tertiary hyperparathyroidism?

A

Occurs after prolonged secondary glands become autonomous, producing excessive PTH even after cause of hypocalcaemia is corrected

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97
Q

How does tertiary hyperparathyroidism present?

A

Symptoms and signs are due to hypercalcaemia so can be similar to primary hyperparathyroidism

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98
Q

What investigations are done for tertiary hyperparathyroidism?

A 
Serum Calcium (Raised)
Serum PTH (Raised)
Serum phosphate (Raised)
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99
Q

How do you manage tertiary hyperparathyroidism?

A

Cincalet
Total or subtotal parathyroidectomy recommended
Auto transplantation is an easily accessible site

100
Q

What is Hypogonadism?

A

Female: Impairment of ovarian function

Male: A syndrome of decreased testosterone production, sperm production or both

101
Q

What are the causes of Female hypogonadism?

A

Primary - Gonadal dysgenesis, gonadal damage, premature ovarian failure, androgen excess
Seconary - Functional, pituitary/hypothalamic tumours, Hyperprolactinaemia, Congenital GnRH deficiency, Post pill amenorrhoea

102
Q

What are the Risk Factors for female hypogonadism?

A

Turner’s/Kallman’s
T2DM
Alkylating agents/opioids/glucocorticoids/ sex hormones/ GnRH analogues

103
Q

What are the symptoms of female hypogonadism?

A 
Night sweats
Hot flushing
Vaginal dryness
Dyspareunia
Decreased libido
Infertility
Oligo/amenorrhoea
Features of Turner's: Short, cubitus valgus, poor breast development
104
Q

What are the signs of female hypogonadism?

A

Pre-pubertal (Delayed puberty, Eunuchoid)
Post-pubertal (Regression of secondary sexual characteristics, Perioral and periorbital wrinkles)
Kallman’s syndrome - anosmia
Turner’s syndrome - Short, low posterior hairline, high arched palate, widely spaced nipples, short 4th and 5th metacarpals, congenital lymphoedema)
AI primary ovarian failure

105
Q

What investigations are done for female hypogonadism?

A 
Pregnancy test (Negative)
Serum oestradiol (Low)
Serum FSH/LH
Serum prolactin
TFTs 
Karyotype 
Pelvic imaging
Screen for fMRI
Pituitary function test
Visual field testing
Turner's syndrome
AI oophoritis
106
Q

What causes Male hypogonadism?

A

Primary:

  • Gonadal dysgenesis
  • Gonadal damage
  • Rare causes: Renal failure, liver cirrhosis or alcohol excess

Secondary:

  • Pituitary/hypothalamic lesion
  • GnRH deficiency (Kallman’s)
  • Hyperprolactinaemia
  • Genetic mutations
  • Laurenec-moon-biedl syndrome
  • Age
  • Prader-willi syndrome
107
Q

What is Laurence-moon-biedl syndrome?

A

Secondary cause of hypogonadism seen by obesity, polydactyly, retinitis pigmentosa, learning difficulties)

108
Q

What are examples of gonadal dysgenesis?

A

Klinefelter’s syndrome

Undescended testicles

109
Q

What are the risk factors for male hypogonadism?

A 
Age
Kallman's
Prader willi
Klinefelter's
T2DM
Alkylating agents
Opioids
Glucocorticoids
Sex hormones
GnRH analogues
Hyperprolactinaemia
110
Q

What are the symptoms of Hypogonadism?

A 
Delayed puberty
Decreased libido
Impotence
Infertility
Symptoms of underlying disease: (Intellectual dysfunction [Klinefelter's])
111
Q

What are the signs of Hypogonadism?

A 
Measure testicular volume using Prader's orchidometer (15-25mL)
Pre-pubetal:
- Signs of delayed puberty (High pitched voice, Decreased pubic hair/ small or undescended testicles/ small penis)
- Gynaecomastia
- Eunuchoid proportions
- Features of underlying cause
Postpubertal:
- Decreased hair
- Soft and small eyes
- Gynaecomastia
- Fine perioral wrinkles
- Features of underlying cause (Visual defects)
112
Q

What investigations are done for male hypogonadism?

A 
Serum total testosterone (Low)
Sex hormone binding globulin 
Albumin
LH and FSH
Karyotyping 
Secondary
- Pituitary functions test
- MRI of hypothalamus
- Visual field test / smell test
- Iron testing 
Assess bone age
113
Q

In both forms of Hypogonadism (male and female), what is seen when discovering LH and FSH?

A

In primary: Raised

In secondary: Normal/Low

114
Q

What is Hypopiruitarism?

A

Partial or complete deficiency of one or more pituitary. May arise from a congenital defect during development of the pituitary gland or as a result of acquired diseases of the pituitary gland, the parasellar structure, or the hypothalamus

115
Q

What can cause Hypopituitarism?

A 
Neoplastic causes
Vascular causes
Inflammation and infiltrative lesions
Infection
Congenital
Radiotherapy
PItuitary surgery
Other
116
Q

What neoplasms cause hypopituitarism?

A

Pituitary adenoma
Craniopharynigioma
Sellar meningiomas
Pituitary metastases

117
Q

What vascular issues cause hypopituitarism?

A

Pituitary apoplexy
Sheehan syndrome
Intrastellar aneurysms

118
Q

What inflammatory and infiltrative lesions cause hypopituitarism?

A

Lymphocytic hypophysitis
Hypophysitis
Haemochromatosis
Sarcoidosis, TB and langerhans cell histiocytosis X

119
Q

What infections

cause hypopituitarism?

A

Pituitary abscess formation
Pituitary Tuberculomas
Fungal pituitary disease occurs as a complication of aids but uncommon

120
Q

What are the congenital causes of hypopituitarism?

A

Pituitary or hypothlamic origin
Transcription factor defects
Mutations in PROP1 cause of familial and sporadic congenital pituitary hormone deficiencies

121
Q

What are the other (Radiotherapy, Pituitary, other) causes of Hypopituitarism?

A

May follow treatment with external radiation
Pituitary surgery
Traumatic brain injury
Empty sella syndrome
Hypothalamic damage from mass lesions, infections, radiation
Chronic opiate use leads to deficiencies of gonadotrophin

122
Q

What are the Risk Factors for hypopituitarism?

A 
Pituitary tumour
Pituitary apoplexy
Pituitary surgery
Cranial radiation
Traumatic brain injury
Genetic defects
Hypothalamic disease
Inflammatory disorders
Empty sella syndrome
Syphillis
Tuberculous meningitis
Severe postpartum haemorrhage (Sheehan)
123
Q

What are the signs and symptoms of ACTH deficiency?

A

Acute: Weakness, dizziness, nausea, vomiting, circulatory collapse, fever, shock
Chronic: Fatigue, pallor, anorexia, weight loss
Children: Delayed puberty, failure to thrive
Hypoglycaemia, hypotension, anaemia, lymphocytosis, eosinophilia, hyponatraemia

124
Q

What are the signs for TSH deficiency?

A

Tiredness, Cold intolerance, constipation, hair loss, dry skin, hoarseness, cognitive slowing
Weight gain, bradycardia, hypotension
Children: Delayed development, growth restriction and intellectual impairment

125
Q

What are the signs and symptoms of Gonadotrophin deficiency?

A

Women: Oligomenorrhoea, loss of libido, dyspareunia, infertility, osteoporosis
Men: loss of libido, impaired sexual function, mood impairment, loss of facial, scrotal and body hair, decreased muscle mass, osteoporosis, anaemia

126
Q

What are the signs and symptoms of Growth hormone deficiency?

A

Decreased muscle mass
Dyslipidaemia, premature atherosclerosis
Children: Growth restriction

127
Q

What are the signs of ADH deficiency?

A

Polyuria
Polydipsia
Decreased urine osmolality
Hypernatraemia

128
Q

What may also present with features attributable to the underlying cause?

A

Space-occupying lesions - headaches or visual field deficits

Large lesions involving hypothalamus - polydipsia and inappropriate ADH

129
Q

What investigations are done for hypopituitarism?

A 
Pituitary functions test
Dynamic tests
Serum electrolytes
Serum and urine osmolality
MRI/CT pit
Metyrapone testing of adrenal axis
130
Q

How do you manage hypopituitarism?

A

Apoplexy - IV hydrocortisone + surgery
ACTH - Oral corticosteroids + IV/IM for stressful events
TSH - Levothyroxine after adrenal replacement
Female (with gonadotrophin-releasing hormone) - oestrogen with progesterone, if want fertility: Gonadotrophins.
Males with GNRH - testosterone + gonadotrophins if want to be fertile
Growth hormone - recombinant human growth hormone
ADH - Desmopressin
Anti-CTLA-4 Ab therapy associated hypophysitis - high dose glucocorticoids

131
Q

What are the complications of hypopituitarism?

A 
Male infertility
Female infertility
Corticosteroid over-replacement
Thryoxine over-replacement
Desmopression over-replacement
Growth hormone over-replacement
Testosterone over replacement
132
Q

What is Hypothyroidism?

A

Insidious onset with significant morbidity.

Clinical features often subtle and nonspecific

133
Q

What are the three types of hypothyroidism?

A

Primary
Secondary
Transient

134
Q

What causes primary hypothyroidism?

A 
AI hypothyroidism
Iatrogenic 
Drugs
Congenital defects
Infiltration of the thyroid
135
Q

What causes secondary hypothyroidism?

A

Isolated TSH deficiency
Hypopituitarism - neoplasm, infiltrative, infection and radiotherapy
Hypothalamic disorders - neoplasm and trauma

136
Q

What causes transient hypothyroidism?

A

Withdrawal of thyroid suppressive therapy
Postpartum thyroiditis
Subacute/chronic thyroiditis with transient hypothyroidism

137
Q

What are the Risk factors for hypothyroidism?

A 
Iodine deficiency
Female sex
Middle age
Family history of AI thyroiditis
AI disorders
Graves' disease
Post-partum thyroiditis
Turner's and Down's
Primary pulmonary hypertension
MS
Radiotrharpy
Amiodarone, Lithium
T1DM
Textile workers
138
Q

What are the symptoms of hypothyroidism?

A 
Tiredness
Lethargy
Cold intolerance
Dry skin
Hair loss
Slowing of intellectual activity
Constipation
Decreased appetite with weight gain
Deep hoarse voice 
Menorrhagia and later oligomenorrhia or amenorrhoea
Impairedhearing due to fluid in middle ear
Reduced libido
139
Q

What are the signs of Hypothyroidism?

A

Dry coarse skin, hair loss and col peripheries
Puffy face, hands and feet (myxoedema)
Bradycardia
Delated tendon reflex relaxation
Carpal tunnel syndrome
Serious cavity effusions e.g. pericarditis or pleural effusion

140
Q

What are the other presentations for Hypothyroidism?

A 
AKI
Female sexual dysfunction
Hypercholesterolaemia
Can develop into myxoedema: Expressionless dull face with peri-orbital puffiness; swollen tongue, sparse hair, pale, cool skin with rough, doughy texture; enlarged heart
Megacolon/intestinal obstruction
Cerebellar ataxia
Psychosis
Encephalopathy
141
Q

How does Hashimoto’s and atropic thyroiditis present?

A

Subclinical AI thyroiditis represents early stages of chronic thyroiditis with a soft/firm thyroid gland, usually normal in size or slightly enlarged

142
Q

How does postpartum thyroiditis present?

A

Occurs in 5-7% within first 6 months

Most show remission but some may progress to permanent

143
Q

How does subacute thyroiditis?

A

Referred to as granulomatous, giant cell or de quervian’s thyroiditis
Viral infection produces local symptoms and exquisite tenderness of the thyroid gland with nodularity

144
Q

What investigations cause hypothyroidism?

A 
Serum TSH - elevated
Free serum T4 - low
Serum cholesterol - often raised
FBC - anaemia
Fasting blood glucose - elevated
Serum CK - may be raised
Serum sodium - may be decresed
Antithyroid peroxidase antibodies - may be elevated
145
Q

How do you treat clinical hypothyroidism?

A

Levothyroxine and maybe liothyronine
For some, it starts at 25 micrograms daily up by 25 every 4 weeks - including: Cardiac disease, severe hypothyroidism, over 50 years old
Drugs e.g. ferrous sulphate, calcium supplemets, rifampicin and amiodarone interfere with T4 absorption

146
Q

How do you treat subclinical hypothyroidism?

A

Occurs when a patient has TSH over normal but T4 in normal range
TSH > 10 benefits from levothyroxine
Treat those with a history of radio-iodine treatment or positive thyroid

147
Q

How do you treat hypothyroidism in special groups ?(Children, pregnancy, older patients with comorbidity, myxoedema coma)

A

Children - Levothyroxine can cause pseudotumour cerebri in children

Pregnancy - Wait untill euthyroid to be pregnant
Measure TFT during first, second and third trimester

Older patients - Start at 25 and up in 25mg segments every 4 weeks

Myxoedema coma - elderly patients, presents with reduced consciousness, seizures, hypothermia, features of hypothyroidism

148
Q

What are complications of hypothyroidism?

A 
Angina
Resistant hypothyroidism
Atrial fibrillation
Osteoporosis
Myxoedema coma
Complications in pregnancy
149
Q

What is Multiple endocrine neoplasia?

A

An AD condition characterised by a predilection to develop tumours of endocrine glands. They are functioning hormone producing tumours in multiple organs.

150
Q

What are the types of MEN?

A

MEN 1

  • Pituitary adenomas
  • Parathyroid tumours
  • Pancreatic islet-cell tumours
  • Fascial anglofibromas and collagenomas

MEN 2a

  • Parathyroid tumours
  • Medullary thyroid cancers
  • Phaeochromocytoma

MEN 2b
- Same as Men 2a with: marfanoid appearance, neuromas of the GI tract

151
Q

What are the signs and symptoms of MEN1?

A

Age of onset of tumours is teenage years
Diagnosis in 4th decade of life
Symptoms and signs depend on organs affected!
Pituitary tumours may cause visual defects

152
Q

What symptoms and signs are seen in different MEN1 tumours?

A

Parathyroid tumours - Hyperparathyroidism - Hypercalcaemia + Nephrolithiasis

Hypergastrinaemia - Zollinger-Ellison syndrome (gastrin secretion)

Hyperinsulinaemia - cancer of pancreatic islet cells

Hyperprolactinaemia
Hypersomatotrophinaemia

153
Q

What are the signs and symptoms of MEN2?

A

Medullary thyroid cancer - HTN, Episodic sweating, Diarrhoea, pruritic skin lesions, lump in neck
Hypercalcaemia - renal stones, abdominal moans and psychic groans (Constipation, polyuria/polydipsia, depression, kidney stones, fatigue)

154
Q

What are the investigations for MEN1?

A

Screening first or second degree relatives
Hormone hypersecretion blood tests
DNA testing

155
Q

What are the investigations for MEN2?

A

Phaeochromocytoma test - 24hr urine metanephrines (followed by abdominal MRI)
Medullary thyroid cancer test - elevated calcitonin conc..
Parathyroid tumours - simultaneously elevated Ca2+ and PTH

156
Q

What is Obesity?

A 
A BMI >30 
OR defined as waist circumference
- Men
     - Low risk = <94cm
     - Very high risk = >102cm
- Women
     - Low risk = <80cm
     - Very high risk = >88cm
157
Q

What are the causes for Obesity?

A

There are genetic factors that affect the risk of becoming obese
There are a few monogenomic forms of obesity (e.g. Leptin deficiency, prader-willi syndrome)

158
Q

What are the signs and symptoms of Obesity?

A

Noticing that you are gaining weight
Symptoms of complications: T2DM, CHD, Obstructive sleep apnoea
High body weight, BMI, waist circumference

159
Q

What are the investigations for obesity?

A 
Measure serum lipids
Measure HbA1c
Hormone profile check 
TFTs - hypothyroidism can cause obesity
Other investigations depend on comorbidities
160
Q

What is Osteomalacia?

A

Disorder of mineralisation of bone matrix (Osteoid). There is normal bone but its mineral content is low

161
Q

What causes Osteomalacia?

A 
Vitamin D deficiency
- Lack of exposure to sunlight
- Dietary deficiency
- Malabsorption
- Decreased Hydroxy vit-D
- Decrased 1alpha hydroxy vit D
Renal osteodystrophy
Drug-induced - anti-convulsants
Renal phosphate wasting 
Fanconi syndrome (phosphaturia, glycosuria, aminoaciduria)
Renal tubular acidosis
Hereditary hypophosphataemic rickets
Tumour induced osteomalacia
162
Q

What are the Risk Factors for Osteomalacia?

A 
Dietary calcium and Vitamin deficiency
Chronic kidney disease
Limited sunlight exposure
Inherited disorders
Hypophosphaturia
Anticonvulsant therapy
Mesenchymal tumours
Fanconi's syndrome
Pregnancy
Obeisty 
Poverty
Alcoholism
Living in countries at high latitude
163
Q

What are the symptoms of Osteomalacia?

A

Osteomalacia

  • Bone pain
  • Fractures, especially femoral neck
  • Proximal myopathy - waddling gait
  • Weakness
  • Malaise
164
Q

What are the symptoms for Rickets?

A

Rickets

  • Hypotonia
  • Growth retardation
  • Skeletal deformities
  • Knock-kneed, bow legged
165
Q

What are the signs for Osteomalacia?

A

Bone tenderness
Proximal muscle weakness
Waddling gait
Sign of hypocalcaemia (Trousseau’s sign, chvostek’s sign)

166
Q

What are the signs for Rickets?

A 
Bossing of frontal and parietal bones
Swelling of costochondral junctions
Bow legs in early childhood
Knock knees in later childhood
Short stature
167
Q

What are the investigations for Osteomalacia?

A 
Serum calcium level (Low)
Serum 25-hydroxy-vit D (Low)
Serum Phosphate level (Low)
Serum urea and creatinine (Ratio elevated)
Intact PTH (High)
Serum ALP (High)
24-hour urinary calcium (Low)
168
Q

What is the management of osteomalacia?

A

Vitamin D and calcium replacement
In malabsorption/hepatic disease: Give Vit D2 (ergocalciferol)
In renal disease or vitamin D resistance give alfacalcidol
Monitor 24hr urinary calcium and weekly plasma calcium
Also monitor: Serum calcium, phosphate, ALP, PTH, Vitamin D
Treat underlying cause!

169
Q

What are the complications of Osteomalacia/rickets?

A

Insufficiency fractures or pseudofractures
Secondary hyperparathyroidism
Metastatic calcification in renal failure
Hypercalcaemia
Hypercalciuria and kidney disease

170
Q

What is Osteoporosis?

A

Reduced bone density (-2.5 on DEXA) resulting in bone fragility and increased fracture risk. This is reduced bone mass

171
Q

If trabecular bone affected what types of fractures are common?

A

Crush fractures of vertebrae (hence littleness and dowagers humps of old women)

172
Q

If cortical bone is affected, what type of fractures are common?

A

Long bone fracture more likely

173
Q

What causes Osteoporosis?

A 
Primary 
- Idiopathic
- Post-menopausal
Secondary 
- Malignancy
- Endocrine (Cushing's disease, thyrotoxicosis, primary hyperparathyroidism, hypogonadism)
- Drugs - corticosteroids, heparin
- Rheumatalogical 
- Gastrointestinal (Malabsorption, liver disease, anorexia)
174
Q

What are the Risk factors for Osteoporosis?

A

SHATTERED + L

S - Steroid use
H - Hyperparathyroidism, hyperthyroidism, hypercalciuria
A - Alcohol and tobacco use
T - Thin (BMI <22)
T - Testosterone low
E - Early menopause
R - Renal or liver failure
E - Erosive/inflammatory bone disease
D - Dietary calcium
\+
L - Low/malabsorption
175
Q

What are the symptoms of Osteoporosis?

A 
Often asymptomatic until fractures occur
Characteristic features:
- Neck of femur (after minimal trauma)
- Vertebral fractures (leading to loss of height, stooped posture)
- Colles' fracture
176
Q

What are the signs of osteoporosis?

A

Often NO signs until complications develop

  • Tenderness on percussion
  • Thoracic kyphosis
  • Severe pain when hip flexed and externally rotated
177
Q

What are the investigations for osteoporosis?

A 
Calcium (Normal in primary)
Phosphate (Normal in primary)
ALP (Normal in primary)
X-ray diagnosign fractures
Isotope bone scan
DEXA scan
178
Q

On a DEXA scan what does the T score indicate?

A

T >-1 is normal
T -1> or >-2.5 is osteopenia
T

179
Q

What is Paget’s disease of the bone?

A

Characterised by excessive bone remodelling at one (monostotic) or more (polyostotic) sites resulting in bone that is structurally disorganised
Increased bone turnover with increased number of osteoblases and osteoclasts with resultant remodelling, bone enlargement, deformity and weakness

180
Q

What causes Paget’s disease of the bone?

A

Unknown
Genetic factors and viral infection
Excessive bone resorption by abnormally large osteoclasts followed by increased bone formation by osteblasts in a disorganised fashion
Results in an abnormal pattern of lamellar bone
Marrow spaces filled by an excess of fibrous tissue with a marked increase in blood vessels

181
Q

What are the Risk factors for Paget’s disease of the bone?

A 
Family history
Age > 50 years
Male sex (45-74 years)
Infection
Environmental factors
182
Q

What are the symptoms of Paget’s disease of the bone?

A 
Asymptomatic
Present with insidious onset pain, aggravated by weight bearing and movement
Headaches
Deafness
Increasing skull size
Fractures
183
Q

What are the signs of Paget’s disease of the bone?

A

Bitemporal skull enlargement with frontal bossing
Spinal kyphosis
Anterolateral bowing of femur, tibia or forearm
Skin over affected bone may be warm
Sensorineural deafness

184
Q

What investigations are done for Paget’s disease of the bone?

A

Very high ALP
Ca2+ and phosphate - normal
Bone radiographs (enlarged, deformed bones), lytic and sclerotic appearance, lack of distinction between cortex and Medulla
Skull changes (Osteoporosis circumscripta, enlargement of frontal and occipital areas, cotton wool appearance)
Bone scan (assess extent of skeletal involvement, pagetic bone lesions)
Resorption markers (monitor disease activity)

185
Q

What is a Phaeochromocytoma?

A

Tumour arising from catecholamine-producing chromaffin cells of the adrenal medulla. Occasionally extra adrenal (Phaeochromocytomas or paragangliomas)

186
Q

What are the causes for Phaeochromocytoma?

A

90% in adrenal medullary catecholamine-producing chromaffin cells
5-10% are multiple
May be sporadic, 40% are hereditary in adults and up to 40% in children
MEN 2A, 2B, von hippel-lindau syndrome

187
Q

What are the Risk factors for Phaeochromocytoma?

A

MEN 2A/2B
Von Hippel-Lindau
Succinate dehydrogenase
Neurofibromatosis type 1

188
Q

What are the signs and symptoms of Phaeochromocytoma?

A 
Headache
Palpitations
Diaphoresis
Hypertension
Hypertensive retinopathy
Pallor
Impaired glucose tolerance/diabetes mellitus
Family history of endocrine disorders
Orthostatic hypotension
Hypercalcaemia
Cushing syndrome
Diarrhoea
Fever 
Papilloedema
Abdominal masses
189
Q

What are the investigations for phaeochromocytoma?

A

24-hour urine collection (Raised catecholamines, normetanephrines and creatinine)
Plasma catecholamines (elevated)
Genetic testing (familial disorders)
Complete blood count (Eryhtrocytes)
Serum calcium (elevated)
Serum potassium (Low)
MRI of abdomen and pelvis (hyper-intense to liver)
CTAP (masses, cenral area of low attenuation)

190
Q

What is a non-functioning pituitary tumour?

A

Benign tumours of the pituitary gland formed from pituitary cells that do not produce any active pituitary hormones
The adenomas can be classes as microadenomas (<1cm) or macroadenomas (>1cm)

191
Q

What are the histological classifications of pituitary tumours?

A

Chromophobe (70%) - most non-secretory, some cause hypopituitarism, 50% produce prolactin
Acidophil (15%) - secrete GH or prolactin
Basophil (15%) - secrete ACTH

192
Q

What are the causes of Pituitary tumours?

A

No specific cause
Cause symptoms due to local pressure effect
Can occur as part of MEN 1 syndrome

193
Q

What are the Risk Factors for Pituity tumours (non-functioning)?

A

MEN 1
Familial isolated pituitary adenomas
Can occur as part of MEN 1 syndrome

194
Q

What are the signs and symptoms of non-functioning pituiary tumours?

A 
Develop VERY SLOWLY 
Headaches
Pressure on surrounding structures:
- Optic chiasm - Bitemporal hemianopia)
- Cavernous sinus - Palsy CN III, IV, VI
- Normal pituitary gland - Panhypopituitarism
195
Q

What are the investigations for non-functioning pituitary tumours?

A

MRI
CT
Bloods - check hormone levels
Visual field testing

196
Q

What is PCOS?

A

Hormonal disorder characterised by oligomenorrhoea/amenorrhoea and hyperandrogenism (clinical or biochemical)
Frequently associated with: Obesity, Insulin resistance, T2DM, Dyslipidaemia

197
Q

What is the cause of PCOS?

A

Environmental and genetic factors
Hyperinsulinaemia results in increased ovarian androgen synthesis and reduced hepatic sex hormone binding globulin
Leads to an increase in free androgens (Which gives rise to the symptoms)

198
Q

What are the Risk factors for PCOS?

A 
Family history of PCOS
Premature adrenarche
Low birth weight
Fetal androgen exposure
Environmental endocrine disruptors
199
Q

What are the symptoms of PCOS?

A

Menstrual irregularities
Dysfunctional uterine bleeding
Infertility
Hyperandrogenism: Hirsutism, Male-pattern hair loss, acne

200
Q

What are the signs of PCOS?

A

Hirsutism
Male-pattern hair loss
Acne
Acanthosis nigricans (signs of severe insulin resistance) - velvety thickening and hyperpigmentation of skin of the axilla or neck

201
Q

What are the investigations for PCOS?

A

Serum LH - High
Serum LH:FSH - High
High testosterone, androstenedione and DHEA-S
Test for: Hyperprolactinaemia, Hypo/hyperthyroidism
CAH
Cushing’s syndrome
Look for impaired glucose tolerance

202
Q

What are the diagnostic criteria for PCOS?

A

Must have atleast 2 of the following:

  • Amenorrhoea/Oligomenorrhoea
  • Clinical/biochemical signs of androgen excess (elevated free testosterone)
  • PCOS seen on USS
203
Q

What is Primary hyperaldosteronism?

A

Aldosterone production exceeds the body’s requirements and is relatively autonomous with regard to its normal chronic regulator, the renin-angiotensin II system

204
Q

What causes primary hyperaldosteronism?

A

Aetiology unknown in most cases
Genetic basis
Excessive aldosterone levels act at the distal renal tubule, promoting sodium retention, which results in water retention and volume expansion with hypertension.
There is excretion of potassium resulting in hypokalaemia

205
Q

What are the risk factors for primary aldosteronism?

A

Family history of primary aldosteronism

Family history of early onset of hypertension and/or stroke

206
Q

What are the signs and symptoms of primary aldosteronism?

A 
Hypertension
20-70 years old
Nocturia
Polyuria
Lethargy
Mood disturbances (Irritability, anxiety, depression)
Difficulty concenctrating
Paraesthesia, muscle cramps
Muscle weakness
Palpitations
207
Q

What are the investigations for Primary hyperaldosteronism?

A 
Plasma potassium (normal or low)
Aldosterone/Renin ratio (>70)
208
Q

How do you manage primary hyperaldosteronism?

A

Unilateral:
Unilateral laparoscopic adrenalectomy with preoperative aldosterone antagonists (spironolactone) and post-operatively.

Bilateral:
No adrenal lesions, aldosterone antagonists
2nd line: laparoscopic adrenalectomy with pre- and post- operative spironolactone

Familial hyperaldosteronism type I:
Glucocorticoids > Aldosterone antagonists
Children: Amiloride > eplenerone

209
Q

What are the complications of Primary hyperaldosteronism?

A 
Peioperative complications
Stroke
Myocardial infarction
Heart failure
Atrial fibrillation
Impaired renal function
Aldosterone antagonist or mineralocorticoid receptor antagonist-induced hyperkalaemia
210
Q

What is a prolactinoma?

A

Benign lactotroph adenomas expressing and secreting prolactin

211
Q

What causes a prolactinoma?

A

Different types of prolactinoma:

  • Microadenoma
  • Macroadenoma
  • Giant pituitary adenomas
  • Malignant prolactinoma
212
Q

What are the risk factors for prolactinoma?

A

Female gender (20-50)
Genetic predisposition
Oestrogen therapy
Male gender (30-60)

213
Q

What are the symptoms for Prolactinoma?

A 
Amenorrhoea or Oligomenorrhoea
Galactorrhoea
Loss of libido 
Erectile dysfunction
Visual deterioration (e.g. bitemporal hemianopia)
Headaches
Dry Vagina
Reduced beard growth
214
Q

What are the signs for prolactinoma?

A 
Osteoporosis
Ophthalmoplegia
Infertility
Hypopituitarism
Cranial nerve palsies
215
Q

What investigations are done for Prolactinoma?

A 
Exclude pregnancy
TFTs (Normal)
Serum Prolactin (Raised)
Pituitary MRI (Characteristic features)
Visual-field exam
216
Q

What managements are done for Prolactinoma in pre-menopausal women?

A

Asymptomatic Microprolactinomas - observe

Symptomatic microprolactinomas - Dopamine agonist (Cabergoline then bromocriptine) > Combined oral contraception > Trans-sphenoidal surgery > Sellar radiotherapy

Microprolactinomas who desire pregnancy or macroprolactinomas - Dopamine agonist (Cabergoline then bromocriptine)> Trans-sphenoidal surgery > Sellar radiotherapy

217
Q

What managements are done for post-menopausal women?

A

Microadenomas - observations

Macroadenomas - Dopamine agonist (Cabergoline > Bromocriptine) > Trans-sphenoidal surgery > Sellar radiotherapy

218
Q

What are the complications for Prolactinoma?

A

Visual field impairment
Anterior pituitary failure and/or diabetes insipidus
Hypopituitarism associated with radiotherapy
Cabergoline-associated valvular insufficiency
Pituitary apoplexy
Cerebrospinal fluid leakage

219
Q

What is SIADH?

A

Continuous secretion of ADH, despite the absence of normal stimuli for secretion. Plasma vasopressin concentration is inappropriate for teh existing plasma osmolarity

220
Q

What is the cause SIADH?

A

Drugs (SSRI, amiodarone, carbamezapine)
Pulmonary processes (Infections)
Malignancy (Gastro, lung)
CNS disorders: CNS infections, brain trauma
Lung: Pneumonia, TB, abscess, aspergillosis
Anaesthesia and postoperative state
Nephrogenic SIADH or pseudo siadh caused by gain of function mutations in V2

221
Q

What are the risk factors for SIADH?

A 
Age >50 years
Pulmonary condition (e.g. pneumonia)
Nursing home residence
Malignancy
Medicine associated with SIADH induction
CNS disorders
Postoperative state
Endurance exercise
222
Q

What are the symptoms for SIADH?

A 
Decreased urine volume, concentrated urine
Mild hyponatraemia
Headache
Nausea/vomiting
Muscle cramp/weakness
Irritability
Confusion
Drowsiness
Convulsions
Coma
223
Q

What are the signs for SIADH?

A 
Mild hyponatraemia (no signs)
Severe hyponatraemia (reduced reflexes, extensor plantar reflexes)
Signs of underlying cause
224
Q

What investigations are done for SIADH?

A 
Serum Sodium (<135)
Serum Osmolality (<280)
Serum Urea (<3.6)
Urine sodium (>40)
Urine osmolality (>100)
Serum cortisol (>138)
CXR
CT/MRI
225
Q

What is the management for SIADH?

A

Severe symptoms
IV hypertonic saline + fluid restriction, treat cause + furosemide

Mild to moderate: Treat cause + fluid restriction

Asymptomatic (Na+ = 125)
Fluid resuscitation + treat underlying cause

How do you treat ongoing SIADH?
Fluid restriction + treat underlying cause > Tolvaptan > Sodium chloride > Demeclocycline

226
Q

What are the complications of SIADH?

A

Central pontine myelinolysis - brain used to hyponatraemia.

Overcorrection of hyponatraemia, seizures, death and come can occur

227
Q

What is thyroid cancer?

A

Malignancy arising in the thyroid gland

228
Q

What are the types of Thyroid cancer?

A 
Papillary
Follicular
Medullary
Lymphoma
Anaplastic
229
Q

What are the causes of thyroid cancer?

230
Q

What are the risk factors for Thyroid cancer?

A

Childhood exposure to radiation
Medullary thyroid cancers may be familial or associated with MEN 2a or 2b
Lymphoma associated with Hashimoto’s thyroiditis

231
Q

What are the symptoms of Thyroid cancer?

A

Slow-growing neck lump
Discomfort swallowin
Hoarse voice

232
Q

What are the signs of thyroid cancer?

A

Palpable nodules or diffuse enlargment of thyroid gland
Cervical lymphadenopathy > suspect malignancy
Patient is usually euthyroid!

233
Q

What are the investigations for Thyroid cancer?

A

TFTs (TSH normal)
Bone profile
Thyroid autoantibides if hashimotos/graves
Tumour markers (thyroglobulin (papillary and follicular), calcitonin (medullary))
CXR with thoracic inlet (goitres and mets)
USS
Radionulcide scan
FNA cytology

234
Q

What are thyroid nodules?

A

Abnormal growth of thyroid cells that forms a lump in the thyroid gland

235
Q

What causes thyroid nodules?

A

Vast majority of thyroid nodules are benign, small proportion turn into thyroid cancer
Most nodules are adenomatous and most are multiple
Nodules are usually non-functioning

236
Q

What are the risk factors for thyroid nodules?

A

Family history
Age
Women
Radiation

237
Q

What are the symptoms for Thyroid nodules?

A

Asymptomatic
Potential pain/rarely tracheo-oesophageal compression
Nodular goitre rather than smooth
Single nodule more likely to be malignant

238
Q

What are the signs for thyroid nodules?

A

Nodule moves when swallowing

Check for regional lymphadenopathy (consider malignancy)

239
Q

What investigations are done for thyroid nodules?

A 
TFTs (normal, can be hypo)
Ultrasound 
FNA (Allows cytological analysis)
Radionuclide isotope scanning (Checks iodine uptake)
CT/MRI - detect spread
240
Q

What is thyroiditis?

A

Inflammation of the thyroid gland

241
Q

What causes thyroiditis?

A 
Hashimoto's - AI condition
De Quervian's thyroiditis - Painful dysphagia, pyrexia (Virus attacks - present hyperthyroid, once virus void, euthyroid)
Post partum thyroiditis
Drug-induced thyroiditis
Acute or infectious thyroiditis
Riedel's thyroiditis
242
Q

What are the symptoms of thyroiditis?

A

Hypothyroidism (Fatigue, constipation, dry skin, weight gain, cold intolerance, acute or infectious thyroiditis, riedel’s thyroiditis)
Of rapid enlargement of the thyroid gland:
- Dyspnoea
- Dysphagia
- Tenderness

243
Q

What are the investigations for thyroiditis?

A 
Histology: diffuse lymphocytic and plasma cell infiltration with formation of lymphoid follicles
TSH - Raised
Anti-TPO / Anti-thyroglobulin antibodies
Thyroid ultrasound
Radiomuclide isotope scanning
CRP/ESR raised
244
Q

What is the management of thyroiditis?

A

Pharmacological
- Thyroid hormone replacement - oral levothyroxine sodium
- Titrate dose based on patients need
Surgical
- Considered if large goitre causing symptoms

245
Q

What are the complications of Thyroiditis?

A

Thyroid hormone over-replacement
Hyperlipidaemia
Hashimoto’s encephalopathy
Myxoedema coma

Conditions (18 decks)

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