Endocrinology (Quesmed) Flashcards

1
Q

What is Acromegaly?

What usually causes it?

A

It is a hormone condition due to Excess Growth Hormone Secretion, usually due to a secreting Pituitary Adenoma

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2
Q

What are the signs of Acromegaly?

A
  • Outward growth of the Jaw and Head with increased Interdental Spacing and Macroglossia
  • Increased Sweating (Oily)
  • Large Heads and Feet

Coarse Facial Features
Headaches
!!!!Erectile Dysfunction
Mood Disturbances

Voice Change
Fatigue

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3
Q

What investigations should be ordered in Acromegaly?

What is done first?
What big thing is measured next?
What are the 2 imaging options?

A

IGF-1 (to Screen)

If it is raised or equivocal- measure GROWTH HORMONE following the intake of Oral Glucose (ORAL GLUCOSE TOLERANCE TEST) to see if Growth Hormone is Inappropriately Suppressed (this Confirms)

If Acromegaly has been diagnosed, an MRI should be performed to assess the size and the extent of the tumour

If MRI is contraindicated, CT is second line. If the tumour is too close to the optic chiasm, assess Visual Fields

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4
Q

What is the management of Acromegaly?

A

Trans-sphenoidal Surgery

If Refractory or if they can not undergo surgery-
- Somastatin Receptor Ligands (OCTREOTIDE)
- Pegvisomant (GH Analogue)
- Cabergoline (Dopamine Agonist)
- Radiotherapy

Measure IGF1 and random Growth Hormone 3 months after the surgery

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5
Q

What are the complications of Acromegaly?

One that happens in 80% of people?
3Cs and 3Hs what is seen in Congestive cardiac failure (2)
5 more

A

Sleep Apnoea (happens in 80%)

Congestive Heart Failure (Cardiomegaly and LVH- ECHOCARDIOGRAPHY to CHECK for THIS)
Hyperhidrosis
Carpal Tunnel Syndrome
Hypertension
!!!!!!!Cerebrovascular Disease
!!!!!!Hypopituitarism

Arthritis
Increased Risk of Colonic Polyps that can turn cancerous (so COLONOSCOPY every 5 years)
!!!!Visual field defects
Ischaemic Heart Disease
Type 2 Diabetes Mellitus

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6
Q

What kind of Tumours are associated with the 3 Multiple Endocrine Neoplasias (MEN)?

A

MEN1 (3Ps)
- Pituitary
- Pancreas
- Parathyroid

MEN2a (3Cs)
- Calcitonin (Medullary Thyroid)
- Calcium (Parathyroid)
- Catecholamines (Pheochromocytoma)

MEN2b (Big and Belly)
- Medullary Thyroid
- Phaeochromocytoma
- Mucosal tumours (GI Tract)

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7
Q

What is Adrenal Insufficiency?

A

Destruction of Adrenal Cortex leading to reduction of Glucocorticoid Production

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8
Q

What are the Primary Causes of Adrenal Insufficiency? (Addison’s)

What should be suspected if there is haemorrhagic shock?

What is the most common cause and most common cause in the developing world?

What 3 are the least common but still happen?

A

Autoimmune (most common)

Surgical removal

Trauma

Infections (TB- most common in developing world)

Haemorrhage (Waterhouse-Friderichsen Syndrome) (look for SHOCK)

Infarction

!!!!!(Neoplasm, Sarcoidosis, Amyloidosis (less common))

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9
Q

What are the Secondary Causes of Adrenal Insufficiency?

(Brain causes)

A

Congenital
Base of Skull Fracture
Surgery/ Radiotherapy
Neoplasm
Infiltration or Infection of the Brain
!!!!!CRH Deficiency

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10
Q

What are the signs of Adrenal Insufficiency?

What is only seen in Primary?

A

!!!!Fatigue and Weakness
!!!!GI Symptoms (nausea, vomiting, weight loss)
!!!!Syncope

  • Hyperpigmentation (due to HIGH ACTH Precursors)- Palmar Creases- !!!!only seen in PRIMARY- not secondary
  • Hypotension
  • Hypoglycaemia
  • Hyponatraemia, Hyperkalaemia and !!!!!Weight Loss- Addison’s
    so SALT CRAVING
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11
Q

What Investigations should be ordered in Adrenal Insufficiency/ Addison’s?

What is the first line and second line?

When are the Renin and Aldosterone levels affected and how are they affected?

What things should be done to establish the cause?

A

!!!!!FIRST LINE- Morning Serum Cortisol (low)
SECOND LINE- Short Synacthen (Cortisol Levels do not rise)

LOW Sodium
Low Glucose
Low Cortisol
Low Aldosterone (in Addison’s)

HIGH Potassium
High Renin (in Addison’s)

ACTH is high in Primary Insufficiency, low in Secondary Insufficiency

ACTH (Short Synacthen Test) is used to confirm the diagnosis

To Establish Cause-
1) Adrenal Auto-antibodies
2) Chest Xray
3) CT of the Adrenals
4) MRI of the Brain

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12
Q

What is the management of Adrenal Insufficiency?

What should be done in an Addisonian Crisis?

A

Hydrocortisone for Glucocorticoid Replacement
Fludrocortisone for Mineralocorticoid Replacement

What is the management of Addisonian Crisis?
- Aggressive Fluid Resuscitation (1L of Saline) and IV Steroids (Hydrocortisone)
- !!!!!!Glucose is used if there is Hypoglycaemia

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13
Q

What are some facts about Amiodarone Induced Thyrotoxicosis?

What investigations should be ordered?

A

TFTs should be completed as part of drug monitoring with Amiodarone

Amiodarone can directly trigger thyroid disease through Thyroiditis or can trigger an underlying Autoimmune Thyroid Disease

To correctly diagnose the type of Amiodarone Induced Thyrotoxicosis- check the Patient’s Antibody Status and undertake Specialist Imaging of the Thyroid Gland like
1) Thyroid Uptake Scan
2) Colour Flow Doppler Ultrasound

Amiodarone Induced Thyrotoxicosis Type 1 show NORMAL UPTAKE on scans and INCREASED VASCULARITY on Doppler Imaging

Amiodarone Induced Thyrotoxicosis Type 2 show DECREASED UPTAKE and REDUCED VASCULARITY

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14
Q

What is the Management of Amiodarone Induced Thyrotoxicosis?

A

Steroids plus Antithyroid (Carbimazole)

Discuss whether Amiodarone needs to be continued

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15
Q

What are the Mechanisms of Action of the 7 types of Antidiabetics?

A

Biguanides (Metformin)
- Increase Peripheral Insulin Sensitivity and Hepatic Glucose Uptake

Sulfonylureas (Gliclazide)
- Depolarise Islet Cells in the Pancreas increasing the Insulin Release

Thiazolidinediones (Pioglitazone)
- Increases Peripheral Insulin Sensitivity

SGLT2 Inhibitors (Dapgliflozin)
- Increase Urinary Glucose Loss

DPP4 Inhibitors (Sitagliptin)
- Inhibit GLP1 Breakdown

GLP1 Analogues (Exenatides)
- Increase Insulin Secretion and Sensitivity

Intestinal Alpha-Glucosidase Inhibitors (Acarbose)
- Delay Intestinal Carbohydrate Absorption

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16
Q

What are Carcinoid Tumours?

A

Malignant tumours that develop in the Neuroendocrine System. The Appendix and Small Intestine are common origins. 5-10% of the tumours secrete Hormones- especially SEROTONIN

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17
Q

What are the signs of Carcinoid Tumours?

What are the 3 core symptoms?

A

*Diarrhoea
*Flushing
*Wheeze

Abdominal Pain
Pulmonary Stenosis

These symptoms are caused by Serotonin and its breakdown products on the Systemic Circulation.

Patients with Gastrointestinal Carcinoid Tumours only experience these symptoms if they have LIVER METASTASES, as the products of the tumours can drain straight into the Hepatic Veins without undergoing metabolism in the liver itself.

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18
Q

What is the management of Carcinoid Tumours?

A

Octreotide to inhibit the tumour products

Surgical Resection to decrease the Tumour Size

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19
Q

What investigation should you order if you suspect Carcinoid Tumours?

A

Urinary 5HIAA (it is a product of Serotonin)

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20
Q

What is Charcot Arthropathy?

A

The Bones and Joints get destroyed after the Sensory Nerves are Lost

It is a Chronic Destructive Disease of the Bone and Joints in Patients with Neuropathy

It is characterised by Painful or Painless Bone and Joint Destruction in Patients with Limbs that have lost Sensory Innervation

Bones get destroyed after sensory nerves stop working

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21
Q

What is the main cause and other cause of Charcot Arthropathy?

A

Diabetes causing Autonomic and Peripheral Neuropathy

Also SYPHILIS can cause it

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22
Q

What is the main differential to rule out in Charcot’s Arthropathy?

A

Osteomyelitis

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23
Q

What are the signs of Charcot’s Arthropathy?

A

Swollen, red, inflamed joint that is most likely painful in the context of NEUROPATHY

5Ds

Destruction
Deformity
Degeneration
Dense Bones
Debris

Generally affecting the TARSOMETATARSAL JOINTS in the feet

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24
Q

What is the management of Charcot Arthropathy?

A

Conservative (Avoid using the joints/ bones)
- Prolonged Immobilisation (Offloading)
- Orthotics (braces, splints)

Medications (Bone, Nerve, Pain)
- Bisphosphonates
- Neuropathic Pain Agents
- Topical Anaesthetics

Surgical
- Resection of Bony Prominences
- Deformity Correction
- Amputation

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25
Q

What are the causes of Cushing’s Syndrome?

A

ACTH-dependent= Pituitary Tumour, Ectopic ACTH-producing Tumours

Non-ACTH dependent= Adrenal Adenomas, Adrenal Carcinomas

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26
Q

What are the signs of Cushing’s Syndrome

A

Moon Face
Obesity with Centripetal Obesity
Striae
Bruising
Interscapular and Supraclavicular Fat Pads (Buffalo Hump)

!!!!!!!!!!Erectile Dysfunction (Impotence)

!!!!!!!Osteopenia and Osteoporosis

!!!!!!!Acne and Hirsutism

!!! Opposite of Adrenal Insufficiency -HYPOKALAEMIA and HYPERTENSION
HYPERGLYCAEMIA

Proximal Myopathy
Thin Skins
Thin Limbs

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27
Q

What Investigations should be ordered in Cushing’s Syndrome?

A

FIRST= Wean them off any steroid medications they are on

To confirm High Cortisol=
1) Low dose Dexamethasone Suppression Test
2) 24 Hours Urinary Cortisol

To Localise it=
1) Plasma ACTH
2) High dose Dexamethasone Suppression Test
3) !!!!!!Inferior Petrosal Sinus Sampling
4) MRI of the Pituitary
5) CT Chest and Abdomen (suspected Tumour)

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28
Q

What is the management of Cushing’s Syndrome?

A

First= MEDICAL THERAPY before Surgery

Medical=
- Metyrapone (to block Synthesis of Steroids)
- Also can give Ketoconazole (Adrenolytic Agent), Mifepristone (Glucocorticoid Antagonist) and Pasireotide (Somatostatin Receptors)

Surgical=
- Pituitary Tumour Resection
- If high cortisol continues after surgery- Radiotherapy is needed

Post surgery= Steroid Replacement, give them a STEROID CARD and MEDIC ALERT BRACELET

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29
Q

What is Nelson’s Syndrome?

A

After a Bilateral Adrenalectomy has been done (like AFTER CUSHING’s TREATMENT)

There is LOSS of feedback to the brain so we get high CRH from the hypothalamus

This leads to an increase in Anterior Pituitary activity and the formation of an Adenoma

This causes Headaches, Visual Field Defects and Skin Pigmentation

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30
Q

How does Cortisol increase Plasma Glucose?

A

It Inhibits Insulin-mediated Glucose Disposal

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31
Q

What is the most common type of Ectopic ACTH Production? And what are the investigations that should be ordered?

A

Small Cell Lung Carcinoma- Increased Skin Pigmentation
- Plus look out for signs of OTHER Lung conditions (COPD, Weight Loss, Pneumonia)

NO Suppression of cortisol in Low or High Dose Dexamethasone administration

High ACTH

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32
Q

What is the most common cause of Exogenous Cushing’s Syndrome?

A

Oral Corticosteroids

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33
Q

What are the investigations for a Pituitary Adenoma in Cushing’s?

A

!!!!!!!!!!!!!Both Cortisol and ACTH are SUPPRESSED after High Dose Dexamethasone

Cortisol High after Low Dose Dexamethasone
Cortisol Normal after High Dose Dexamethasone
ACTH high

Perform MRI of the Pituitary

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34
Q

What are some of the main side effects of Steroids?

A

1) Cushing’s symptoms
2) Psychiatric- Mania, Psychosis, Depression
3) Increased appetite
4) IMMUNOSUPPRESSION
5) !!!!!!GLAUCOMA and CATARACTS
6) !!!!!!Intracranial Hypertension

MINERALOCORTICOID
- Fluid Retention
- Hypertension

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35
Q

What should be suspected if a patient presents with Cushing’s like Symptoms with Raised 24 Hour Cortisol and raised ACTH but NORMAL DIURNAL VARIATION of Cortisol?

What other test can you use to differentiate this?

A

Chronic Alcoholism

Use the Insulin Test to differentiate

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36
Q

What is Diabetes Insipidus?

A

It is the Abnormal Quantity of ADH (Cranial Cause)

or Abnormal Response to ADH (Nephrogenic Cause)

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37
Q

What are the signs of Diabetes Insipidus?

A

Large Volumes of Dilute Urine
(>3 litres in 24 hours and Serum Osmolality<300)

Patients also have Nocturia and Excessive Thirst

Signs of Hypernatraemia
- Lethargy
- Thirst
- Weakness
- Confusion
- Coma

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38
Q

What are the causes of Cranial (5) and Nephrogenic (4) Diabetes Insipidus?

A

Cranial
- Head Trauma
- !!!!!!!!!Inflammatory Disease (Sarcoidosis)
- Cranial Infections (Meningitis)
- Vascular Conditions (Sickle Cell Disease)
- Rare Genetic Cause

Nephrogenic
- Drugs (Lithium)
- !!!!!!!!!!!!! Metabolic Disturbance (Hypercalcaemia, Hyperglycaemia, Hypernatraemia, Hypokalaemia)
- Chronic Renal Disease
- Rare Genetic Cause (Wolfram’s Syndrome)

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39
Q

What investigations should be ordered in Diabetes Insipidus?

What can be done to confirm if still uncertain?

A

Baseline=
1) Urea and Electrolytes
2) Blood Glucose (to rule out Diabetes Mellitus)
3) Urine Dip
4) Paired Serum and Urine Osmolality

SERUM Osmolality is raised (>290), URINE Osmolality is low (<700)

SERUM Sodium is raised, URINE Sodium is low

You can also do a Fluid Deprivation Test if the diagnosis is unclear

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40
Q

What is the management of Cranial and Nephrogenic Diabetes Inspidus?

What should be monitored with treatment for Cranial Diabetes Insipidus?

A

Cranial
- Desmopressin
- Sodium should be monitored as there is a risk of HYPONATRAEMIA

Nephrogenic
- !!!!!!!!!!!!THIAZIDES
- Correcting Metabolic Abnormalities and stopping any offending drugs
- High dose Desmopressin can be used
- Other treatments= Thiazide Diuretics and NSAIDs to reduce Urine Volume

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41
Q

What are the causes of Diabetic Ketoacidosis?

A

Infection (so may have Fever cos of this)
Dehydration
Fasting
First Presentation of Type 1 Diabetes

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42
Q

What are the signs of DKA?

There is basically just 4 with others linked to them

A

1) Fruity Acetone Breath

2) !!!!!!Hyperventilation (Kussmaul)

3) Abdominal Pain

4) Vomiting

  • Therefore-

Dehydration

!!!!!Hypovolaemic Shock

Drowsiness

Coma

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43
Q

What investigations should be ordered if DKA is suspected?

What metabolic sign is seen?- consider the fact that they are going to be vomiting a lot

A

Blood Glucose (>11.1mmol/L)
Blood Ketones (>3mmol/L)
pH<7.3 or Bicarbonate<15

Blood Gas
Urinary Ketones and Glucose
HYPOKALAEMIA may be present- ECG may show HYPOKALAEMIA or ISCHAEMIC Changes

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44
Q

What are the 5 types of Diabetic Neuropathy?

A

Distal Symmetry Sensory Neuropathy
- MOST COMMON
- Caused by loss of Large Sensory Fibres
- Glove and Stocking Distribution
- Often Affecting Touch, Vibration and Proprioception

Small-fibre Predominant Neuropathy (Touch is NOT AFFECTED- so no tingling- just loss of pain and temp)
- Caused by loss of Small Sensory Fibres
- Presents with Deficits in Pain and Temperature Sensation in a Glove and Stocking Distribution along with episodes of Burning Pain (Touch Preserved)

Diabetic Amyotrophy (Amyotropy= Hips/ Thighs instead of Glove/ Stocking)
- Caused by Inflammation of Lumbosacral Plexus or Cervical Plexus
- Severe pain around Thighs or Hips
- Proximal Weakness

Mononeuritis Multiplex (loss of REFLEXES in the affected area)
- Invariable Pain
- Neuropathies involve TWO Peripheral Nerves

Autonomic Neuropathy (Non-myotome/dermatome specific)
- Postural Hypotension
- Gastroparesis
- Constipation and Urinary Retention
- Arrhythmias
- Erectile Dysfunction

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45
Q

What is the first line treatment of Diabetic Neuropathy?

A

Pregabalin, Duloxetine and Gabapentin

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46
Q

What is the first line management of Gastroparesis in Autonomic Neuropathy in Diabetes?

A

Stabilise the Blood Sugar Levels

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47
Q

What are the types of Diabetes Retinopathy?

A

Non-Proliferative Diabetic Retinopathy (NPDR)

Proliferative Diabetic Retinopathy (PDR)

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48
Q

What is seen in the Fundoscopy for Diabetic Retinopathy?

A

If Milder Disease-
- Dots (Microaneurysms)
- Hard Yellow Exudates (Lipid Deposits)
- Blots (Haemorrhages)

If Significant Ischaemia-
- Engorged Tortuous Veins
- !!!!Cotton Wool Spots
- Large BLOTS (Haemorrhages)

In PDR, new blood vessels can be seen in the retina

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49
Q

What is Diabetic Maculopathy?

A

It is a Macular Oedema caused by Leakage of the Vessels close to the Macula

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50
Q

What 3 features on Ophthalmology warrant IMMEDIATE Referral to an Opthalmologist in Diabetes Retinopathy?

A
  • Proliferative Retinopathy (New Blood Vessels)
  • Vitreous Haemorrhage
  • Advanced Retinopathy with Retinal Detachments
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51
Q

What are the 5 possible causes of Erectile Dysfunction?

A
  • Vascular Diseases (Atherosclerosis)
  • Autonomic Neuropathy (Penile Denervation due to Diabetes or !!!!!Increased Alcohol Intake)
  • !!!!!!Drugs (Antihypertensives)
  • Psychogenic
  • !!!!!Endocrine Causes (!!!!!Prolactinoma, Hypogonadism)
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52
Q

What are the 7 possible causes of Erectile Dysfunction?

A
  • Vascular Diseases (Atherosclerosis)
  • Autonomic Neuropathy (Penile Denervation due to Diabetes or Increased Alcohol Intake)
  • Drugs (Antihypertensives)
  • Psychogenic
  • Endocrine Causes (Prolactinoma, Hypogonadism)
  • Pelvic Surgery (Bladder, Prostate)
  • Anatomical Abnormalities (Peyronie’s Disease)
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53
Q

What investigations should be ordered in Erectile Dysfunction?

A

Sexual and Psychological History

9am TESTOSTERONE is the most important

Blood Tests- Full Blood Count, Urea and Electrolytes, Thyroid Function, Lipids, Testosterone, Prolactin

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54
Q

What is the management of Erectile Dysfunction?

A

Oral Phosphodiesterase Inhibitors (Sildenafil)

Psychosexual Therapy

Vacuum Aids

Intra-cavernosal Injections

Prosthesis

Tell them to STOP CYCLING if they cycle more than 3 times a week

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55
Q

What are the Contraindications and Cautions of using Sildenafil?

A

Contraindicated in:
1) !!!!!!Those taking Nitrates
2) Uncontrolled Hypertension (>170/100)/ Hypotension
3) Arrhythmias
4) Unstable Angina
5) Stroke (last 6 months)
6) Recent Myocardial Infarction (last 3 months)
7) Heart Failure (last 6 months)

Caution in:
1) Angina
2) !!!!Peptic Ulcer
3) !!!!!!Liver or Kidney Impairment
4) !!!!!Peyronie’s Disease
5) !!!!!!Complex Antihypertensive Regimes (Remember this is a cause of Erectile Dysfunction as well)

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56
Q

What are the possible results of a Fluid Deprivation Test?

(Does giving Desmopressin help with the Urine Osmolality?)

A

1) Cranial Diabetes Insipidus-
- Low Urine Osmolality (<300) after Fluid Deprivation
- But Normalised Osmolality after DESMOPRESSIN is given as issue is that the hormone isn’t produced

  • Treat with Desmopressin

2) Nephrogenic Diabetes Insipidus-
- Urine Osmolality is low even after Desmopressin is given as issue is that there is resistance to the hormone

  • Treat the reversible causes and ensure Adequate Fluid Intake. Desmopressin, Thiazide Diuretics and Prostaglandin Synthase Inhibitors can be given

3) Primary Polydipsia-
- Urine Osmolality is normal after Fluid Deprivation and after Desmopressin

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57
Q

What are the causes of Galactorrhoea in Men?

What are the 4 drugs associated with it?

A
  • Idiopathic
  • Prolactinoma
  • !!!!!!!Drugs- Antipsychotics, SSRIs, Cimetadine, Beta Blockers
  • Metabolic Conditions- Hypothyroidism, Liver Disease, Chronic Renal Impairment
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58
Q

What is the management of Galactorrhoea in Men?

A

Switch medications if that is the suspected cause

!!!! If they have a significant mental health issue (like Schizophrenia), then give a dopamine agonist like Cabergoline/ Bromocriptine to help counter the side effects of the Antipsychotic they are taking

But this can make the original drug less effective

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59
Q

What are the causes of Smooth and Nodular Goitres?

Which 2 drugs cause a smooth goitre and which condition causes a painful one?

What 2 infiltrations can cause Smooth Goitres?

A

Smooth Goitres-
- Grave’s Disease
- Hashimoto’s Disease
- Drugs (Lithium and Amiodarone)
-!!!!!Iodine Deficiency or Excess
- De Quervain’s Thyroiditis (PAINFUL)
- !!!!!!!!!!!!!!!!!Infiltration (Sarcoid/ Haemochromatosis)

Nodular Goitres (Cysts and Cancers)-
- Toxic Solitary Adenoma
- Non-Functional Thyroid Adenoma
- Multinodular Goitre
- Thyroid Cyst
- Cancer

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60
Q

What investigations should be conducted if there is a Goitre in the context of Hyperthyroidism?

A

Ultrasound Scan and Radioisotope Scan

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61
Q

What is the First Line Management of a Toxic Adenoma (Thyroid)?

A

RadioIodine Administration

62
Q

What are the causes of Gynaecomastia?

A

High Oestrogen or Low Testosterone

  • Obesity
  • Anabolic Steroid
  • Tumours (Sertoli, Leydig)
  • Chronic Illness (Testosterone is suppressed more than Oestrogen in Malnourishment)
  • Exogenous Oestrogen
  • Hyperthyroidism
  • Hypogonadotrophic Hypogonadism (Low FSH, LH and Testosterone)
  • Hyperprolactinaemia (Pituitary Disease)
  • Testicular Failures (Infection or Chemotherapy Damage)
  • Medications (Spironolactone, GnRH Agonists, some Chemotherapy Agents, Digoxin, Ketoconazole)
63
Q

What is the management of Gynaecomastia?

A
  • Observation and Reassurance
  • Treat underlying cause- Hypogonadism with Testosterone
  • Tamoxifen
  • Danazol
  • Breast Reduction Surgery
64
Q

What are the signs of Klinefelter’s?

A

Tall Stature
Gynaecomastia
Delayed Puberty and Hypogonadism

47XXY

65
Q

What is Hirsutism and what are the causes of Hirsutism?

Remember Hypothyroidism/ T2DM and the medications SCP

A

Excess Hair in Females- in back, chest due to Increased Testosterone and Increased Sensitivity to Androgens
- Deep Voice, Acne, Frontal Balding, Large Muscles, Mood Changes

1) PCOS- most common cause
2) Androgen secreting tumours
3) Congenital Adrenal Hyperplasia
4) Cushing’s Syndrome
5) Acromegaly
6) Severe Insulin Resistance (Diabetes)
7) Idiopathic
8) Certain Medications- Steroids, Phenytoin, Ciclosporin
9) Anorexia Nervosa
10) Underactive Thyroid
11) Familial Trait

66
Q

What Investigations should be ordered in Hirsutism?

A

Serum Testosterone

Check for Rotterdam Criteria for PCOS Diagnosis
(Biochemical and Clinical Evidence of Testosterone Excess and Ultrasound evidence of Polycystic Ovaries)

67
Q

What are the causes of Hyperaldosteronism and Conn’s Syndrome?

A

Adrenal Adenoma (Conn’s Syndrome)
Bilateral Adrenal Hyperplasia (which is the most common cause)
Familial Hyperaldosteronism
Adrenal Carcinoma

68
Q

What are the signs of Hyperaldosteronism/ Conn’s Syndrome?

Hypertension PLUS Hypokalaemia with no other obvious features

A

Hypertension
Hypokalaemia
Metabolic Alkalosis

!!!!Polyuria
!!!!Polydipsia
Lethargy
!!!!Headaches
!!!!Osteoporosis

69
Q

What investigations should be ordered in Hyperaldosteronism/ Conn’s Syndrome?

What is the Gold Standard?

A

FBC/ UE/ LFTs
ESR
Bone Profile (for Osteoporosis)
TFTs
ECG
Chest X ray

1) FIRST- Aldosterone/ Renin Ratio
2) CT/MRI for the Adrenal lesions
3) GOLD STANDARD= Adrenal Venous Sampling

70
Q

What is the management of Hyperaldosteronism/ Conn’s Syndrome?

A

Identify the cause with Specialist Imaging or Adrenal Venous Sampling

Surgically remove the affected Adrenal Gland

Or if Bilateral- Potassium Sparing Diuretics (Amiloride, Spironolactone, Eplerenone)

71
Q

What should be suspected if the ratio of Renin to Aldosterone is fine but the actual levels are elevated in the Context of Hypertension?

so that means that renin is also high

A

Secondary Hyperaldosteronism

Like- Nephrotic Syndrome and other Congestion Diseases (Liver Cirrhosis, Congestive Cardiac Failure, Renal Artery Stenosis)

72
Q

What are the 2 Drug Causes of Hyperthyroidism?

A

Amiodarone and Lithium

73
Q

What is the management of Hyperthyroidism?

A

Symptomatic Relief- Propanolol
Medical Management- Carbimazole (avoid in Pregnancy, but safe in LATE pregnancy)/ Propylthiouracil- P for Pregnancy

74
Q

What is the management of a Thyroid Storm?

Standard Thyroid Management + 2 others

A

1) IV Propanolol

2) !!!!!IV Digoxin

3) Propylthiouracil through NG Tube, followed by Lugol’s Iodine 6 hours later

4) Prednisolone and Hydrocortisone

75
Q

What are the signs of a Thyroid Storm?

A

Agitation and Confusion

Vomiting

High Temperature

Palpitations and Tachycardia

76
Q

What is the most common cause of Hyperthyroidism?

A

Graves’ Disease (Anti-TSH)

77
Q

What is Subacute Thyroiditis and how is it managed?

A

A Viral Illness releases Preformed Hormones which is converted into T3 and T4

So standard Thyroid treatment is ineffective and you have to use Supportive Care

78
Q

How does Carbimazole work?

A

It inhibits Thyroid Peroxidase
- Stops T3 and T4 production

79
Q

What is the most serious side effect of Carbimazole?

A

Agranulocytosis- so watch out for Infections

(So like Clozapine)

80
Q

What thyroid conditions cause Radioisotope Uptake to be increased and decreased?

A

/Remember DTG for uptake in that order/

De Quervain’s= DECREASED UPTAKE

Toxic Thyroid Adenoma= INCREASED UPTAKE on ONE SIDE

Graves’= INCREASED UPTAKE

81
Q

Does De Quervain’s cause Hyperthyroidism or Hypothyroidism?

A

Hyperthyroidism first followed by a phase of Hypothyroidism

82
Q

What is the main risk factor for Thyroid Eye Disease in Graves’ Disease?

A

SMOKING increases the risk of THYROID EYE DISEASE in Graves

83
Q

What should be given to postpartum women presenting with Hyperthyroidism symptoms?

A

Propanolol (as it is transient) so just manage the symptoms- no need to worry about the actual thyroid levels

84
Q

What are the 6 causes of Hypocalcaemia?

A

1) Vitamin D Deficiency
(Malnutrition (Osteomalacia), Malabsorption, CKD)

2) Hypoparathyroidism
(Postparathyroidectomy, Inherited, Pseudohypoparathyroidism)

3) Hyperphosphataemia
!!!!!(Tumour Lysis Syndrome, Rhabdomyolysis, Phosphate Administration)

4) Acute Pancreatitis

5) Hypomagnesaemia

6) Acute Alkalosis

85
Q

What are the signs of Hypocalaemia?

A

SPASMODIC

Spasms (Trosseau’s sign)
Perioral Paresthesia
Anxiety/ Irritability
Seizures
Muscle Tone Increase (Colic, Dysphagia)
Orientation Impairment (Confusion)
Dermatitis
Impetigo Herpetiformis
Chvostek’s Sign

86
Q

What investigations should be ordered in Hypocalcaemia is suspected?

A

!!!!!!!!ECG (look for prolonged QT/ arrhythmia)
Bone Profile (Calcium, Phosphate, Magnesium, Albumin, Total Protein, ALP)
!!!PTH
Magnesium
Vitamin D
Amylase (if Suspected Pancreatitis)
Xrays (if suspected Osteomalacia)

87
Q

What is the management of Hypocalcaemia?

usually just go for the severe option

Remember EDTA can give false low calcium readings

Also WHAT is given in the context of CKD?

A

Management of Acute Hypocalcaemia
- Mild- Oral Calcium Supplementation
- Severe (Spasms or ECG Changes)- IV Calcium Gluconate

Long term-
- Treat the cause
- Encourage Dietary Calcium and Vitamin D intake
- Calcium and Vitamin D supplements
- Alphacalciferol if CKD
- Magnesium Supplements if Recurring Hypomagnesaemia

88
Q

What are the signs of Hypoglycaemia?

A
  • Blood glucose concentrations <3.3 mmol/L cause autonomic symptoms due to the release of glucagon and adrenaline (average frequency in brackets):

1) Sweating
2) Shaking
3) Hunger
4) Anxiety
5) Nausea

  • Blood glucose concentrations below <2.8 mmol/L cause neuroglycopenic symptoms due to inadequate glucose supply to the brain:

1) Weakness
2) Vision changes
3) Confusion
4) Dizziness

  • Severe and uncommon features of hypoglycaemia include:

1) Convulsion
2) Coma

89
Q

What investigations should be ordered in Hypoglycaemia?

A

Check medication for drug causes

Serum Insulin, C Peptide and Proinsulin
(High Insulin and High C Peptide and Proinsulin= Endogenous. High Insulin and Low C Peptide and Proinsulin= Exogenous)

72 Hour Fast Test- to demonstrate Episodic Hypoglycaemia (Insulinoma)

8am Cortisol and/or Synacthen Test- for Adrenal Insufficiency

Abdominal CT/ MRI/ PET to localise an Insulinoma

90
Q

What is the gold standard investigation for an Insulinoma?

A

A 72 Hour Fast

91
Q

What are the signs of an Insulinoma?

Manage with Surgery

A

Whipple’s Triad
1) Symptomatic Hypoglycaemia
2) Glucose Levels of 2.2 or lower
3) Resolution of Symptoms with Glucose

92
Q

What is Impaired Fasting Glucose?

Hepatic Insulin Resistance

A

It is a Prediabetic State where

Fasting Glucose is 6.1-7
2 Hour Glucose <7.8

They are able to metabolise a Bolus of Ingested Glucose as normal but have abnormal control of their Basal Blood Sugar (Can control Bolus, but not Basal)

They are at higher risk of getting Diabetes

93
Q

What is Impaired Glucose Tolerance?

Muscle Insulin Resistance

A

It is a Prediabetic State where

Fasting Glucose <7
2 Hour Glucose 7.8-11

They are at higher risk of getting Diabetes than IFG as 2 hours glucose is >7.8 here but <7.8 for IFG

94
Q

What are the causes of Mineralocorticoid Excess?

A

The majority of cases are due to Hyperaldosteronism (Treatment-resistant High Blood Pressure and Low Potassium)

95
Q

What are the signs of Mineralocorticoid Excess?

What condition is it associated with?

A

Hypertension and _Cardiac Failure_ due to LEFT VENTRICULAR HYPERTROPHY

The Hypokalaemia is usually asymptomatic but can be associated with Rhythm Disturbances and ECG Abnormalities. They may have MUSCLE WEAKNESS and TETANY

There is also an association with Osteoporosis

96
Q

What is the management of Mineralocorticoid Excess? (same as Hyperaldosteronism)

A

Identify the cause (Specialist Imaging or Adrenal Venous Sampling)

Then Surgically remove the affected Adrenal Gland

If Bilateral- then use Potassium-SParing Diuretics (Spironolactone, Eplenerone)

97
Q

What is the most common cause of Hyperaldosteronism?

A

Bilateral Adrenal Hyperplasia

(Conn’s is SECOND most common)

98
Q

What are the 3 types of Multiple Endocrine Neoplasia (MENs)?

A

MEN 1
- Mutation in MEN 1 Gene
- Parathyroid (Hyperplasia and Adenomas)
- Pancreas (Gastrinoma and Insulinoma)
- Pituitary (Prolactinoma)

MEN 2a
- Mutation in RET gene
- Thyroid (Medullary Thyroid Cancer)
- Adrenal (Pheochromacytoma)
- Parathyroid (Hyperplasia/ Adenomas)

MEN 2b
- Thyroid (Medullary Thyroid Cancer)
- Adrenal (Pheochromacytoma)
- Parathyroid (Hyperplasia/ Adenomas)
- Mucosal Neuromas (Skin Lesions)

99
Q

What are the 2 types of Oesophageal Carcinoma?

A

Squamous Cell Carcinoma
- Most common
- Seen in Upper 2/3s of the Oesophagus

Adenocarcinomas
- Leading cause in the West
- Present in Lower 1/3
- Associated with Obesity and GORD (ongoing reflux converts cells into Mucin-producing tissue called Barret’s Oesophagus which can turn into Adenocarcinoma)

100
Q

What are the risk factors for Oesophageal Carcinoma (aka Squamous Cell Carcinoma)?

A

Smoking is the most important Risk Factor

  • High Alcohol Intake
  • Achalasia
  • Zenker’s Diverticulum
  • Oesophageal Web
  • High Intake of Hot Beverages
  • Dietary Intake of Areca or Betal Nuts and dietary nitrosamines
101
Q

What are the signs of Oesophageal Carcinoma?

A

Progressive Dysphagia from SOLIDS to LIQUIDS
(Spasms and Achalasia have Dysphagia to both Solids and Liquids from the start)

Odynophagia may also be present

Weight loss is the second most common symptom

Hoarseness can develop if the Laryngeal Nerve is affected

102
Q

What Investigations should be ordered in Oesophageal Carcinoma?

CMFEL

A

Initial- Upper GI Endoscopy. Allows for visualisation of the tumour and grading

Then STAGE the tumour to decide whether it is Resectable (may not be resectable if there is extensive local spread or if has metastasised)

1) CTAP FIRST after Endoscopy- Check size and metastasis to Lungs and Liver

2) MRI- can identify Liver Metastasis

3) FDG-PET- good for identifying Distal and Nodal Metastases but it is bad at identifying size of tumour (often done BEFORE ENDOSCOPI ULTRASOUND, as if there is metastasis then surgery is not going to be done anyway so no point)

4) Endoscopic Ultrasound (most accurate method of local staging but you can’t see Metastatic Spread)

5) Laparoscopy- useful in identifying Intraabdominal metastases if all other imaging has been negative. However, non-invasive investigations are preferred

103
Q

What is Osteomalacia?

A

It is a condition caused by inadequate levels of Calcium, Vitamin D and Phosphate

Bones become SOFTER as a result and fracture easily

104
Q

What are the signs of Osteomalacia?

Suspect if Proximal Weakness and Abnormal Waddling Gait with Bone Pain

What 5 additional symptoms are seen in children?

A

In Adults
1) Bone Pain (Lower Back, Pelvis and Lower Extremities)
2) Myalgia and Weakness (Quadriceps and Gluteal Muscles) and Impaired Physical Function
3) Leads to a WADDLING GAIT

In Children-
1) BOWING of Knees
2) Knock Knees
3) !!!!Swelling of the Costochondral Junctions
4) !!!Skull Softening
5) !!!Delayed Tooth Eruption
6) May also have Bone Pain and Muscular Weakness

105
Q

What are the causes of Osteomalacia?

A

1) Vitamin D Deficiency
2) Malabsorption (Coeliac) OR LIVER DISEASE

3) Renal Tubular Acidosis (Loss of Phosphate leads to Osteomalacia due to Failed Reabsorption)
4) Chronic Kidney Disease- Renal Osteodystrophy can develop as Renal Failure leads to reduced 1-25Dihydroxycholecalciferol Production. Phosphate Levels rise here due to Failure of Excretion

5) Cadmium Poisoning
6) Drugs (Anticonvulsants such as Carbamazepine and Phenytoin)

7) Tumour-induced Osteomalacia (Paraneoplastic Tumours can inhibit Phosphate Reabsorption, leading to Increased Renal Phosphate Loss and Deficiency as a result)

106
Q

What are the biochemical and radiological findings of Osteomalacia?

A

Low Vitamin D
High ALP

Low Calcium
Low Phosphate

High PTH

Xrays: Looser Lines (translucent lines) which are Lucencies going part of the way through the bone

107
Q

What is the management of Osteomalacia?

A

Vitamin D <25 = deficiency (you need high dose treatment and maintenance treatment)

Vitamin D 25-50= Insufficiency- you will only need the maintenance treatment

Lifestyle advice
- Safe Sun exposure
- Dietary Intake of Vitamin D and Calcium
- Long term Maintenance Supplements

108
Q

What is Osteoporosis?

A

It is a disease where the protein and mineral content of the bone is lower than normal
It is an Osteopaenic Disease

109
Q

What are the risk factors for Osteoporosis?

A

Age (>50 for women and>65 for men)
Female Sex

SHATTERED FAMILY
- Steroid Use
- Hyperthyroidism/ Hyperparathyroidism
- Alcohol and Smoking
- Thin (BMI<22)
- Testosterone Deficiency
- Early Menopause
- Renal/ Liver Failure
- Erosive/ Inflammatory Bone Disease
- Diabetes
- Family History

110
Q

Who should be investigated for Osteoporosis?

(10 year fracture risk score calculated via FRAX or QFracture)

A

1) All Men> 75
2) All Women>65
3) All Men and Women>50 if:
- FFF (Low BMI) DDD
- Family History of Hip Fractures
- Falls History
- Previous Fragility Fracture
- Low BMI
- Drink>4 Units of Alcohol per day of Alcohol
- (Drugs) Are/ Were on Steroids
- Disease associated with Osteoporosis (Coeliac Disease, Inflammatory Bowel Disease, Hyperparathyroidism)

111
Q

What 3 investigations are used to confirm Osteoporosis and what 6 investigations are used to exclude Mineral Bone Disease?

A

To Confirm-
- DEXA Scan (Gold Standard)
- Xrays (Wrist, Heel, Spine, Hip) if Fractures are suspected
- MRI Spine (to look for a Vertebral Fracture)

To exclude Metabolic Bone Disease-
- Bone Profile (Calcium, Phosphate, Albumin, Total Protein, ALP)
- Vitamin D level
- TFTs
- Urinary Free Cortisol
- Testosterone
- Bence-Jones Protein

112
Q

What T Score suggests Osteoporosis in DEXA Scans?

What about Osteopaenia?

A

Score between -1 and -2.5 means OSTEOPAENIA

<2.5 is Osteoporosis

113
Q

What is the Lifestyle Advice given to someone with Osteoporosis and What is the First Line Management?

A

Lifestyle
- Reduce Risk Factors (Stop Smoking, Better Diabetic Control)
- Diet (Adequate Vitamin D, Calcium, Protein)
- Regular Weight-bearing Exercise
- Hip Protectors in Nursing Home Patients

First Line-
- BISPHOSPHONATES (Alendronic Acid)
- Sit up for at least 30 minutes after taking it and drink glass of water to reduce risk of developing Oesophageal Ulcers
Other Side effects= Atrial Fibrillation, Osteonecrosis of the Jaw, Atypical stress fractures

  • Also give Vitamin D and Calcium if there is evidence of deficiency

Second Line-
- Denosumab (Inhibits the receptors which activate Oseoclasts)
- Raloxifene- used in Postmenopausal Women (has the same protective action on bones that Oestrogen has)
- HRT if women have Premature Menopause
- Teriparatide (Stimulates Bone Growth)
- Strontium Ranelate (reduces rate of Bone Turnover and stimulates Bone Growth)

114
Q

What is the most common cause of Primary Hyperparathyroidism?

A

Parathyroid Adenoma

115
Q

What is the most common type of Pituitary Tumour and how does it present? How is it diagnosed and managed?

A

Pituitary Adenoma (Benign and Non Secretory)

Signs
- Headache and Visual Field Defects

Diagnosis
- MRI Brain
- Screening for Visual Field Defects
- Hormone Tests as appropriate

Management
- Neurosurgery- Trans-sphenoidal
- Radiotherapy- for Residual Tumour after Surgery or for Recurrence

116
Q

What is the most common Hormone-secreting Tumour of the Pituitary and how does it present? How is it diagnosed ana managed?

A

Prolactinoma (microadenoma if <10mm, macroadnoma if >10mm)

Signs-
- High Levels of Prolactin
- In Women= Oligomenorrhoea or Amenorrhoea, Galactorrhoea, Infertility and Vaginal Dryness
- In Men= Erectile Dysfunction and Reduced Facial Hair
- Mass effects from the tumour itself- Headache and Visual Field Defects

Investigations-
- MRI Brain (Microadenoma= Lesions in the Pituitary, Macroadneoma= Space-occupying Tumour)
- Serum Prolactin

Management-
- Dopamine Agonist (Cabergoline)- results in decreased Prolactin
- HRT- Oestrogen- given when Fertility and Galactorrhoea are not an issue

  • Surgery- Trans-sphenoidal Resection if Pharmacological Management doesn’t work
117
Q

What is Syndrome of Inappropriate ADH Production?

A

Excess production of ADH which may be caused by Primary Pituitary Pathology, or a Non-Pituitary Pathology

118
Q

What are the 6 causes of SIADH?

A

1) Pituitary Tumour
2) Other Tumours (small cell lung cancer, thymoma, lymphoma)- SMALL CELL LUNG CANCER
3) Pulmonary Disease (Infections, Pneumothorax, Asthma, Cystic Fibrosis)
4) !!!!!!!!!!!!!!!!CNS Disease (Infection, Head Injury)
5) Drugs (Chemotherapy, Carbamazepine, SSRIs/ TCAs, Sulphonylureas)
6) Idiopathic

119
Q

What are the signs of SIADH?

A

Hyponatraemia (Euvolaemic) signs
- !!!!!Muscle Cramps
- Nausea and Vomiting
- Confusion and Coma
- Seizures

120
Q

What investigations should be ordered in SIADH?

A

1) U/Es- Hyponatraemia
2) Plasma Osmolality will be LOW (<270)

3) Urine Sodium will be high (>20)
4) Urine Osmolality will be concentrated (>100)

5) MRI for Pituitary Tumour

121
Q

What is the management of SIADH?

Why should they be corrected slowly in SIADH?

A

Fluid Restriction
Surgery if Pituitary Cause

Correct them SLOWLY to avoid CENTRAL PONTINE MYELINOLYSIS

122
Q

What is Pituitary Apoplexy and what are the signs?

What is low in these patients and how is this condition managed?

A

Bleeding into the Pituitary Gland- occurs in individuals with Pituitary Tumours or Infarction of the Tumour

(It is usually the initial presentation of Pituitary Tumours)

Symptoms- Sudden Onset, Retroorbital HEADACHE + Nausea and Vomiting

Majority of patients will have a deficiency of hormones (low ACTH for example which results in Low Sodium)

Management- Give HYDROCORTISONE due to the loss of ACTH first then perform MRI

123
Q

In Hypopituitarism, what is the most important hormone to replace?

A

Cortisol

124
Q

In Hypopituitarism, which hormones disappear first?

A

Growth Hormone

Then

LH
FSH
TSH
ACTH
Prolactin

125
Q

What is the most common cause of Hypopituitarism?

A

Pituitary Adenoma

126
Q

What is the most likely cause of Hyperprolactinaemia in Mental Health Patients?

A

Risperidone

but can also be due to Haloperidol, TCAs, SSRIs

127
Q

What is Pseudohypoparathyroidism?

A

It is a genetic condition that results in the failure of target organs to respond to normal levels of parathyroid hormone (so resistance)

In normal Hypoparathyroidism- the issue is the low levels of PTH

128
Q

What are the signs of Pseudohypoparathyrodism?

A

The same signs as Hypoparathyroidism

PLUS

  • Short stature and fingers (4th and 5th metacarpals plus blunting of knuckles)
  • Also Rounded Faces
  • Hypocalcaemia (Numbness and tingling of fingers and toes, Muscle Cramps, Seizures, Carpopedal Spasms)
  • Vitamin D Deficiency (Bone pain and Fractures)
129
Q

What are the investigations of Pseudohypoparathyroidism?

A

Calcium Levels (Low Calcium)
Parathyroid Hormone Levels (will be normal)

cos it’s the same amount of pth as normal but it is being resisted by downstream organs

130
Q

What is the management of Pseudohypoparathyroidism?

A

Calcium Supplementation

Vitamin D Supplementation

131
Q

What is Rhabdomyolysis?

A

It is Skeletal Muscle Breakdown which leads to the release of Intracellular Content (like Myoglobin and Potassium) into the blood stream

Excess Myoglobin can precipitate in the Glomerulus, leading to Renal Obstruction, Direct Nephrotoxicity and AKI

132
Q

What are the causes of Rhabdomyolysis?

A

Trauma- Prolonged !!!!!!!!Immobilisation (long lie in the elderly), Crush injuries, Burns, Seizures, Compartment Syndrome

Ischaemia- Embolism, Surgery

Toxins- STATINs, Fibrates, Ecstasy, Neuroleptics (FENS)

It can also present following a Strenuous Exercise (Spin Class)

133
Q

What are the signs of Rhabdomyolysis?

A

Muscle Pain/ Swelling

Red/ Brown Urine

AKI 10-12 hours after the initial pain/ injury

134
Q

What investigations should be ordered in Rhabdomyolysis?

A

Creatine Kinase- 5 fold rise from the upper limit suggests Rhabdomyolysis (if it is only 4 times then it is not high enough)

Raised LDH (suggests Muscle Damage)

Hyperkalaemia
Hyperphosphataemia
Hyperuricaemia
Hypocalcaemia (calcium is taken into damaged muscle by several mechanisms)

Urine Tests- often Falsely Positive for Blood on Dipstick with NO RED BLOOD CELLS seen on Microscopy. This is due to the Myoglobinuria (urine is tea- or cola-coloured)

135
Q

What is the management of Rhabdomyolysis?

A

IV Fluids and Hyperkalaemia management (IV Calcium Gluconate)

136
Q

What are the Secondary Causes of Diabetes?

A

Pancreatic Causes-
- Cystic Fibrosis
- Chronic Pancreatitis
- !!!!!!!!!!!!!!!!!Haemochromatosis
- Cancer

Endocrine causes- (CAPT CAPT CAPT CAPT CAPT)
- Cushing’s
- Acromegaly
- Phaeochromocytoma
- Thyrotoxicosis

Drug Causes
- Steroids (give Sulphonylurea (like Gliclazide) as treatment)
- Atypical Neuroleptics
- Thiazides
- !!!!!!!!!Beta Blockers

Glycogen Storage Disorders
- Glycogen Storage Disease 1 (von Gierkes)
- Glycogen Storage Disease 2 (Pompe)

137
Q

What are the main side effects of Amiodarone?

Happy Harry Can See Grey Lungs

A

1) Hypothyroidism (more common than Hyperthyroidism)

2) Hyperthyroidism

3) Corneal Deposits

4) Stevens-Johnson Syndrome

5) Grey Discoloration of the Skin

6) Liver Failure

7) Pneumonitis (leads to Pulmonary Fibrosis)

138
Q

What are the main side effects of the Anti-Diabetic Drugs?

A

Biguanides (Metormin)
- Lactic Acidosis and GI Disturbance

Sulfonylurea (Gliclazide)
- Hypoglycaemia and Weight Gain

Thiazolidinediones (Pioglitazone)
- Fluid Retention, Weight Gain and Worsening Heart Failure

SGLT2 Inhibitors
- DKA when used with Insulin
- Higher risk of UTIs

DPP4 Inhibitors
- Hypoglycaemia and GI Disturbance

GLP1 Analogues
- Hypoglycaemia and GI Disturbance
- Higher risk of Pancreatitis when used with DPP4

Intestinal Alpha-Glucosidase Inhibitors
- Flatulence and GI Disturbance

139
Q

What is Subclinical Hypothyroidism/ Hyperthyroidism?

A

Hypo- High TSH, Hyper- Low TSH

But NORMAL T3 and T4

140
Q

What is the management of Subclinical Hyperthyroidism?

A

1) Excluding other causes of high TSH (illness)

2) Rechecking Thyroid Function in 3 months

3) Most patients need no treatment

4) Antithyroids (although not much evidence that it works)

141
Q

What is the management of Subclinical Hypothyroidism?

A

1) Assess for features of Hyperthyroidism

2) Exclude causes of transiently-suppressed TSH (medications like Steroids and Lithium and Parkinson medications)

3) Repeat TFTs in 3 months

4) LEVOTHYROXINE IF:
- Symptoms of Hypothyroidism
- if still low 3 months apart

142
Q

What are the signs of Type 1 Diabetes?

A

Polyuria
Polydipsia
Weight Loss

143
Q

What is the management of Type 1 Diabetes?

A

Insulin Replacement with Short Acting and Long Acting Insulin (Basal-Bolus Teaching)

Delivered Subcutaneously through a Pen Device or with a Continuous Infusion Pump

Monitor Diet, Glucose Levels and Insulin Therapy

144
Q

What is the Honeymoon Period in Type 1 Diabetes?

A

Insulin Requirement may be low if pancreas is able to produce a Significant Amount of Insulin

This is the Honeymoon Period

Monitor children during this time as their insulin requirements can suddenly increase

Blood glucose may be normal on very low insulin doses and parents can think that the condition has gone away

145
Q

What are the signs of Hypoglycaemia?

A

Irritability, Sweating, Abdominal Pain, Dizziness, Loss of Consciousness and even Fits

146
Q

What are the complications of Type 1 Diabetes?

A

Growth and Pubertal (delay in Puberty and Obesity)

Hypertension

Renal Disease

Retinopathy

Feet

Associated Illnesses
- Thyroid Disease (most associated)
- Coeliac Disease

147
Q

How do you work out the dosage for the Short and Long Acting Insulin?

A

Give 3/5s of the required Insulin dose as Short Acting

Give 2/5s as Long Acting

148
Q

What kind of Visual Defects do the Following Lesions Cause?

1) Optic Nerve

2) Optic Tract (Optic Chasm to Ipsilateral LGN)

3) Optic Chiasm

4) Optic Radiation (LGN to Visual Cortex)

A

1) Monocular Vision Loss

2) Contralateral Homonymous Hemianopia

3) Bitemporal Hemianopia)

4) Contralateral Homonymous Hemianopia

149
Q

What do Lesion in the following lobes cause in terms of Visual Defects?

Temporal Lobe

Parietal Lobe

Occipital Lobe

A

Temporal= Contralateral Homonymous SUPERIOR (upper) Hemianopia

Parietal= Contralateral Homonymous INFERIOR (lower) Hemianopia

Occipital= Contralateral Homonymous Hemianopia

150
Q

What is Waterhouse-Friderichsen’s Syndrome?

A

It is caused by Severe Bacterial Infection which results DIC and Adrenal Haemorrhage and Failure

The Adrenal Haemorrhage is usually Bilateral but can be Unilateral

151
Q

What are the causes of Waterhouse Friderichsen Syndrome?

A

N. Meningitidis but may also be other bacterial infections

152
Q

What are the signs of Waterhouse Friderichsen Syndrome?

A

Non-specific Infection which progresses to a Macular, Petechial and Purpuric Rash along with SEPTIC SHOCK