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Endocrinology Flashcards

1
Q

Causes of hyperthyroidism

A

Graves disease
Thyroid adenomas (solitary or multinodular)
Postpartum thyroiditis
Aminodarone induced hyperthyroidism
Ectopic thyroid tissue
Exogenous (levothyroxine, excessive iodine, contrast)
De Quervain’s thyroiditis

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2
Q

What is De Quervain’s thyroiditis? What are specific/prominent signs and symptoms? How is it treated differently? What should be watched for?

A

Transient hyperthyroidism post viral infection
Neck pain and fever at onset. Thyroid tenderness. Raised esr
Treat with aspirin and steroids.
Watch for following hypothyroidism

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3
Q

Generic symptoms of hyperthyroidism

A 
Weight loss
Increased appetite
Palpitations
Heat intolerance
Irritability 
Anxiety
Tremor
Diarrheoa
Goitre
Oligomenorrhoea
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4
Q

Generic signs of hyperthyroidism

A 
Tachycarida / AF
Full pulse
Warm
Hyperkinesis 
Lid-lag (upper eyelid not following down as eye looks down revealing sclera above iris)
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5
Q

What is graves disease?

A

Autoimmune condition where antibodies stimulate tsh receptors

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6
Q

What signs differentiate graves disease from other forms of hyperthyroidism?

A

Eye signs - proptosis/exopthalmos, lid retraction, optic nerve atrophy, pain, grittiness, conjunctival swelling
Pre-tibial myxoedema

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7
Q

What is a bad prognostic indicator for eye signs in graves disease?

A

No protrusion - higher pressure!

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8
Q

What blood abnormalities are seen in graves disease other than the normal TFTs?

A

Raised tsh receptor antibodies

Raised antithyroid peroxidase (tpo)

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9
Q

What is the clinical course of graves disease?

A

Fluctuating

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10
Q

What examination findings and tests would suggests a nodule (single or multiple) is responsible for hyperthyroidism?

A

Can feel nodules!
Radioactive iodine shows hot nodules
Poor response to carbimazole and constant symptoms

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11
Q

General treatments for hyperthyroidism

A 
Carbimazole
Propulthiouracil (ptu)
Beta blockers
Radioactive iodine
Thyroidectomy
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12
Q

How does carbimazole work?

What is its t1/2? What consequence is this? Serious adr?

A

Inhibits t3/t4 formation
Weeks - takes a while to work
Agranulocytosis

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13
Q

What should patients on carbimazole immediately report to a dr?

A

Mouth ulcers

Sore throats

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14
Q

What should be done prior to radioactive iodine therapy or thyroidectomy?

A

Render the patient euthyroid first

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15
Q

Compliactions of thyroidectomy

A

Laryngeal nerve palsy
Hypoparathyroidism
Transient hypocalcaemia
Hypothyroidism

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16
Q

Signs and symptoms of thyroid storm

A 
Pyrexia 
Tachycardia
Restlessness
Hypertension
Cardiac failure
Liver dysfunction
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17
Q

What can trigger a thyroid storm?

A

Stress
Infection
Surgery
Radioactive iodine therapy

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18
Q

Treatment of thyroid storm

A

Propanolol
Potassium iodide
Carbimazole
Corticosteroids

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19
Q

Risks of hyperthyroidism during pregnancy?

A

Graves - mothers antibodies effect fetus - manage by treating mother
Use ptu in first trimester as carbimazole has rarely been teratogenic

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20
Q

Side effect of ptu?

A

Hepatotoxicity.

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21
Q

What regimes of antithyroid drugs can be used to treat hyperthyroidism?

A

Use carbimazole or ptu to lower thyroid hormones to normal levels
Block thyroid hormones completely and replace with thyroxine

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22
Q

Causes of hypothyroidism?

A 
Hashimotos thyroditis
Postpartum thyroiditis
Primary atrophic hypothyroidism
Iodine deficiency 
Drugs - carbimazole, ptu, amiodarone, lithium
Hypopituitism
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23
Q

Presentation of hypothyroidism?

A 
Dry hair
Weight gain
Cold intolerance
Bradycardia
Depression
Goitre
Constipation
Myxoedema 
Tiredness
Anaemia
Amenorrhoea
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24
Q

What would hashimoto’s thyroiditis present with on bloods?

A

Raised tsh
Normal or decreased t3/4
TPO antibodies
Anaemia (of chronic disease)

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25
Q

What is a myxedema coma? How does it present?

A

Decompensated hypothyroidism often following acute insult (infection, stroke)
Confusion to coma
Hypothermia
Cardiac failure (bradycardia and low stroke volume)
Hypoglycaemia
Hyponatremia (decreased Na/katpase in kidneys)
Hypoventilation with T2 respiratory failure

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26
Q

Treatment for myxedema coma

A 
ABCDEs inc ventilation
IV T3
Steroids 
Glucose and sodium as required 
Passive rewarming
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27
Q

Why are steroids used in the treatment of myxoedema coma? What raises suspicion of need?

A

Incase it is secondary to hypopituitarism with associated adrenal insufficiency
No previous thyroid surgery, no previous goiter

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28
Q

Why is t3 used in myxoedema coma not t4. Risks?

A

T3 is active thus much faster action.

Higher risk of hyperthyroid issues like arrhythmia

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29
Q

General treatment for hypothyroidism

A

Thyroxine

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30
Q

What patients should get a lower starting dose of thyroxine?

A

Elderly
Long standing disease
IHD patients

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31
Q

How long after starting thyroxine would you expect symptom resolution?

A

6 months

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32
Q

What are four main diabetic eye changes?

A

Blurring due to high sugar
Cateracts
Diabetic retinopathy
Maculopathy

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33
Q

What are the subdivisions and features of diabetic retinopathy

A

Background - microaneurysms (small red dots), superficial haemorrhage (blots), hard exudates (small yellow/white blobs), cotton wool spots (oedema from infarcts)
Proliferative - blood vessels on retina surface, retinal fibrosis and detachment, surface haemorrhages, blood in vitreous humour

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34
Q

What is diabetic maculopathy?

A

Anurysms form and lead causing fluid, fat and protein deposition (oedema and exudate) with central loss of vision

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35
Q

Treatment option for diabetic retinopathy and maculopathy? Outcome?

A

Aggressive sugar control

Laser treatment - stops progression but doesn’t reverse

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36
Q

What is the mechanism behind diabetic kidney disease?

A

Glomerular damage with

  • thickened basement membrane
  • detached podocytes
  • scarring
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37
Q

What is the physiological consequence of diabetic kidney disease?

A

Diabetic nephropathy

- proteinurea, hypoalbuminia, oedema

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38
Q

Is eGFR typically effected in early diabetic kidney disease?

A

No

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39
Q

What is an early sign of diabetic kidney disease? What treatments are important?

A

Microalbuminuria
Aggressive diabetes control
Ace inhibitors even in presence of normal BP

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40
Q

Mechanisms behind diabetic neuropathy?

A

1 - Uptake of glucose independent of insulin into neurones and schwann cells through glut3. Glucose - sorbitol catalysed by aldose reductase. High sorbitol interferes with neuronal conduction and mylination.
2 - Microvascular damage by non enzymatic glycosylation and vasoconstrictors reduces neuronal perfusion
3 - Oxidative stress from increased ROS production

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41
Q

Clinical pictures of diabetic neuropathy?

A

Symmetrical sensory neuropathy
Painful neuropathy
Mononeuropathy
Autonomic neuropathy

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42
Q

How are nerves physically effected in diabetic neuropathy?

A

demylination then axonal degridation

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43
Q

Senses lost in diabetic symmetrical sensory polyneuropathy

A

Vibration
Pain
Temperature
Proprioception

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44
Q

What complications result of a diabetic autonomic neuropathy?

A

Vagal neuropathy - tachycardia, gastroparesis
Sympathetics to blood vessels - postural hypotension
Nerves to bladder - incomplete emptying, stasis
Nerves to sexual organs - impotance

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45
Q

Causes of impotance in diabetes?

A 
Neuropathy 
Anxiety/depression
Vascular
Medications
Unrelated to diabetes at all!
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46
Q

Which sign of background diabetic retinopathy suggests proliferative retinopathy is imminent?

A

Cotton wool spots

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47
Q

What comorbidity should be aggressively treated in a patient with diabetic nephropathy

A

Htn

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48
Q

What are major complications of diabetic sensory neuropathy?

A

Lack of injury sense in foot leading to ulcerations, gangrene and amputation
Charcot arthropathy - microtrauma not detected resulting in chronic fractures and subluxation. Autonomic neuropathy causes hyperaemia and thus increases osteoclast activity causing bone destruction.

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49
Q

Differentials for charcots arthropathy?

A 
DM
Syphillis
Leprosy
Spinal cord injury
Chronic alcoholism (b12 deficiency)
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50
Q

Features of charcots arthropathy

A 
Deformity
Swelling
Pain
Erythema
Warmth (key!  Check temp) 
Decreased sensation
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51
Q

Treatment of charcots arthropathy

A

Fitted boots
Diabetic control
Surgery to reduce ulceration risk if extremity in bad position

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52
Q

What sort of pain do patients with diabetic neuropathy often experience?

A

Electrical

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53
Q

What is the key pathological mechanism for diabetic macrovascular disease?

A

Injury to arterial wall
Chronic inflammation
Athrosclerosis

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54
Q

In addition to athroscleosis what other pathological mechanisms play a role in diabetic macrovascular disease?

A

Hypercoagubility
Impaired nitric oxide generation
Impaired fibrinolysis
Comorbidites - metabolic syndrome!!

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55
Q

Key macrovascular disease in diabetes?

A

CVD
Stroke
HTN
Gangrene

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56
Q

What leaves a diabetic at greater risk of a fatal MI as a direct result of the diabetes?

A

Athrosclerosis and hypercoagubility
Autonomic neuropathy causing tachycardia
Sensory neuropathy decreasing detection
CKD!

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57
Q

Treatment options for diabetic macrovascular prophylaxis?

A

Blood sugar control
Ace i and other htn control
Lipid control

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58
Q

When would you start statins in some one with t2dm? What about t1dm?

A

T2 - qrisk2 >10

T1 - over 40, diabetic for > 10 years, nephropathy or other risk factor

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59
Q

Causes of diabetes?

A 
T1DM
T2DM
Gestational 
Metabolic
Drugs
Pancreatic disease
Single gene disorders
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60
Q

Drugs that can cause diabetes?

A

Steroids
Antipsychotics
Thiazides

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61
Q

Metabolic causes of diabetes?

A

Acromegally
Cushings
Glucagonoma

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62
Q

Single gene disorders associated with diabetes

A

Prader willi
Maternally inherited diabetes and deafness
Insulin receptor mutations

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63
Q

Why are diabetics more at risk of infection?

A

Impaired chemotaxis and phagocytosis

Impaired superoxide generation

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64
Q

What hand sign may diabetics exhibit? Cause? Implication?

A

Prayer sign - unable to flatten fingers
Cherioarthropathy - thickened skin and limited joint mobility
Implication for anaesthetics

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65
Q

Commonest cause of hypoglycaemia in diabetics?

A

Treatment related

Insulin/sulphonylureas

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66
Q

What happens to long term diabetics with regards to hypoglycaemia?

A

Hypoglycaemia unawareness

Decreased glucagon and adrenaline response so no classic warning symptoms

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67
Q

Rarer causes of hypoglycaemia?

A 
Insulinoma
Paraneoplastic 
Postparandial hypoglycaemia 
Hepatic or renal failure reducing respective ability to release glucose 
Addisons / ACTH deficiency 
Drug induced 
Alcohol
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68
Q

What are the characteristic features of a insulinoma?

A

Whipples triad

  • symptoms on fasting and exercise
  • with confirmed hypoglycaemia
  • relieved by glucose
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69
Q

What are causes of postparandial hypoglycaemia?

A

Excessive insulin for size of meal
Surgery removes food!
Alcohol with meal exaggerates insulin response

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70
Q

How dose alcohol cause hypoglycaemia?

A

Poor nourishment in alcoholics

Inhibits gluconeogenesis

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71
Q

Causes of type 1 diabetes?

A

Genetic susceptibility (HLA)
Diet
Hygiene hypothesis
Coxsackie virus

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72
Q

Presentation of type 1 diabetes?

A 
Young
Acute
Weight loss
Polyuria
Polydipsia 
Ketoacidotic
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73
Q

Precipitants of diabetic ketoacidosis

A

First presentation
Omitting insulin
Incurrent illness

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74
Q

What occurs to potassium in diabetic ketoacidosis?

A

Potassium deficit due to urinary loss

Lack of insulin means less potassium shifted into cells so appears normal - high in spite of actual deficit

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75
Q

Causes of dehydration in DKA?

A

Osmotic diuresis

Vomiting

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76
Q

What contributes to potassium leaving cells into the ecf in dka?

A

Lack of insulin decreases nakatpase reducing potassium uptake
Acidosis increases ecf H so increased potassium release in exchange
Increased ecf tonicity pulls water out of cells increasing icf k concentration resulting in K release.

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77
Q

What effect does acidosis have on renal handling of k in dka? In what cells is potassium secreted renally?

A

Decreases k secretion maintaining k in body

Principal cells

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78
Q

Diagnosis of DKA?

A

Hyperglycaemia (>11)
Kentonaemia or heavy ketonuria
Acidosis

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79
Q

Management of DKA?

A

Fluids - 1L in 1, 2l in 4, 2 in 8, 2 in 12
Stat SC insulin 10 units
FRIVII (0.1unit/kg/hr)
Add glucose once BM

80
Q

When should the FRIVII be switched off in DKA?

What should be done?

A

pH >7.3 OR bicarb >18 OR Ketones

81
Q

Complications of DKA?

A

Hypovolaemic shock
Acidotic coma
DVT

82
Q

Complications of DKA treatment?

A

Cerebra or pulmonary oedema
Hypoglycaemia
Hypokalaemia

83
Q

Risk factors for T2DM

A 
Genetic
Ethnicity - asian, african
Low birth weight
Age
Obesity 
Diet
Sedentary lifestyle
Hypertension
High cholesterol
84
Q

Presentation of T2DM

A 
Old and fat
Insidious
Polyuria
Polydipsia 
Weight loss
Candidia infection
Visual blurring
Low energy 
Complications (retinopathy, neuropathy, large vessel disease)
85
Q

Skin change associated with T2DM?

Other conditions seen in?

A

Acanthosis nigricans

PCOS, Cushings, acromegally, hypothyroid

86
Q

Diagnostic criteria for DM?

A

Symptoms and one or asymptomatic and 2 of:

  • fasting BM >7
  • Glucose tolerance test >11
  • HbA1c >6.5%
  • Random BM >11
87
Q

How is a Glucose tolerance test performed?

A

12 hr fast followed by 75g glucose. Measure 2 hours later

88
Q

What is happening if someone is just under on a glucose tolerance test (e.g 9)

A

Impaired glucose tolerance - on the way to DM. Still at high risk of macrovascualr complications

89
Q

What are the diagnostic values for maternal diabetes?

A

Fasting BM >5.6

GTT >7.8

90
Q

Conservative management options for t2dm?

A

Diet - low sugar, high complex carbs, high fibre, low fat, low alcohol
Exercise - both informal and formal

91
Q

Oral medical management of T2DM

A 
Biguanides - metformin
Sulfonylureas - gliclazide
Glitazones - piogliazone 
Acarboze inhibitors 
Gliptins - saxogliptin
SGLT2 inhibitors - dapagliflozin
92
Q

Injectiable management of T2DM

A

GLP1 agonist - exenatide

Insulin

93
Q

Non drug management of DM (not conservative)

A

Gastric banding

94
Q

What is a typical management regime for T2DM with failure of 1st and 2nd line options. What would change 3rd line option?

A

Lifestyle mods
Metformin
Sulfonylurea - use pioglitazone if hypo risk high eg. Driver.

95
Q

If lifestyle and 2 meds are not controlling t2dm what should be considered?

A

Triple oral therapy
Add insulin
Novel therapies

96
Q

What is HONK?

A

Hyperosmolar hyperglycaemic state

Severe hyperglycaemia without ketosis

97
Q

Presentation of honk?

Include notable absences

A

Severe dehydration with hyperosmolality
Hypernatraemia
Coma
No ketones or acidosis

98
Q

Treatment of HONK

A

Isotonic fluids

Slowly increasing insulin

99
Q

Predisposing factors for HoNK

A

Glucose rich food
Steroids
Illness
Thiazides

100
Q

What is the mechanism behind PCOS?

A

Increased GNrH resulting in high LH and low FSH causing androgen secretion but not conversion into oestrogen.
There is also associated insulin resistance

101
Q

Signs and symptoms of PCOS

A 
Hirtuism
Irregular or absent periods
Infertility 
Acne
Obesity 
Virilisation (baldness, clitoromegally)
102
Q

Complication of PCOS?

A

Metabolic syndrome

103
Q

What investigations should be done in suspected PCOS? What would you expect to see? Pitfalls?

A

Serum testosterone - high - must check for sex hormone binding globulin
LH - low - depends when taken as pulsetyle
USS - polycystic ovaries

104
Q

Diagnostic criteria for PCOS

A

2 of

  • clinical evidence of hyperandrogenism
  • oligo or anovulation
  • polycystic ovaries on USS
105
Q

Treatment for PCOS?

A

Symptomatic - hair removal
Conservative - exercise, diet
Medical - OCP, spironolactone, metformin

106
Q

What OCP to use in PCOS? What is the active ingredient? How does it work?

A

Dianette - cyproterone acetate

Progesterone - an antiandrogen

107
Q

Why give PCOS spironolactone?

A

Antiandrogen properties hence side effect of gynacomastia

108
Q

Why give PCOS metformin?

A

No only helps with insulin resistance but also with menstrual regularity and infertility

109
Q

Differentials for PCOS for hirsutism?

A

Idiopathic hirsutism
Congenital adrenal hyperplasia
Cushings
Virilizing tumour of ovary or adrenal

110
Q

What causes congenital adrenal hyperplasia?

A

Lack of enzyme in steroid metabolism that usually converts progesterone into aldosterone and cortisol. Causes a deficiency in aldosterone and cortisol with an excess in androgens as progesterone is pushed down this pathway.
Lack of cortisol causes high ACTH and thus adrenal hypertrophy

111
Q

How does congenital adrenal hyperplasia present at birth if severe?

A 
Ambiguous genitalia in females (cliteral hypertrophy, fused labia)
Adrenal crisis (hypotension, hypoglycaemia)
Mineralcorticoid deficiency (hypotension, hyponatraemia)
112
Q

If not too severe, how would congenital adrenal hyperplasia present in adult life?

A

Precocious puberty
Hirsutism
Primary amenorrhoea

113
Q

How can you test for congenital adrenal hyperplasia?

A

Administer ACTH and measure response

114
Q

Treatment of congenital adrenal hyperplasia?

A

Replacement of glucocorticoids and mineralocorticoids

Genetic councilling

115
Q

In diabetes glucose is found in the urine? Why? How is it normally dealt with by the kidney?

A

Freely filtered at the glomerulus so [high] in blood means the same in urine exceeding the transport maximum.
Usually glucose is reabsorbed in the PCT fully. On the luminal membrane using a glucose:Na cotransporter (SGLT2) and using Na/K ATPase with GLUT1/2

116
Q

When are serum cortisol levels highest? Lowest? What can change the cycle?

A

High early morning
Low at midnight
Stress will cause a raise

117
Q

What inhibitory trophic hormones are released by the hypothalamus into the portal circulation? What do they inhibit?

A

Dopamine - prolactin

Somatostatin - gh, tsh

118
Q

Local effects of a pituitary tumour?

A

Compression of optic chiasm - bitemporal hemianopia
Compression of cavernous sinus - CN III, IV and VI dysfunction
Meningeal irritation - headache
Compression of hypothalamus - appetite, sleep, thirst disturbance, DI
Compression of ventricles - hydrocephalus
Sphenoid sinus invasion - csf rhinorrhoea

119
Q

Effects of CN3,4 and 6 dysfunction in cavernous sinus compression?

A

3 - SR, IR, MR, IO, LPS, sphincter pupillae - ptosis, eye down and out, fixed dilated pupil
4 - SO - diplopia on looking down
6 - LR - cant abduct
All three together causes completely immobile eye

120
Q

Causes of hypopituitarism?

A 
Tumour 
Sheehans syndrome following post partum haemorrhage 
Infections
Trauma 
Sarcoidosis 
Radiation/chemotherapy 
Anorexia nervosa / starvation
121
Q

Zones of the adrenals with what they produce?

A

Zona glomerulosa - mineralocortiocoids
Zona fasicularis - corticosteroids
Zona reticularis - androgens

122
Q

Major effects of glucocorticoids

A 
Gluconeogenesis 
Protein catabolism 
Fat and glycogen deposition 
Sodium retention and potassium loss 
Immunosuppression
123
Q

How does negative feedback work on the hpa axis?

A

Cortisol inhibits CRH and ACTH formation

124
Q

When should basal cortisol and acth levels be taken? What consideration?

A

At peak between 0800 and 0900

Stress should be minimised

125
Q

What main tests are used in patients with high levels of cortisol to determine cause? How do they work?

A

Dexamethasone suppression tests
Low dose - patients with Cushing’s syndrome will not significantly suppress cortisol on administration of dexamethasone
High dose - patients with Cushing’s disease will significantly suppress cortisol indicating cause is likely ectopic or adrenal if failed to suppress

126
Q

If cortisol levels are low what main tests can be used to identify the cause? Differentiate them.

A

Synacthen
Short - if no response to ACTH confirms hypoadrenalism but could be primary, secondary or iatrogenic
Long - if no response suggests primary adrenal failure

127
Q

Why does secondary hypoadrenalism result in a positive short synacthen test? Why does this change with a long one?

A

Adrenal atrophy

On a long test the adrenals are kicked into life unless there is a primary pathology

128
Q

What CLINICALLY would differentiate addisons from secondary hypoadrenalism?

A

Pigmentation from high ACTH

Low mineralocorticoids producing hypotension and electrolyte imbalance

129
Q

What tests can be used in suspected addisons disease (generally)

A 
Random cortisol 
Synacthen tests 
U+Es
BM
Adrenal antibodies
Abdo xray 
Serum aldosterone
130
Q

What might be seen in an abdominal xray of an addisons patient?

A

Calcified adrenals

Evidence of tb

131
Q

Causes of addisons disease?

A 
Autoimmune
TB
Surgical removal 
Haemorrhage/infarction
Malignant destruction
132
Q

Causes of secondary hypoadrenalism

A

Exogenous steroids

Pituitary disease

133
Q

Emergency management of addisons crisis?

A

NaCl
Hydrocortisone
Glucose

134
Q

Long term treatment of hypoadrenalism?

A

Gluticorticoids - e.g. Hydrocortisone

Mineralocorticoids - e.g. Fludrocortisone

135
Q

What is the most common cause of cushings syndrome?

A

Exogenous steroids

136
Q

What are causes of cushings syndrome?

A

Iatrogenic
Disease - increased ACTH from pituitary
Atopic ACTH from a tumour
Endogenous cortisol secretion from adrenals

137
Q

A patient with a history of cushing type symptoms has a positive low dose dexamethasone suppression test. What tests will help diagnose the source?

A 
Adrenal ct
Pituitary mri 
K levels
High dose dexamethasone test
Plasma acth 
Cheat xray
138
Q

A patient with a history of cushing type symptoms has a positive low dose dexamethasone suppression test. A high dose dexamethasone suppression test is negative, his potassium is normal and there are no signs on the chest xray. A ct of adrenals is negative and there is nothing on a pituitary mri. Where is the likely lesion? Why?

A

Pituitary. Most acth secreting tumours are too small to see on mri. Normal potassium suggests not ectopic and a response to the high dose tests suggests a pituitary source.

139
Q

What causes death in untreated cushings?

A

Htn with mi and heart failure

Infection

140
Q

How is cushings treated?

A

Ketoconazole to reduce plasma cortisol
Removal of source if possible
If not bilateral adralectomy with replacement

141
Q

What is the risk with bilateral adrenelectomy for cushings?

A

Nelsons syndrome

No feedback so massive enlargement of pituitary

142
Q

Hazards to discuss on starting steroids for any condition

A 
Infection
Suppress own steroids
Hypertension
Pancreatitis
Weight gain
Diabetes
Depression
Osteoporosis
Thin skin and bruising
Cataracts
143
Q

What is diabetes insipidus?

A

Deficiency ir insensitivity to adh resulting in polyurea, nocturea and compensatory polydipsia

144
Q

What is the biochemical profile of diabetes insipidus?

A

High plasma osmolality
Low urine osmolality
High plasma sodium
High urine volumes

145
Q

You suspect diabetes insipidus. How do you test for it?

A

Water deprivation test for up to eight hours
Plasma osmolality should stay the same whilst urine osmolality should increase in a normal person.
If this does not occur sufficiently give synthetic ADH (desmopressing) and monitor change to differentiate cranial from renal.

146
Q

When should a water deprevation test be stopped?

A

If >3% body weight reduction

147
Q

Causes of cranial diabetes insipidus?

A 
Hypothalmic-pituitary surgery
Trauma
Infection
Tumour
Necrosis - sheehans 
Famililal 
Idiopathic
148
Q

Causes of nephrogenic diabetes insipidus

A 
Familial
Idiopathic
Renal disease
Lithium
Hypokalaemia
Hypercalcaemia 
Sickle cell disease
149
Q

Treatment of cranial diabetes insipidus

A

Desmopressin

150
Q

Treatment of nephrogenic diabetes insipidus

A

Reverse cause if possible

151
Q

Other causes of polyuria and polydipsia not diabetes insipidus

A

Diabetes mellitus
Hypokalaemia
Hypercalcaemia
Primary polydipsia - psychiatric, too much water, low plasma osmolarity

152
Q

How does SIADH present?

A

Dilutional hyponatraemia with low plama osmolality
Euvolemic with no hypotension
Normal potassium
No response to 1-2 L of 0.9% sodium chloride

153
Q

Treatment of SIADH

A

Fluid restriction
Demeclocycline to inhibit adh
Cautious use of hypertonic saline in severe illness

154
Q

Causes of siadh

A 
Tumours
Pneumonia
Head injury 
Alcohol withdrawal 
Drugs carbamazepine
155
Q

Causes of hyponatraemia with hypovolaemia?

A

Vomiting, diarrheoa, burns, haemorrhage, osmotic diuresis, diuretics, addisons,

156
Q

Causes of hyponatraemia with euvolaemia?

A 
SIADH
Overenthusiastic 5% glucose use
Exertion with only water replacement 
psychogenic polydipsia
Desmopressin 
Addisons 
Mannitol 
Sickle cell syndrome
157
Q

Causes of hyponatraemia with hypervolaemia

A

Heart failure, liver failure, hypoalbuminaemia

158
Q

What is the mechanism behind hyponatraemia with hypovolaemia with respect to adh.

A

Loss of salts out of proportion to loss of water causing low osmolarity
Due to volume depletion adh still released to maintain volume lowering osmolarity further still

159
Q

What are signs and symptoms of very low sodium concentrations? What sort of values do they occur at? Why do they occur?

A

Caused by water moving into neurones - hyponatraemic encephalopathy

160
Q

Who are most at risk of hyponatraemic encephalopathy?

A

Children,
Premenopausal women
Hypoxaemic patients

161
Q

What should be done in a patient with hyponatraemia with euvolaemia to further diagnose?

A

Plasma and urine electolytes and osmalarities

Screen for addisons and siadh

162
Q

Treatment of hyponatraemia with euvolaemia

A

Fluid restriction
Slow 0.9% nacl
Severe neurological signs - hypertonic saline

163
Q

Causes of hypernatraemia?

A 
Water deficite (impaired thirst, unable to drink, diabetes insipitus, osmotic diuresis)
Excessive sodium administration (NaCl overuse, drugs with high na content)
164
Q

Symptoms of hypernatraemia?

A 
Nausea
Vomiting
Fever
Confusion
Polydipsia
165
Q

Investigations of hypernatraemia

A

Urine and plasma osmolality and sodium

166
Q

Symptoms and signs of acromegally

A

Bone - pronounced brow, wide nose, large jaw, macroglossia, wide spaced teeth, large hands and feet
Skin - acanthosis nigracans, darker skin, curly hair
Physiological - snoring, OSA, DM, HTN, headaches, decreased libido, carpal tunnel

167
Q

Tests in suspected acromegally

A

Glucose tolerance test - +ve with failed suppression of growth hormone
MRI pituitary

168
Q

Treatment of acromegaly

A

Lesion removal
Somatostatin analogues
GH antagonist

169
Q

Causes of hyperprolactinaemia

A

Pituitary adenoma secreting prolactin
Compression of pituitary stalk
Medications - antipsycotics, metaclopramide, ecstacy
Physiological - pregnancy, breastfeeding

170
Q

Presentation of hyperprolactinaemia

A

Female - amenorrhoea, oligomenorrhoes infertility, galactorrhoea
Male - galactorrhoea, impotence, hypogonadism,
Both - osteoporosis,

171
Q

Test in suspected hyperprolactinaemia

A

Prolactin levels between 8 and 160

Pregnancy test

172
Q

Differentiate cause of hyperprolactinaemia from prolactin levels

A

> 5000 from prolactinoma

>10000 from macroprolactinoma

173
Q

Treatment of microprolactinoma

A

Dopamine agonist eg bromocryptine

174
Q

Treatment of macroprolactinoma

A

Bromocriptine

If no response and visual symptoms etc then surgery

175
Q

Causes of diabetes insipidus

A

Cranial - idiopathic, trauma, congenital, tumour, haemorrhage
Renal - inherited, lithium, ckd, hypokalaemia

176
Q

Tests to run in suspected diabetes insipidus?

A

DM screen
U+E
Serum and urine osmolarities

177
Q

What changes in osmolarity would you see in urine and plasma (and ratio!) in diabetes insipidus?

A

Raised plasma
Lowered urine
U:P ratio

178
Q

Diagnostic test for diabetes insipidus

A

Water deprivation test - urine should normally concentrate

If it fails to give desmopressin and urine should then concentrate if cranial and not if nephrogenic

179
Q

Differentials of diabetes insipidus

A

DM
Lithium
Diuretic use
Primary polydipsia

180
Q

Treatment of diabetes insipidus

A

Cranial - desmopressin, treat cause

Renal - treat cause, nsaids, bendroflumethiazide

181
Q

Commonest hormones secreted by pituitary tumours

A

Prolactin
ACTH
GH

182
Q

A patient with a know pituitary tumour presents with sudden headache, meningism and visual field defect. What should be considered?

A

Pituitary apoplexy - bleed into tumour

183
Q

Features of growth hormone deficiency

A

Loss of muscle, difficulty exercising, decreased cardiac output, low glucose, osteoporosis

184
Q

Treatment of gh deficiency

A

Somatotrophin

185
Q

Causes of primary hyperaldosteronism

A

Adenoma - conns

Bilateral adrenocortical hyperplasia

186
Q

If someone has hyperaldosteronism but their k is nor,al what other blood test will be deranged?

A

Alkalosis

187
Q

What should be tested in suspected hyperaldosteronism

A

U+e

Renin and aldosterone levels

188
Q

What tests to run on a patient with proven primary hyperaldosteronism?

A

Mri

If adrenal mass seen take adrenal vein sampling bilat to see if it the source

189
Q

Treatment of primary hyperaldosteronism?

A

Conns - remove adenoma

Spironolactone

190
Q

Causes of secondary hyperaldosteroneism

A

High renin due to low renal perfusion
Renal artery stenosis
Diuretics
Ccf

191
Q

What is the 10% rule in phaeochromocytomas

A

10% malignant, extra adrenal, bilateral, familial

192
Q

Where are most extraadrenal phaeochromocytomas

A

Aortic bifurcation

193
Q

Who should be screened for thyroid problems?

A 
AF
Hyperlipidaemia
Lithium 
DM
Amiodarone
Downs
194
Q

What independantly influences prognosis and risk of thyroid eye disease

A

Smoking

195
Q

What causes a goitre in hashimotos?

A

Wbc infiltration

IPE (17 decks)

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