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Phase 2a Basic Knowledge > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Define T1DM

A

Autoimmune destruction of pancreatic B-cells leading to absolute insulin deficiency

T4 Hypersensitivity reaction

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2
Q

T1DM epidaemiology

A

Young
Lean
Northern European descent (Finland!)

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3
Q

Risk factors for T1DM

A

HLADR2 DQ3
HLADR4 DQ8
Other autoimmune condition
Environmental infection - could be a trigger!

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4
Q

Pathophysiology for T1DM

A

Autoimmune destruction of B-cells in islet of langerhan leads to absolute deficiency in insulin production —>
Hyperglycaemia and lower cellular glucose —>
Increased lipolysis & gluconeogenesis.

Insulin helps draw potassium in along with glucose [therefore, Hyperkalaemia even though full body k+ is low]

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5
Q

Signs/symptoms of T1DM

A

Young, lean
Polyuria, polydipsia, polyphagia
Weight loss
Glucosuria (+/- signs of ketogenesis)

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6
Q

When can T1DM Sx be diagnostic

A

When signs and symptoms are present with diabetes complications

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7
Q

Investigations and diagnosis for T1DM

A

Fasting blood glucose (FBG): < 7.0 mmol/L = normal
> 7.0 mmol/L = T1DM

Random blood glucose (RBG): < 11.1 mmol/L = normal
> 11.1 mmol/L = T1DM

HBA1C: > 48 mmol/L or 6.5% = T1DM

OGTT: Give 75g fast acting glucose… then measure blood glucose 2hrs later… > 11.1 mmol/L diagnostic

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8
Q

Prediabetic values for T1DM

A

None - no pre-diabetes
No lifestyle modification will affect this type of diabetes from developing.

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9
Q

Treatment for T1DM

A

Basal Bolus Insulin

Basal = longer acting, maintain stable insulin level throughout the day
Bolus = faster acting, 30 mins preprandial (before meal) to give “insulin spike”

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10
Q

4 types of insulin

A

Rapid - Novorapid, Aspart
Short - regular insulin
Intermediate - NPH
Long - detemir

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11
Q

The main complication for T1DM

A

Diabetes ketoacidosis

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12
Q

Define diabetes ketoacidosis (DKA)

A

Occurs from poorly managed T1DM
Or from infection/illness

Characteristic Px = 10y/o presents to A&E with severe dehydration + Hx of T1DM

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13
Q

Pathophysiology of diabetes ketoacidosis

A

Absolute insulin deficiency leads to unrestrained lipolysis + gluconeogenesis

You get so much gluconeogenesis (not all glucose is usable) therefore, converted to ketone bodies.

Ketone bodies = acidic therefore, increased concentration -> ketoacidosis

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14
Q

Signs or symptoms of DKA

A

T1DM Sx +

Kussmaul breathing (deep laboured breaths, to blow off CO2 - as compensation)

Pear drop breath (fruity ketone breath smell)

Reduced tissue turgor, hypotension + tachycardia

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15
Q

Investigation and diagnosis for DKA

A

Bloods:

Ketones > 3mmol/L
Hyperglycaemic > 11.1 mmol/L (RPG)
Acidosis (metabolic) < 7.3 pH or <15 mmol HCO3-
(These 3 = diagnostic)

+ Ketonuria, Glycosuria, Hyperkalaemia

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16
Q

Treatment for DKA

A

ABCDE (emergency)

1st line ALWAYS fluids - in most patients because of dehydration first

Then

Insulin (+ glucose, prevent hypoglycaemia)
( + potassium, replenish K+ stores)

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17
Q

Define T2DM

A

Peripheral insulin resistance with partial insulin deficiency
(Cholesterol/lipid and Beta amyloid deposits in pancreas)

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18
Q

T2DM epidaemiology

A

Presents later in life (30+)
M>F

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19
Q

Cause of T1DM

A

Autoimmunity
Genetics
Idiopathic
LADA —> Latent Autoimmune Diabetes in Adults

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20
Q

What is LADA

A

Latent Autoimmune Diabetes in adults
It’s a slower variant of T1DM… so… slower progression of insulin deficiency.

Harder to differentiate between it and T2DM

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21
Q

What is MODY

A

Maturity onset diabetes of the young
It is rare autoimmune condition similar to T2DM but presents in youth rather than older age.

TREATMENT - sulfonylurea (gliclizide)

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22
Q

Risk factors for T2DM

A

Genetic link (fHx - much stronger than HLA link in T1DM)
Smoking
Obesity
Hypertension
Sedentary lifestyle

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23
Q

What is T2DM a risk factor for…

A

Hypertension
Silent MI
Nephrotic syndrome
CKD

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24
Q

Pathophysiology for T2DM

A

Repeated exposure could lead to peripheral insulin resistance (i.e malfunctional insulin intracellular activation pathway)

Therefore, decreased GLUT-4 expression
Also
+ minor destruction of pancreatic islets (amyloid + cholesterol/lipid deposits)

All leading to hyperglycaemia with increased insulin demand from a depleted B cell population

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25
Q

Signs / symptoms for T2DM

A

Obesity
Hypertensive older Px
Polydipsia, polyuria + nocturia, glycosuria

Acanthosis nigracans; dark pigmented skin folds (sign of severe insulin resistance)

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26
Q

Investigation and diagnosis of T2DM

A

Same as T1DM
FPG > 7 mmol/L, RBG > 11.1 mmol/L, HBA1C > 48 or 6.5%

However, patient in T2DM could have a pre-diabetic state

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27
Q

Diagnosing prediabetic state

A

Diagnosed for T2DM, you have…

Impaired glucose tolerance
Plasma glucose after 2hrs 7.8 - 11.1 mmol/L (OGTT)

Impaired fasting glucose
Blood glucose 6.1 - 6.9 mmol/L

HBA1C
Between 42 - 47 mmol/mol

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28
Q

Treatment for pre diabetics

A

Lifestyle change / Modify risk factors
Like diet and exercise

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29
Q

Treatment for T2DM

A

1st line: Metformin
2nd line (if HBA1C is > 58 or 7.5%): add another drug Sulfonylurea - Gliclizide
3rd line: if persistently high, add another drug DPP-4 inhibitor or SGLT-2 inhibitor
4th line: last resort consider giving insulin

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30
Q

What type of drug is Metformin

A

Biguanide - increases insulin sensitivity and decreases liver production of glucose.

Weight neutral
Does NOT typically cause hypoglycaemia

Side effects:
Lactic acidosis
Diarrhoea and abdominal pain

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31
Q

Type of drug is Gliclazide

A

Sulfonyluria - stimulate insulin release from the pancreas

Weight gain
CAN cause hypoglycaemia
Increased risk of MI

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32
Q

Main complication of T2DM

A

HHS
Hyperosmolar hyperglycaemic state

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33
Q

Explain what to do in HHS

A

Often precipitated with infection - pneumonia
Pathophysiology - excessive hepatic gluconeogenesis (not totally insulin deficient, therefore you don’t get ketosis) - instead glucose = osmotically active so the excess glucose causes Hyperosmolar blood
Sx - severe T2DM, REDUCED CONCIOUSNESS
Dx - heavy glycosuria, increased plasma osmolality (> 300 mmol/L) with hyperglycaemia - NO ketonuria / hyperketonemia
Tx - first INSULIN (+ glucose, K+)
Then give fluids - 0.9% saline
Could give LMWH - anticoagulant as they have thicker blood.

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34
Q

What are the complications of DM

A

Macro-vascular
Cardiovascular (MI)
Cerebrovascular (Ischaemic stroke)
Peripheral arterial (PVD)

Micro-vascular
Retinopathy
Neuropathy (charat foot)
Nephropathy (nephrotic syndrome / CKD)

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35
Q

Define hypoglycaemia

A

Abnormally low blood glucose
< 3.3 mmol/L

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36
Q

Signs/symptoms of someone who is hypoglycaemic

A

Reduced conciousness
Dizziness
Syncope

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37
Q

Treatment for hypoglycaemia

A

IV glucose, if no IV acces give
IM glucagon

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38
Q

What could cause someone to be hypoglycaemic

A

Could be a result of diabetes drugs - sulfonylureas / insulin
In non-diabetics - diet, liver failure or Addison’s

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39
Q

What are the causes of hyperthyroidism

A

Graves (most common)

Toxic multinodular goitre - nodules secreting thyroid hormones

Toxic adenoma (solitary toxic thyroid nodule)

Ectopic TSH secretion - from ovarian Teratoma

De quervains thyroiditis - swollen, red, tender goitre (could be post viral infection)

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40
Q

Hyperthyroidism epidaemiology

A

F > M

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41
Q

Define hyperthyroidism

A

Hyperthyroidism is where there is over-production of thyroid hormone by the thyroid gland.
AKA thyrotoxicosis

Primary hyperthyroidism is due to thyroid pathology

Secondary hyperthyroidism is the condition where the thyroid is producing excessive t3/t4 as a result of overstimulation by TSH. The pathology is in the hypothalamus or pituitary

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42
Q

Pathophysiology of hyperthyroidism

A

In most common case: TSH-R autoantibodies

Mimic TSH and stimulate the TSH receptors on the thyroid.
I.e. Grave’s disease (an autoimmune condition).

Remember the role of t3/t4 is metabolism… so in excess the symptoms of metabolism are heightened

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43
Q

Symptoms of hyperthyroidism

A

Weight loss + hyperphagia
Anxiety
Heat intolerance
Diarrhoea
Oligomenorrhoea

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44
Q

Signs of hyperthyroidism

A

Tachycardia
Goitre (usually diffused, unless Toxic M.G)
Muscle wasting
Fine tremor

Specific to graves… (triad of…)
Exophthalmos (opthalmopathy)
Pretibial myxoedema (dermopathy)
Acropachy (clubbing + swelling + new bone formation)

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45
Q

Investigation / diagnosis of hyperthyroidism

A

TFTs: Low TSH… high T3/4 = primary hyperthyroidism

      High TSH… high T3/4        = secondary hyperthyroidism 

      Low TSH… normal T3/4   = sub-clinical hyperthyroidism 

      High TSH… normal T3/4  = sub-clinical hypothyroidism

Other tests:
Blood levels: TSH-R autoantibodies +ve in Grave’s
In 80% of cases anti-TPO Ab’s (more in hypothyroidism though)
Thyroid UltraSound Scan: differentiates diffused from toxic MG

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46
Q

1st line treatment for hyperthyroidism

A

Carbimazole

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47
Q

When is carbimazole Contraindicated for hyperthyroidism

A

In pregnancy
Give propylthiouracil

Use “block and replace” effect… dose is sufficient to block all production and the patient takes levothyroxine titrated to effect

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48
Q

Side effects of carbimazole

A

Agranulocytosis
Presents as a sore throat

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49
Q

Treatment for hyperthyroidism

A

1st line = Cabimazole
+ propranolol (beta blocker for symptomatic relief)
2nd line = propylthiouracil

Could give radioactive iodine (definitive - destroys excess thyroid tissue) - contraindicated: pregnancy

Last resort = surgery (thyroidectomy)

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50
Q

Complications for hyperthyroidism

A

Thyroid storm (main comp)

Heart failure - because increased workload on heart due to increased metabolism

Osteoporosis - increased metabolism of the bone (increased bone resorption)

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51
Q

What is thyroid storm

A

Rapid deterioration of thyrotoxicosis and have extremely high levels of T3/4
Systemic decompensation:
A Fib
Hypertension
Coma

Treatment: propylthiouracil + KI (high dose)

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52
Q

Signs related to Graves’ disease

A

Exophthalmos - build up glycosaminoglycan + inflammation and swelling around the eye causes it to bulge
Pretibial myxoedema
Acropachy

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53
Q

Role of triiodothyronine (t3)

A

Speeds up basal metabolic rate
Cells produce more proteins & burn more energy (using lipids and sugar)

Increases cardiac output

Increases bone resorption

Activates sympathetic nervous system

Remember most thyroxine converts into t3 to produce an effect

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54
Q

Epidaemiology of hypothyroidism

A

F > M
Ageing
Postpartum

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55
Q

Cause of hypothyroidism (primary)

A

Developed world:
Most common = Hashimoto’s thyroiditis

Developing world + worldwide:
Iodine deficiency

Drugs - Amiodarone (can also cause hyperthyroidism) / lithium
De quervains (progressed)
Treatment for hyperthyroidism- surgery / radioactive iodine / too much carbimazole/propylthiouracil

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56
Q

Define hypothyroidism

A

Hypothyroidism is the term used to describe an inadequate output of thyroid hormones by the thyroid gland.

Primary hypothyroidism - inability of the thyroid gland to produce hormones

Secondary hypothyroidism - pituitary / hypothalamus is failing to stimulate the the thyroid gland by not secreting TSH

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57
Q

Explain Hashimoto’s thyroiditis and what disease does it cause

A

Most common cause of hypothyroidism

An autoimmune inflammation of the thyroid gland.
Associated with Antithyroid peroxidase (anti-TPO) antibodies
And antithyroglobulin antibodies.

Initially it causes a goitre and eventually leads to atrophy of thyroid gland.

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58
Q

Causes of secondary hypothyroidism

A

Hypopituitarism
-tumour
-radiation
-surgery
-infection

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59
Q

Symptoms of Px with hypothyroidism

A

Weight gain
Cold intolerance
Constipated
Lethargy
Menorrhagia

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60
Q

Signs of Px with hypothyroidism

A

Bradycardia
Slow reflexes
Goitre (if Hashimoto’s / iodine deficient)
Myxoedema

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61
Q

Investigations / diagnosis of hypothyroidism

A

TFT’s:
High TSH… Low T3/4 = primary hypothyroidism
Low TSH… Low t3/4 = secondary hypothyroidism
High TSH… Normal T3/4 = sub-clinical hypothyroidism

Anti-TPO / Anti-TGA Ab’s

May be anaemic ( can be all types; microcytic / Normacytic normachromic / Macrocytic)

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62
Q

Treatment for hypothyroidism

A

Levothyroxine (T4) - careful with dose, can cause iatrogenic hyperthyroidism
and the dose is titrated until TSH levels are normal

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63
Q

What is the complication of hypothyroidism

A

Myxoedema coma
Often infection induced

Rapid decrease in thyroid hormones

Px seen as: hypothermic, loss of consciousness, heart failure
Treatment: levothyroxine, ABx + hydrocortisone (until adrenal insufficiency hasn’t been ruled out

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64
Q

What types of thyroid carcinomas are there

A

Papillary (most common - 70%)

Follicular (25%)

Anaplastic (worst prognosis) - metastasises the most

Medullary cell carcinoma

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65
Q

What are the most common sites of metastases for thyroid cancers

A

Remember as LBLB:

LUNG - 50%
BONE - 30%
LIVER - 10%
BRAIN - 5%

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66
Q

Signs / symptoms of patient with thyroid carcinoma

A

Hard + irregular thyroid nodules
Could have hoarse voice (if theres compression of recurrent laryngeal nerve)

Other signs of carcinomas like… sudden weight loss, bleeding

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67
Q

How to diagnose thyroid carcinoma

A

Fine needle aspiration biopsy

TFTs

Thyroid USS

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68
Q

Treatment for thyroid carcinoma

A

For papillary + follicular:
Thyroidectomy or radiotherapy

For anaplastic:
Mainly palliative care

Remember any removal of thyroid will need lifelong hormone replacement - levothyroxine

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69
Q

Define Cushing disease and syndrome

A

Cushings disease = increased cortisol levels due to pituitary adenoma
Cushings syndrome = increased cortisol level from any cause

Note: pseudo-Cushing’s is due to alcohol… this resolves in 1-3 weeks.

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70
Q

Role of cortisol

A

Free coritisol is part of the circadian rhythm… peaks in morning, reduces by night

The ‘stress’ hormone:
Increased gluconeogenesis, proteolysis and lipolysis… increased glucose

Increased sensitivity for catecholamines (sympathetic innervation) in peripheries… narrowed blood vessels

Dampens immune response, so reduced inflammatory mediators and t-lymphocyte proliferation.

Inhibits GnRH decreased ovarian and testicular function.

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71
Q

Causes of Cushing’s syndrome

A

ACTH DEPENDENT
Most common = Cushing disease (pituitary adenoma)
Ectopic ACTH (SCLC)

ACTH INDEPENDENT
Most common OVERALL cause = Iatrogenic (steroid use)
Adrenal adenoma

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72
Q

Pathophysiology of Cushing’s

A

CRH—>ACTH—> Cortisol (in a -ve feedback loop) - this feedback loop either doesn’t work or have increased secretion of cortisol independent to the loop… causing Sx

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73
Q

Signs and symptoms for Cushing’s syndrome

A

Moon face, central obesity, buffalo hump
Abdominal striae
Peripheral limb weakness and muscle atrophy
Osteoporosis
Plethoric complexion
Susceptible to infection

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74
Q

Investigation / diagnosis for Cushing’s

A

Rule out oral steroids - if on steroids… ween them off

Random serum cortisol test if high then measure cortisol at 12am (should be low here but if high then thats abnormal)

If first line +ve, then measure plasma ACTH
High = ACTH dependant —> look for C.disease on pituitary MRI
Low = non-ACTH dependent —> consider adrenal adenoma.

Gold standard: dexamethasone suppression test (overnight - Giving synthetic cortisol to see if the negative feedback kicks in to suppress the cortisol (non-Cushing’s <50 nmol/L)
In Cushing, there is no suppression of cortisol.

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75
Q

Treatment for Cushing’s

A

Cushing disease:
Trans-sphenoidal resection /
bilateral adrenalectomy (complication of this = Nelson’s syndrome - pituitary continues to enlarge with excess ACTH secretion + hyperpigmentation, no -ve feedback from the adrenal gland)

Otherwise, treat the cause…
Adrenal adenoma:
Unilateral adrenalectomy
Ectopic ACTH = surgical removal of SCLC

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76
Q

Complications of Cushing’s

A

Osteoporosis
Secondary diabetes mellitus
Depression

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77
Q

Define acromegaly

A

Clinical manifestation of excessive growth hormone

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78
Q

How does high GH manifest in adults and children

A

Acromegaly in adults - after epiphyseal fusion

Gigantism in children - before epiphyseal fusion

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79
Q

Cause of acromegaly

A

Functional pituitary adenoma

80
Q

Pathophysiology for acromegaly

A

GHRH —> GH (from somatotrophs) —> IGF-1 (liver) which exerts effects on the rest of the body

In acromegaly… IGF-1 is abnormally high

81
Q

Signs and symptoms of acromegaly

A

Large hands and feet
Prognathism
Frontal bossing
Macroglossia
Vision change (bitemporal hemianopia)
Large interdental spaces
Carpel tunnel syndrome
Arthralgia / back pain

82
Q

Investigations / diagnosis for acromegaly

A

1st line screening: IGF-1 serum level high
Gold standard: OGTT

83
Q

Treatment for acromegaly

A

1st line: always trans-sphenoidal surgery
Or medication…
Dopamine agonist… Bromocriptine
Somatostatin analogue… ocreotide
GH antagonist… pegvisomant

84
Q

Complications of acromegaly

A

T2DM
Sleep apnoea

85
Q

What is the growth hormone inhibiting hormone

A

Somatostatin
Note: more potent at inhibition than dopamine
Very high glucose can also inhibit it

86
Q

Define Conn’s syndrome

A

Primary hyperaldosteronism
I.e. excess aldosterone, independent of the RAAS

Most common cause of secondary hypertension

87
Q

Difference between primary and secondary hyperaldosteronism

A

Primary is excess aldosterone independent of RAAS -
for example…
adrenal adenoma (conns syndrome) - 2/3
Or
Bilateral adrenal hyperplasia - accounts for 1/3 of cases

Secondary is excess aldosterone release because of RAAS activation (due to excess renin) -
For example…
renal artery stenosis
Renal artery obstruction
Heart failure

88
Q

Where is renin secreted from

A

Juxtaglomerular cell in kidney

89
Q

How does aldosterone affect the kidneys

A

Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts

90
Q

Pathophysiology for Conns

A

Adrenal adenoma causes excess release of aldosterone which raises blood pressure… -ve feedback so renin is suppressed.

In secondary hyperaldosteronism, renin is raised.

End up with hypertension with hypokalaemia

91
Q

Signs and symptoms of hyperaldosteronism

A

Resistant hypertension (unfixable with ACEi / B blockers)
Hypokalaemia
Muscle weakness
Parasthesia
Polydipsia + polyuria

92
Q

1st line investigation for conns syndrome / hyperaldosteronism

A

Renin:angiotensin

93
Q

Investigations / diagnosis for conns syndrome

A

1st line: Renin : Aldosterone ratio
Diagnostic: high aldosterone NOT suppressed with 0.9% IV saline or Fludrocortisone

ECG: for hypokalaemia will see… (long PR, U waves and ST depression)

94
Q

Treatment for conns syndrome / hyperaldosteronism

A

Surgery - laparoscopic adrenelectomy
SPIRONOLACTONE (aldosterone antagonist) - should be use 4 weeks pre-op
And for bilateral adrenal hyperplasia

95
Q

What can renal artery stenosis be confirmed by

A

Renal Doppler ultrasound scan
CT angiogram
MRA

96
Q

To diagnose DKA you require…

A
97
Q

Treatment for DKA

A

FLUIDS - 0.9% iv saline (sodium chloride)
I
G
P
I
C
K

98
Q

Risk factor for acromegaly

A

MEN 1

99
Q

Define adrenal insufficiency

A

Reduce secretion of adrenal cortex hormones
Particularly cortisol and aldosterone

100
Q

Name primary adrenal insufficiency

A

Addison’s disease

101
Q

Different types of adrenal insufficiency and why… their pathophysiology

A

Primary (Addison’s): damage to the adrenal cortex results in reduced hormone secretion… feedback means theres still high ACTH —> only adrenal insufficiency leading to hyperpigmentation

Secondary: reduced ACTH causing a reduced stimulation of adrenal gland, reduced hormone secretion and reduced ACTH

Tertiary: reduced secretion of CRH form hypothalamus so HPA axis suppression —> reduced hormone secretion.

102
Q

Who’s Addisons more commonly seen in

A

F > M with other autoimmune condition

103
Q

Causes for adrenal insufficiency

A

Primary / addisons:
In developed world =autoantibody mediated adrenal destruction
In developing world = TB (+ sarcoidosis)
Other causes = adrenal metastases (lung, liver, breasts) / Adrenal haemorrhage (e.g. Waterhouse friderichson syndrome—>blood.V in adrenals burst and cause damage to cortex - main cause of this is meningococcal meningitis)

Secondary:
Main cause = iatrogenic ( suppression of HPA axis) - exogenous steroids

104
Q

Signs / symptoms of adrenal insufficiency

A

Weight loss
Postural Hypotension (reduced aldosterone)
Vitiligo + reduced body hair (reduced androgens)
Hypoglycaemia (reduced cortisol)
Hyperpigmentation (only in Addison’s)

105
Q

Investigation / diagnosis of adrenal insufficiency

A

Short synacthen test:
Tests adrenal reserves by…

Measuring basal cortisol level at 9am (highest here - if low then abnormal)
Give synacthen and sample cortisol 30 mins after and 60 mins after… if failure to double from baseline = primary adrenal insufficiency (should be >580nmol/L)

Other tests:
U&Es… Hyperkalaemia, hyponatraemia
CT / MRI adrenals

106
Q

Autoantibodies associated with adrenal insufficiency

A

21-hydroxylase antibodies
Adrenal cortex antibodies

Present in 80% of autoimmune adrenal insufficiency

107
Q

Treatment for adrenal insufficiency

A

Hydrocortisone
Fludrocortisone

In trauma / infection —> double the dose of hydrocortisone (cortisol needed in stress)

108
Q

What is the severe acute presentation of adrenal insufficiency

A

Adrenal crisis - addisonian crisis

When you have severe adrenal insufficiency ESP hypocortisolemia;
Nausea + vomiting
Renal failure
Loss of consciousness

109
Q

Presentation of adrenal crisis

A

Nausea + vomiting
Renal failure
Loss of consciousness

110
Q

Treatment for adrenal crisis

A

Immediate IV hydrocortisone
IV saline (0.9% sodium chloride) + dextrose (if hypoglycaemic)

111
Q

Define diabetes insipidus

A

3L + of dilute urine daily; due to decreased secretion or action of ADH

112
Q

Types of diabetes insipidus

A

Cranial - decreased ADH secretion

Nephrogenic - decreased kidney response to ADH

Other types include: Gestational / Dipsogenic

113
Q

Cause on central/neurogenic diabetes insipidus

A

ADH gene mutation
Pituitary adenomas / brain tumours
Idiopathic

114
Q

Cause of nephrogenic diabetes insipidus

A

Drugs; Lithium
Renal tubular acidosis
ADH-R mutation
Polyuria

115
Q

Pathophysiology for diabetes insipidus

A

Nephrogenic diabetes insipidus is when the collecting ducts of the kidneys do not respond to ADH

Cranial diabetes insipidus is when the hypothalamus does not produce ADH for the pituitary gland to secrete.

116
Q

Signs / symptoms for diabetes insipidus

A

Polyuria
Polydipsia
HYPERNATRAEMIA
Severe Dehydration
Confusion

117
Q

Investigation / diagnosis for diabetes insipidus

A

Osmolality test:
Urine osmolality = low
Serum osmolality = high

Water deprivation test (no fluid for 8hrs):
Measure urine osmolality and administer desmopressin.
8hrs later, check urine osmolality again.

118
Q

What is water deprivation test used for and what its result

A

Diabetes insipidus
Measuring URINE osmolality before and after desmopressin administration

Diagnosis. After deprivation. After desmopressin

Cranial DI. Low. (<300) High (>800)
Nephrogenic DI. Low. Low

119
Q

Treatment for diabetes insipidus

A

Cranial - give desmopressin

Nephrogenic - thiazides diuretics + treat underlying cause

120
Q

Why are thiazides used for nephrogenic diabetes insipidus

A

Increase water loss at distal convoluted tubule… this encourages increased sodium uptake (+ water retention) which then concentrates the urine and helps with retention of water.

121
Q

Define SIADH - syndrome of inappropriate ADH

A

Inappropriate release of ADH - leads to more water retention therefore compensatory sodium excretion to main euvolemia
(Dilute euvolemia)

The excessive water reabsorption is not usually significant enough to cause a fluid overload, therefore you end up with a “euvolaemic hyponatraemia”.

It is OVERDIAGNOSED CAUSE OF HYPONATRAEMIA…

122
Q

What are the causes of SIADH

A

Tumours (SCLC, prostate, pancreatic)
Trauma to the head
Infection (TB, pneumonia)
Drugs - thiazides, carbamazepine (schizophrenia), SSRIs

123
Q

Pathophysiology for SIADH

A

Increased ADH release independent of RAAS —> increased vessel vasoconstriction and…
Increased Aquaporin-II expression of collecting duct therefore, increased blood volume by water retention

Excess H2O retained means more dilute blood & more Na+ loss to try compensate —> hyponatraemia

124
Q

Signs and symptoms of hyponatremia

A

Sx in hyponatremia!!

  • Vomiting
  • Decreased GCS
  • Headaches
  • Muscle weakness

Seizures, neurological complications, brain stem herniation

125
Q

In what condition could a Px get brain stem herniation and what is it

A

SIADH

Brain stem herniation = low sodium mean increased compensatory H2O movement into brain stem and this increases ICP

Causes hyponatremic encephalopathy
Risk of brain stem herniation through foreman magnum (tectorial herniation)

126
Q

Investigation and diagnosis of SIADH

A

U&Es: HYPONATREMIA and normal K+
High urine osmolality - because serum is diluted… urine is concentrated

Definitive diagnosis: to differentiate between Na+ (salt) depletion & SIADH; give 0.9% saline —>

Na+ depletion —> serum osmolality will be correct
SIADH —> serum osmolality fails to correct

127
Q

Treatment for SIADH

A

Fluid restriction + hypertonic saline

Treat underlying cause
-tumour excision

Chronic cases —>
Drugs; Tolvaptan (vasopressin antagonist / ADH receptor blocker),
Furosemide,
Demeclocycline (tetracycline antibiotic)

128
Q

Complication of SIADH

A

Central pontine myelinolysis
- usually due to rapid correction of sodium

2 phases fro CPM:
Phase 1: encephalopathy and confusion - blood sodium levels fall so water moves via osmosis across blood:brain barrier.

Phase 2: spastic quadriparesis, cognitive and behavioural changes - when given Na+ too fast, get demyelination of neurones.

129
Q

What cells produce PTH

A

Chief cells

130
Q

What triggers PTH

A

Hypocalcaemia

131
Q

Role of PTH

A

Increase osteoclast activity - increases bone resorption

Increases calcium absorption in kidney

Increases calcium absorption in gut

Increases Vit D activity by converting into its active form - Vitamin D acts to increase calcium absorption from the intestine.

132
Q

What are PTH disorders related to

A

Related to disorders of Ca2+ metabolism

Hyper PTH = high Ca2+ (cause of 90% of all Hypercalcaemia) - most common cause in community = hyperparathyroidism
Most common in hospital = bone malignancies e.g. myeloma

Hypo PTH = low Ca2+ (main cause is CKD)

133
Q

Causes of hyperparathyroidism

A

Primary (most common) - parathyroid adenoma
Sometimes parathyroid adenoma
[hyperparathyroid —> hypercalcaemia]

Secondary - response to low calcium (Vit d deficiency / CKD)
Get compensatory hypertrophy of the parathyroid gland
Chronic lack of calcitriol - this is an agonist for PTH
[hypocalcaemia —> hyperparathyroid]

Tertiary - after many years of secondary hyperparathyroidism (most common = CKD) —> glands act autonomously + release PTH with no -ve feedback (increased PTH regardless of Ca2+ conc)

Malignant: neoplasms (squamous cell lung cancer, breast, renal) secrete PTHrP; this ectopically mimics PTH

134
Q

Signs and symptoms for hyperparathyroidism

A

Signs of hypercalcaemia:

Renal stones (calcium oxalate)
Painful bones (excess resorption - osteopenia)
Abdominal groan (constipation, nausea, vomiting)
Psychiatric moans (depression, anxiety)

135
Q

Investigation and diagnosis for hyperparathyroidism

A

See haroons table….

PTH - high in all types

Ca+ - high in primary, tertiary…. Low in secondary

Phosphate - low in primary…. High in secondary & tertiary

ALP - high in all types

136
Q

Treatment for hyperparathyroidism

A

For primary - removal of parathyroid gland / parathyrodectomy of all 4 glands

For secondary / tertiary - treat cause

137
Q

complications for hyperparathyroidism

A

Acute severe Hypercalcaemia;

IV fluids + bisphosphonates

138
Q

Define Hypoparathyroidism

A

Reduced PTH hormone secretion

Rarer than hyperparathyroidism

139
Q

Types of Hypoparathyroidism and their causes

A

Primary - parathyroid gland failure (diGeorge syndrome —> familial, where parathyroid glands do not develop /// could be idiopathic)

Secondary - after surgery / parathyroidectomy (most common)

Pseudohypoparathyroid -
when theres peripheral PTH resistance
- Have small stature + small 4th/5th metacarpals

140
Q

Signs / symptoms of Hypoparathyroidism

A

Signs / symptoms of Hypocalcaemia

Symptoms: Remember Numb CAT
- Convulsions, Arrhythmias, Tetany and Numbness

Signs:
Chvostek - twitching of facial muscles (when CN7 traps over parotid)
Trousseau - carpopedal spasm (when tourniquet applied to forearm)

141
Q

Investigation / diagnosis for Hypoparathyroidism

A

TFTs + U&Es :

Low PTH
Low Ca2+
High Phosphate

ECG :

Long QT

142
Q

Treatment for Hypoparathyroidism

A

Remember its low Ca2+

Give calcium supplies + Vit D (AdCal D3)

143
Q

What can cause Hypercalcaemia

A

Hyperparathyroidism
Bone malignancy

^^ most common ^^

Drugs - thiazides
Excess calcium intake
Dehydration
Hyperthyroidism

144
Q

What’s seen on ECG finding for Hypercalcaemia

A

Short QT interval

145
Q

Signs / symptoms for Hypercalcaemia

A

Renal stones
Painful bones
Psychiatric moans
Abdominal groans

Decreased muscle tone + contractions because calcium inhibits fast Na+ influx

146
Q

What will PTH look like in Hypercalcaemia

A

PTH will be low;

-ve feedback

Unless in hyperparathyroidism

147
Q

Causes of hypocalcaemia

A

CKD (decreased activation of Vit D)
Severe Vit D deficiency
Hypoparathyroidism
Drugs; bisphosphonates / calcitonin
Acute pancreatitis

148
Q

ECG finding for hypocalcaemia

A

Long QT interval

149
Q

Signs / symptoms for hypocalcaemia

A

Numb CAT
- Numbness, Convulsions , Arrhythmias, Tetany

Increased muscle tone + contractions

150
Q

What happens to PTH in hypocalcaemic state

A

PTH is high

Unless in Hypoparathyroidism

151
Q

Define Hyperkalaemia

A

> 5.5mmol/L
6.5 mmol/L = emergency

152
Q

Causes for Hyperkalaemia

A

AKI
Drugs; Spironolatone, ACEi
Addison’s
DM ( + DKA)

153
Q

Pathophysiology of Hyperkalaemia

A

Increased K+ decreases threshold for Action Potentials - easier depolarisation for tissue
+ abnormal heart rhythms

154
Q

Signs / symptoms of Hyperkalaemia

A

Fast irregular pulse (increased risk of V.Failure)
Myalgia

155
Q

Investigations / diagnosis for Hyperkalaemia

A

U&Es
High K+ levels

ECG (remember as…
GO Absent p waves
GO LONG Prolonged PR
GO TALL Tall tented T waves
GO UNDER Wide QRS complex

156
Q

Treatment for Hyperkalaemia

A

Urgent (to stabilise cardiac membrane):
1st line: Calcium gluconate
Then: insulin + dextrose (glucose)

Non-urgent (to treat just Hyperkalaemia; no cardiac issues):
Insulin + dextrose

157
Q

Define hypokalaemia

A

< 3.5 mmol/L
<2.5 mmol/L = emergency

158
Q

Causes of hypokalaemia

A

Drugs; thiazides (Na+ sparing, K+ excreting) / loop diuretics
Conn’s (hyperaldosteronism)
Renal Tubular Acidosis 1 + 2
Decreased potassium intake

159
Q

Signs / symptoms of hypokalaemia

A

Hypotonia
Hyporeflexia
Arrhythmias (esp. AFib)

160
Q

Investigation / diagnosis of hypokalaemia

A

U&Es : decreased K+

ECG :
small inverted T waves
Prominent U waves
ST depression
PR prolongation

161
Q

Treatment for hypokalaemia

A

K+ replacement
Aldosterone antagonist / K+ sparing diuretic = spironolactone

162
Q

Define carcinoid tumours / syndrome

A

Poorly malignant tumours of enterochromaffin cells (neuroendocrine cells - can be found all over body; particularly GI organs)

163
Q

Where is carcinoid tumours mostly found

A

GI tract - at appendix + terminal ileum
Can also be found in lungs

Syndrome - when tumour metastasises in liver; causing Sx

164
Q

Difference between carcinoid tumour and syndrome

A

C. Tumours = only referring to the neoplastic cells (little to no symptoms)

C. Syndrome = when tumour metastasises to the liver —> Sx

165
Q

Pathophysiology of carcinoid tumour / symptoms

A

Neuroendocrine cells found particularly in GI tract / lungs
These cells get signals from nerve cells to secrete hormones into blood…
Amines (histamine) / (serotonin)
Polypeptides (bradykinin) - a vasodilator
Prostaglandins - potent vasodilators
These can be regulated by other hormones e.g. somatostatin inhibits serotonin.
Normally: Serotonin enter liver —> some metabolised into 5-hydroxyindolacetic acid (5-HIAA) & excreted via urine…
The rest carried in blood giving various effects.
When theres a N.E tumour, uncontrolled + unregulated N.E cell division (mainly in GI) —> if met. To liver = carcinoid syndrome.
Liver can’t metabolise hormone so build up of above hormones (their increased action) —> Sx!!!

166
Q

Effects or role of serotonin

A

In GI tract:
Increased motility & peristalsis

In vasculature:
Platelets take up serotonin and later use to vasoconstrict

In heart connective tissue:
Stimulates fibroblasts (get increased collagen)

167
Q

Primary site for N.E. Tumours

A

Common: Small/large intestine, lung, liver

Then: stomach, pancreas, ovaries, thymus

168
Q

Secondary sites for neuroendocrine tumour/carcinoid tumour

A

Liver

This can be primary / secondary… but causes carcinoid syndrome

169
Q

What symptoms are experienced in carcinoid syndrome

A

Common Sx :
Flushing + itching, SoB, diarrhoea

Why..?
- Flushing + itching —> increased histamines & bradykinin

  • Right sided heart valve incompetence (tricuspid regurgitation / pulmonary stenosis) - fibrosis
  • SoB - bronchoconstriction because of fibrosis
  • Diarrhoea and renal impairment - fibrosis of abdominal mesenteries + impaired kidney function - fibrosis

^^ all because of increased serotonin^^
Also, increased serotonin decreases tryptophan —> decreases niacin —> get pellagra (Sx: dermatitis, confusion)

170
Q

What exaggerates / heighten carcinoid syndrome Sx

A

Alcohol

Emotional stress

171
Q

Investigation / diagnosis of carcinoid tumours / syndrome

A

Liver USS —> +ve metastisis

Urinalysis —> increased 5-HIAA (serotonin metabolite) in urine ///chromagranin-A is also elevated + coupled with OCTREOSCAN (GoldStandard)

CT/MRI to locate primary tumour

172
Q

Treatment of carcinoid tumour / syndrome

A

Surgical excision - definitive
Octreotide (SST ANALOGUE) —> bind to N.E. Cells to block production of hormones

173
Q

Complications of carcinoid tumour / syndrome

A

Carcinoid crisis - life threatening Sx constellation

Treatment - high dose somatostatin analogue

174
Q

Define Prolactinoma

A

Prolactin = endocrine hormone secreted by anterior pituitary
…..…oma = refers to tumour

So, Prolactinoma is benign tumour (adenoma) of the pituitary gland which secretes excess prolactin

175
Q

Where is prolactin secreted from

A

Lactrotrophs found in anterior pituitary

176
Q

Where does LH + FSH come from and what’s their role

A

Gonadotrophs in anterior pituitary

Role:
Stimulate ovaries in women —> for oestrogen
Stimulates testes in men —> for testosterone

177
Q

What hormones are secreted by hypothalamus to control prolactin release

A

Thyrotropic-releasing hormone —> stimulatory … but …

Dopamine —> inhibitory … and …
overrides TRH for prolactin release so in non-pregnant women there’s a constant release of dopamine to control limited release of prolactin

178
Q

Pathophysiology for prolactin

A

High levels of prolactin should send a -ve feedback to hypothalamus to increase dopamine levels… to then lower prolactin

High levels of prolactin should send a -ve feedback to hypothalamus to decrease GnRH… lowering FSH + LH —> less oestrogen / testosterone production —> decreased ovulation / spermatogenesis
Remember: oestrogen in women also PREVENTS osteoclast activation —> decreased bone breakdown … BUT … when oestrogen reduced you get too much resorption —> fractures and osteopenia

In a tumour… excess release of this hormone regardless of -ve feedback
< 10mm —> micro Prolactinoma
> 10mm —> macro Prolactinoma —> these can press on surrounding structures:
Meninges (pain at brain)
Optic chiasm (bitemporal hemianopia) - tunnel vision

179
Q

Cause of prolactinemia

A

Pituitary adenoma

Drugs; ecstasy

180
Q

How is breast milk produced

A

A. Pituitary secretes prolactin +
From placenta, human placental lactogen + progesterone are secreted

All 3 stimulate breast glandular tissue to make milk

181
Q

Hyperprolactinaemia effects on oestrogen

A

High levels of prolactin should send a -ve feedback to hypothalamus to decrease GnRH… lowering FSH + LH —> less oestrogen / testosterone production —> decreased ovulation / spermatogenesis
Remember: oestrogen in women also PREVENTS osteoclast activation —> decreased bone breakdown … BUT … when oestrogen reduced you get too much resorption —> fractures and osteopenia

182
Q

Signs / symptoms of Prolactinoma

A

Micro Prolactinomas are usually asymptomatic
Macroprolactinomas:
bitemporal hemianopia
Headaches
Galactorrhoea
Amenorrhoea (F)
Gynecomastia (M)
Erectile dysfunction (M)
Decreased libido & infertility

183
Q

Investigation / diagnosis of Prolactinoma

A

Blood test: Increased prolactin

184
Q

Treatment for Prolactinoma

A

Best: Dopamine agonist (Bromocriptine, Cabergoline) - massively shrinks tumour

Surgery

185
Q

Define pheochromocytoma

A

Phoenix… = dark
Chromo = colour
Cyt = cell
oma. = tumor

So, Phoechromocytoma is a adrenal medullary tumor where cells (chromaffin cells) darken when tumour is formed.

186
Q

Pathophysiology of pheochromocytoma

A

Adrenal medulla; chromaffin cells secrete catecholamines (Ad / NaD) - trigger fight / flight
These hormones bind to al[ha / beta recpetors to…
Increase cardiac output
Increased blood pressure
Dilate pupils
Increase blood sugar

Mutation / spontaneous uncontrollable division of these cells increase secretion

Increased catecholamines —> Cause smooth muscle contraction —> vasoconstriction —> increases peripheral vascular resistance —> hypertension

187
Q

Where in the body can chromaffin cells be found

A

Adrenal medullar
Carotid arteries
Bladder
Abdominal aorta

188
Q

Cause of pheochromocytoma

A

Sporadic

Or

Inherited:
MEN 2a / 2b (multiple endocrine neoplasia)
Neurofibromatosis type 1 (tumour deposits along nerve myelin sheaths)

189
Q

What can trigger catecholamine release

A

Stress
Physical exertion
Foods containing tyramine (chocolate, cheese, wine)

190
Q

Complication of pheochromocytoma

A

Hypertensive crisis / emergency:
180/120mmHg

Small vessels break:
Heart - CHF
Brain - Ischaemic / haemorrhagic stroke
Eyes - Retinol haemorrhage
Kidney - Kidney failure

191
Q

Treatment for hypertensive crisis

A

Phentolamine - alpha blocker

192
Q

Signs / symptoms of pheochromocytoma

A

Hypertension - cause of secondary hypertension (rarer than Conn’s)
Palpitations
Sweating
Pallor
Tachycardic

193
Q

Investigations / diagnosis for pheochromocytoma

A

Plasma metanephrine / normetanephrine (diagnostic)
These are more sensitive readings and longer half life

Also:
Urinalysis - catecholamines
CT; image of tumour

194
Q

Treatment of pheochromocytoma

A

Drugs;
Alpha-blockers (phenoxybenzamine)
Then
Beta-blockers (Atenolol)

^^prevents reactive vasoconstriction^^

Surgery; to remove tumour

195
Q

Tx for hypoglycaemia ()

A

If alert; sugary drinks, gels and snack

Unconscious + out of hospital; intramuscular glucagon

Unconscious + in hospital; intravenous dextrose

196
Q

Give 4 medications you can give for diabetic neuropathic pain

A

Amytryptiline
Gabapentin
Pregabalin
Duloxetine

197
Q

Which receptors are commonly seen in graves

A

Anti-TSH receptor antibodies

Phase 2a Basic Knowledge (13 decks)

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