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Phase 2 Quick > Endo > Flashcards

Endo Flashcards

1
Q

Signs / Symptoms of DMT2

A

Polyuria
Polydipsia
Polyphagia
Glycosuria

Usually picked up on routine blood tests

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2
Q

Pathology of DMT2

A

Repeated, prolonged exposure to glucose results in insulin resistance
+
Pancreatic B cells become damaged from hyperglycaemia and produce less insulin
=
Chronic hyperglycaemia

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3
Q

Ix DMT2

A
  1. HbA1C - GS !!
    tells us avg. blood glucose levels for past 3 months

HbA1C > 48 mmol/L = DIABETES
HbA1C between 42 - 47 mmol/L = PRE-DIABETES

  1. Blood tests
    Random plasma glucose > 11.1 mmol/L
    Fasting plasma glucose > 7 mmol/L
  2. Oral glucose tolerance test
    Fasting > 7 mmol/L
    then test 2 hours after glucose

//
If asymptomatic, at least 2 of above
If symptomatic, 1 of above

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4
Q

Tx T2DM

A

1st line - Lifestyle management

2nd line - Metformin

3rd line - if HbA1C rises to 58, depends on drug tolerance/individual factors
Metformin + sulphonylurea e.g. glicazide
Metformin + DPP4-inhibitor e.g. sitagliptin
Metformin + SGLT-2i e.g. glifazon

4th line - Insulin

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5
Q

Mechanism of Sulphonylurea

A

Stimulates pancreatic B cells to secrete insulin

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6
Q

S/E of sulphonylurea

A

Weight gain
Hyponatraemia
Hypoglycaemia

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7
Q

Examples of sulphonylurea

A

Glicazide
Glimepiride

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8
Q

Describe the mechanism of Metformin

A

Increases insulin sensitivity
Decreases hepatic gluconeogenesis

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9
Q

Side effects of Metformin
When is it CI?

A

GI upset
Lactic acidosis

CANNOT be used in Px with eGFR < 30ml/min AKA renal failure!!

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10
Q

Describe the mechanism of DPP4-inhibitors

A

Increase incretin levels
∴ ↓ Glucagon secretion

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11
Q

Side effects of DPP4-i

A

Usually not many side effects
But does increase risk of pancreatitis

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12
Q

Describe the mechanism of SGLT-2 inhibitors

A

Inhibits reabsorption of glucose in the kidney

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13
Q

Side effects of SGLT-2 inhibitors

A

UTI !!
& Weight loss

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14
Q

Example of SGLT-2 inhibitors

A

Glifazone

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15
Q

Example of DPP4-i

A

Sitagliptin

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16
Q

Signs / Symptoms of Cushing’s

A

Round, moon face
Truncal obesity
Abdominal striae
Buffalo hump
Acne
Hirsutism
Mood changes - depression, anxiety
Irregular periods - Amennorhoea
Proximal limb wasting

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17
Q

Define Cushing’s

A

Chronic, abnormal elevation of cortisol

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18
Q

Causes of Cushing’s

A

ACTH-Independent -
> Iatrogenic !! - most common!
usually prednisolone (or other steroids)

> Adrenal adenoma - benign tumour, secretes XS cortisol

ACTH-Dependent
> Cushing’s disease - Ant. pituitary adenoma causes ↑ ACTH ∴ ↑ cortisol
(most common dependent cause)

> Ectopic ACTH production - neoplasm somewhere in body, esp small cell lung cancer!! also carcinoid tumours - produce XS ACTH

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19
Q

Investigations for Cushing’s

A

1st Line - Raised plasma cortisol
(don’t do randomly! bc cortisol levels fluctuate throughout the day)

GS!! DEXAMETHASONE SUPPRESSION TEST - low dose (1mg)

Other -
24hr urinary free cortisol (can be used instead of ^DST but doesn’t indicate cause)
MRI brain - to find pituitary adenoma
Chest CT - SCLC
Abdo CT - adrenal tumours

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20
Q

Describe how you can identify the cause of Cushing’s disease using the dexamethasone suppression test

A

Low dose (1mg) should be suppressed to < 50 nmol after 2 hours if normal
If NOT suppressed = Cushing’s syndrome

THEN high dose,
If Cushing’s disease, Px should suppress within 48 hours.
If NOT, it suggests an ectopic source (high ACTH) or adrenal tumour (low ACTH).

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21
Q

Treatment for Cushing’s

A

If iatrogenic, STOP STEROIDS !!

If adrenal adenoma, adrenalectomy

If Cushing’s disease, transsphenoidal surgery to remove pituitary adenoma

If ectopic ACTH production and hasn’t metastasised, surgery to remove neoplasm
If can’t do surgery, could remove both adrenal glands and give replacement steroid hormones for life

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22
Q

CUSHING
(acronym)

A

Cataracts
Ulcers
Striae
Hyperglycaemia or HTN
Increased risk of infection
Necrosis
Glycosuria

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23
Q

RF Acromegaly

A

MEN-1

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24
Q

Why are plasma GH levels not used as a diagnostic factor in Acromegaly?

A

Bc secretion is pulsatile
increases due to stress, pregnancy, puberty and during sleep

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25
Q

Signs / Symptoms Acromegaly

A

Bitemporal hemianopia
Large, spade-like hands and feet
Frontal bossing
Large ears, tongue, nose
Spacing between teeth
Large protruding jaw
Back ache
Arthralgia
XS sweating
Sleep apnoea
Amenorrhoea
Oily skin
Mood disturbances
Headache
Acroparaesthesia / Carpal tunnel signs

“My rings don’t fit anymore, I’ve gone up a couple of shoe sizes recently and my teeth have become more separated”

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26
Q

Pathophysiology of Acromegaly

A

Hypothalamus secretes GHRH ∴ Ant. pit secretes GH

XS GH causes XS production of IGF-1
∴ inappropriate growth of soft tissue and bone

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27
Q

RF Acromegaly

A

MEN-1

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28
Q

Ix Acromegaly

A

1st Line - Raised IGF-1 (bloods)

GS !! - Oral glucose tolerance test !
Give Px glucose
Serum GH should fall if normal
In acromegaly, serum GH release is not suppressed

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29
Q

Tx Acromegaly

A

If Acromegaly secondary to pit. adenoma, do transsphenoidal surgery to remove

If secondary to cancer, surgically remove tumour

–

If can’t do above, can be treated w/ mediation :
1. Somatostatin analogues e.g. octreotide - blocks GH release
2. Pegvisomant - GH antagonist given via SC daily
3. Dopamine agonist e.g. cabergoline, bromocriptine - blocks GH release

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30
Q

S/E of Somatostatin analogues

A

Pain at injection site
Loose stool
Abdo cramps
↑ Gallstones
Impaired glucose tolerance

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31
Q

When would you use pegvisomant instead of somatostain analogues (SSA) ?

A

If intolerant or resistant to SSA

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32
Q

Monitoring Acromegaly

A

Yearly follow up - vascular assessment, visual fields, GH levels, BMI

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33
Q

Complications / Co-morbidities Acromegaly

A

HTN / Heart disease - due to ↑ GH ∴ hypertrophy of the heart
Sleep apnoea
Arthritis - due to overgrowth of cartilage
T2 Diabetes - bc constantly high blood glucose
Carpal tunnel - muscle growth compresses nerve
Visual field defects - bitemporal hemianopia
Cerebrovascular events + headaches

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34
Q

RF Prolactinoma

A

Female
Peak incidence @ 20 - 40 years

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35
Q

Signs / Symptoms Prolactinoma

A

GENERAL : Headache, visual defect (bitemporal hemianopia), CSF leak (rareee)

FEMALES : Amennorrhoea, oligomenorrhoea, infertility, low libido, galactorrhoea

MALES : Erectile dysfunction, low testosterone, ↓ facial hair, low libido

–
Males can have galactorrhoea too but rarer

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36
Q

Pathophysiology Prolactinoma

A

Tumour of lactotroph cells
∴ hypersecretion of prolactin

∴ inhibits release of GnRH from hypothalamus
∴ ↓ LH, FSH from ant. pituitary

↓ release oestrogen and progesterone in females / in males ↓ release of testosterone

–
2° hypogonadism

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37
Q

Ix Prolactinoma

A

1st Line - Serum prolactin levels (ALSO GS!!! If high = prolactinoma)

2nd Line - Pituitary MRI (to detect adenoma)

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38
Q

Tx Prolactinoma

A

Medication is preferred over surgery!

1st Line - Dopamine agonists
e.g. ORAL cabergoline, bromocriptine
(bc dopamine inhibits prolactin secretion ∴ shrinks the prolactinoma)

Usually see big reduction of macroadenoma, can be sight saving
Microadenoma - responds to small doses, 1 or 2 a week

2nd Line - Hormone replacement therapy e.g. oestrogen
(if galactorrhoea/fertility isn’t an issue)

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39
Q

Complications Prolactinoma

A

Infertility
Sight loss
↑ Intracranial pressure - bc adenoma growth

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40
Q

Quick! What is Addison’s?

A

Too little cortisol and too little aldosterone

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41
Q

What is the fun key phrase to remember for Addison’s?

A

Tanned, Toned (fit and ready), Tired, Tearful

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42
Q

Causes of Adrenal Insufficiency

A

1° - Addison’s aka autoimmune adrenalitis (most common! 90%!)
Adrenal TB
Surgical removal of adrenal glands
Adrenal infarction/haemorrhage (meningococcal septicaemia)
Malignancy

2° - Steroids
CRH deficiency
Trauma
Radiotherapy

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43
Q

Signs / Symptoms Adrenal insufficiency

A

N + V
Fatigue
Postural hypotension
Hyperpigmentation esp in palmar creases for Addison’s
Pallor
Headaches
Depression
Impotence
Amennorrhoea
Weight loss

REMEMBER : Tanned, Toned, Tired, Tearful

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44
Q

Ix Adrenal Insufficiency

A

> GS!! Short synACTHen
If Px healthy, cortisol levels should double
If doesn’t, indicates Addison’s (1°) (or doesn’t indicate between 1° and 2° confused)

> Plasma ACTH levels
If high with low/normal cortisol = 1° (Addison’s)
If low with low cortisol, indicates 2° or 3°

> U&E
Low Na+ and High K+ (bc low aldosterone)
Low aldosterone, high renin

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45
Q

Tx Adrenal Insufficiency / Addison’s

A

STEROIDS!! - double dose if trauma, nightshift work, infection or surgery

Oral Hydrocortisone/Prednisolone - to replace cortisol
Fludrocortisone - to replace aldosterone

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46
Q

Which medication used to treat adrenal insufficiency corrects postural hypotension?

A

Fludrocortisone
Bc by replacing aldosterone, it ↑ Na+ and ↓ K+

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47
Q

What is an Addisonian crisis?

A

Medical emergency!! Sudden drop in aldosterone and cortisol

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48
Q

How does an Addisonian crisis present?

A

Hypotension and cardiovascular collapse
Fever
Hypoglycaemia
Hyponatraemia and hyperkalaemia
Hypovolaemic shock
Confusion

Fatigue
N+V
Abdo and back pain
Muscle cramps

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49
Q

How to treat an Addisonian crisis?

A

Fluid and IV Hydrocortisone

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50
Q

Describe the differences between 1°, 2° and 3° adrenal insufficiency

A

1° - adrenal gland is damaged (Addison’s)
∴ ↓ cortisol and ↓ aldosterone
Most common cause worldwide = TB, in UK = autoimmune adrenalitis

2° - loss/damage of pituitary gland
∴ inadequate ACTH (∴ less stimulation of adrenal gland)

3° - suppression of hypothalamus
∴ inadequate CRH release
Usually bc patients on long term oral steroids (more than 3 weeks)

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51
Q

When treating adrenal insufficiency, what is important to remember?

A

Double dose of steroids if infection, trauma, surgery or nightshift work

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52
Q

Causes Hyperthyroidism

A

GRAVES’ DISEASE (80%!!)

Toxic multinodular goitre
XS iodine consumption
De Quervain’s thyroiditis/Thyroiditis
Drug induced (iodine, amiodarone)
Pregnancy

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53
Q

Signs / Symptoms Hyperthyroidism

A

General :
Weight loss
Heat intolerance
Palpitations
Anxiety
Tremors
Tachycardia

Graves’ Specific :
EYE SIGNS! - Exopthalmos, lid retraction, lid lag, lacrimation, diplopia
Pretibial myxoedema
Thyroid acropachy
Diffuse goitre

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54
Q

Ix Hyperthyroidism

A
  1. THYROID FUNCTION TEST
    If 1° - ↓ TSH, ↑ T3/T4
    If 2° - ↑ TSH, ↑ T3/T4
  2. THYROID AUTO-ANTIBODIES
    Thyroid peroxidase Abs - more in hypothyroidism
    Thyroglobulin Abs
    TSH receptor Abs (TRAb) - ONLY Graves
  3. THYROID ULTRASOUND
  4. RADIOACTIVE ISOTOPE UPTAKE SCAN
    Much higher in Graves’

Important !
If drug induced, everything is normal except ↑Thyroid hormones

–
Might be mild normocytic anaemia and mild neutropenia

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55
Q

Tx Hyperthyroidism

A

Depends on cause !

> Beta blockers - rapid system control in attacks

> Anti-thyroid drugs e.g. Carbimazole - blocks thyroid hormone synthesis

> Radioiodine treatment

nb. can do thyroidectomy but leave a small bit behind so thyroid function can still happen

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56
Q

What is a common S/E of Carbimazole when treating Hyperthyroidism?

A

Agranulocytosis

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57
Q

Contraindications of Radioiodine treatment in Hyperthyroidism

A

Pregnancy
Breast-feeding

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58
Q

Mechanisms for Hyperthyroidism

A
  1. Overproduction of thyroid hormone
  2. Leakage of pre-formed hormone from thyroid
  3. Ingestion of XS thyroid hormone
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59
Q

What are the 2 strategies when giving Carbimazole for hyperthyroidism?

A
  1. Titration - oral carbimazole for 4 weeks then reduce according to TFTs
  2. Block & Replace - oral Carbimazole and thyroxine (has a less risk of going hypo)
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60
Q

Complications of Hyperthyroidism

A

Congestive HF
Atrial Fibrillation
Osteoporosis
Graves’ opthalmopathy complications
Graves’ dermopathy - elephantitis
THYROID STORM

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61
Q

Comp of Radioiodine therapy when treating Hyperthyroidism

A

Could lead to HYPOthyroidism

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62
Q

Mechanism of Radioiodine therapy when treating Hyperthyroidism

A

Iodine taken up and local irradiation and tissue damage causes return to normal
function

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63
Q

What drugs must be adjusted alongside a thyroidectomy when treating hyperthyroidism?

A

Anti-thyroid drugs are stopped 10-14 days prior and replaced w/ oral potassium iodide

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64
Q

Complications of Thyroidectomy

A

Bleeding
Post-op infection
Hypocalcaemia
Hypothyroidism
Hypoparathyroidism
Recurrent laryngeal palsy - due to laceration
Recurrent hyperthyroidism

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65
Q

What is Thyroid Storm / Thyroid Crisis?

A

Rare, life-threatening condition
Rapid deterioration of thyrotoxicosis

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66
Q

Signs / Symptoms Thyroid Storm

A

Hyperpyrexia
Tachycardia
Extreme restlessness
Potentially delirium, coma and death

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67
Q

What is Thyroid Storm usually precipitated by?

A

Infection
Stress
Surgery
Radioactive Iodine therapy

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68
Q

How do you treat Thyroid Crisis/Thyroid Storm?

A

Large doses of Carbimazole
Propanolol
Potassium iodide - to acutely block release of thyroid hormone from gland
Hydrocortisone - inhibits peripheral conversion of T4 to T3

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69
Q

Causes Hypothyroidism

A

Post-partum
Autoimmune thyroiditis (Hashimoto;s)
Iodine deficiency
Drug-induced (Carbimazole, Lithium, interferon Amiodarone)
Iatrogenic (thyroidectomy or radioactive iodine therapy)
Congenital hypothyroidism

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70
Q

Signs / Symptoms Hypothyroidism

A

Symptoms :
Goitre
Weight Gain
Constipation
Lethargy
Poor memory
Puffy eyes
Arthralgia
Hoarse voice
Cold intolerance
Menorrhagia
Tiredness

Signs : BRADYCARDIC
Bradycardic
Reflexes relax slowly
Ataxia
Dry thin hair/skin
Yawning
Cold hands
Ascites
Round puffy face
Defeated demeanour
Immobile - ileus
Congestive HF

–
nB . Women w/ period problems should always have hypothyroidism excluded !!

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71
Q

Ix Hypothyroidism

A

Thyroid Function Tests
1° - ↑ TSH, ↓ T3/4
2° - ↓↓ TSH (inappropriately low for what T3/4 are), ↓ T3/T4

Thyroid Antibodies
Anti-thyroid Peroxidase Abs in Hashimoto’s!!!!

Other Hypo
> FBC - normocytic, normochromic anaemia. Could be macrocytic (menorrhagia) or microcytic (pernicous anaemia)
> Hyperlipidaemia
> Hyponatraemia (bc ↑ ADH)
> ↑ Serum creatinine kinase w/ associated myopathy

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72
Q

Tx Hypothyroidism

A

Lifelong, oral Levothyroxine (T4)

Start w/ 25 mcg, increase incrementally every 3-6 weeks

AIM is to get TSH = 0.5
w/ 1° - titrate dose until TSH normal
w/ 2° - TSH will always be low, monitor T4

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73
Q

Monitoring Hypothyroidism Tx

A

T4 half-life is ~7 days
∴ wait ~ 4 weeks to see new TSH levels after dose adjustment

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74
Q

Hashimoto’s Thyroiditis pathophysiology

A

Cell and antibody mediated autoimmune disease
Causes formation of anti-thyroid antibodies
∴ forming progressive fibrosis

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75
Q

What is Hashimoto’s thyroiditis associated with?

A

DMT1, Addison’s, Pernicious anaemia

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76
Q

RF Hashimoto’s Thyroiditis

A

Down’s syndrome
Turner’s
HLA-DR3
Graves’

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77
Q

Ix Hashimoto’s thyroiditis

A

1st Line = Thyroid Function Tests
↑ TSH, ↓T4

GS = Anti-Thyroid Peroxidase Antibodies

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78
Q

Tx Hashimoto’s thyroiditis

A

Levothyroxine

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79
Q

What is Diabetic ketoacidosis?

A

A life-threatening, medical emergency

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80
Q

Signs / Symptoms of DKA

A

N+V
Severe dehydration - can cause hypotension
PEAR DROP BREATH
Abdo pain
↓ Consciousness
Hyperventilation - Kussmaul’s
Confused
Confusion - could lead to coma
Potassium imbalance

Also, signs of DM - i.e. polyuria, polydipsia etc

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81
Q

What is the associated between DKA and DMT1?

A

Most common way children w/ DMT1 present is with DKA

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82
Q

Is DKA preventable?

A

YES, so preventable
Usually occurs when people w/ DMT1 stop insulin (bc of illness/vomiting)
Pxs SHOULD NEVER STOP INSULIN !!!!!!!!!!!

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83
Q

Causes DKA

A

Untreated DMT1 / Interruption of insulin therapy
Undiagnosed DM
Infection/Illness
Myocardial infection

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84
Q

What is Kussmaul’s breathing?

A

Deep, laboured breathing pattern at consistent pace
Often associated with severe metabolic acidosis

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85
Q

Ix DKA

A

Need 3 of the following for diagnosis !! :
1. Hyperglycaemia - BG > 11mmol/L
2. Ketosis - blood ketones > 3mmol/L
3. Acidosis - ABG, pH < 7.3 and/or bicarbonate < 15mmol/L

Clinical features
+ BG measurement
+ Blood gas

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86
Q

DKA Pathology

A

↓↓↓ Insulin
∴ unrestrained glucose production (hepatic gluconeogenesis)
∴ ↓ peripheral glucose uptake

High levels of circulating glucose
-> Osmotic diuresis by kidneys
∴ DEHYDRATION

Peripheral lipolysis = ↑ FFAs
FFAs oxidised to Acetyl CoA -> ketones
∴ ACIDOSIS

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87
Q

Tx DKA

A

IMMEDIATE ABC management if unconsciousness

Replace fluid loss w/ 0.9% saline

Replace deficient insulin - give insulin AND glucose (will prevent hypoglycaemia, will both inhibit gluconeogenesis and ∴ ketone production)

Treat underlying triggers - e.g. illness w/ Abx

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88
Q

Why can insulin Tx for DKA cause hypokalaemia?
Why is this dangerous?

A

Bc insulin decreases K+ levels
K+ goes into cells bc ↑ Na+ pump activity
∴ Hypokalaemia
∴ can lead to arrhythmias etc

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89
Q

Monitoring DKA

A

Monitor BG closely
Bc therapy can lead to shift of K+ into cells
∴ hypokalaemia

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90
Q

Complications DKA

A

Cerebral oedema

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91
Q

Cell types of Thyroid Cancers

A

Papillary
Follicular
Medullary
Lymphoma
Anaplastic

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92
Q

Behaviour
Spread
Prognosis

for Papillary cell Thyroid Cancer

A

Affects young people
Local spread, followed by pulmonary/skeletal
Good prognosis

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93
Q

Behaviour
Spread
Prognosis

for Follicular Cell Thyroid Cancer

A

Affects middle aged people, 3x more common in Females
Pulmonary & skeletal (lung/bone)
Usually good prognosis if early but poorer than papillary

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94
Q

Behaviour
Spread
Prognosis

for Medullary Cell Thyroid Cancer

A

Often familial
Local and metastases (liver, lung, skeletal)
Poor prognosis - depends on age/stage

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95
Q

Behaviour
Spread
Prognosis

for Lymphoma Cell Thyroid Cancer

A

Variable
/
Usually poor prognosis

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96
Q

Behaviour
Spread
Prognosis

for Anaplastic Cell Thyroid Cancer

A

Aggressive, mean onset = 65years
Local spread
Very very poor prognosis (avg. survival = 3-8 months)

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97
Q

RFs Thyroid Cancer

A

Head & neck irradiation
Females

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98
Q

Signs / Symptoms Thyroid Cancer

A

Palpable thyroid nodule - increased size, hardness and irregularity
Dysphagia
Hoarseness of voice - if tumour presses on recurrent laryngeal nerve

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99
Q

DDx Thyroid Cancer

A

Goitre

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100
Q

Ix Thyroid Cancer

A

1st Line = Ultrasound of neck (thyroid)
Fine needle biopsy cytology (to distinguish between benign and malignant)
Laryngoscopy

TFTs - hypo/hyperthyrodism needs to be treated before surgery

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101
Q

Tx Thyroid Cancer

A

Follicular & Papillary Cancers -
Total thyroidectomy
Ablative radioiodine given after - this is taken up by remaining thyroid tissue or metastatic lesions

Anaplastic & Lymphoma -
Tx is largely palliative :(
But external radiotherapy might provide some respite

102
Q

Complications Thyroid Cancer

A

↑ Risk of recurrent laryngeal nerve damage OR hypoparathyroidism

103
Q

Phases of De Quervain’s Thyroiditis

A

4 Phases

Phase 1 - Lasts 3 to 6 weeks. Hyperthyroidism, painful goitre, ↑ ESR
Phase 2 - Lasts 1 to 3 weeks, Euthyroid
Phase 3 - Weeks to months, Hypothyroidism
Phase 4 - Thyroid structure, function goes back to normal

104
Q

What is De Quervain’s Thyroiditis ?

A

Transient, self-limited inflammation of thyroid gland
Subacute granulomatous thyroiditis
Presents w/ hyperthyroidism
Probs viral

105
Q

Ix De Quervain’s Thyroiditis

A

1st Line =
Total T4/T3
T3 resin uptake
Free thyroxine index
(all of above is elevated)

CRP = elevated

106
Q

Tx De Quervain’s Thyroiditis

A

In HYPERthyroidism phase, NSAIDs and corticosteroids
(Usually only give steroids if v severe)

In HYPOthyrodism phase, no treatment usually. If severe, give small dose of Levothyroxine

107
Q

Complications De Quervain’s

A

Thyroid storm
Long term hypothyroidism

108
Q

DDx De Quervain’s

A

Thyroid cancer!
Toxic multinodular goitre
Hashimoto’s
Graves’

109
Q

How can you clinically detect recurrence with medullary thyroid cancer?

A

Calcitonin !
Medullary thyroid cancer often secretes calcitonin!

110
Q

Causes Hyperparathyroidism

A

1° - XS PTH
Tumour - solitary adenoma

2° - Compensatory hypertrophy of glands in response to HYPOcalcaemia
Vitamin D deficiency!!
Chronic renal disease

3° - After prolonged 2°, causes glands to act autonomously ∴ hyperplastic OR adenomatous change
(∴ ↑ Ca2+ bc no neg feedback bc ↑↑PTH)
Usually seen in CKD!

Malignant - Parathyroid-related protein (PTHrP) is produced by squamous cell lung cancer, breast & renal cell carcinomas
Mimics PTH

111
Q

Describe the Ca2+, PTH and phosphate levels in 1°, 2°, 3° & Malignant Hyperparathyroidism

A

1° - ↑Ca2+, ↑PTH, ↓Phosphate
2° - ↓Ca2+, ↑PTH, ↑Phosphate
3° - ↑Ca2+, ↑↑PTH, ↑Phosphate

Malignant - ↑Ca2+, ↓PTH (bc PTHrP isn’t in assay)

112
Q

Signs / Symptoms Hyperparathyroidism

A

Renal STONES, painful BONES, abdo GROANS, psychiatric MOANS

–
STONES - renal colic from renal stones (can lead to renal failure)
Biliary stones

BONES - painful bones, fractures & osteoporosis
Usually osteotitis fibrosa cystitis

GROANS - GI symptoms
N+V, constipation, indigestion

MOANS - lethargy, fatigue, depression, memory loss, psychosis, insomnia

–
ALSO, thirst, polyuria, HTN

Often asymptomatic at first w/ ↑ Ca2+
In retrospect, it’s not !

113
Q

Describe the 3 reasons that Hyperparathyroidism presents the way it does

A

1. ↑Ca2+
2. Bone resorption effects of PTH
3. ↑BP ( ∴ check Ca2+ in EVERYONE with HTN)

114
Q

Ix Hyperparathyroidism

A

STONES - Ultrasound KUB
BONES - DEXA bone scan for osteoporosis
GROANS - Abdo XR, renal calculi or nephrocalcinosis

BLOODS -
1° - ↑Ca2+, ↑PTH, ↓Phosphate
2° - ↓Ca2+, ↑PTH, ↑Phosphate
3° - ↑Ca2+, ↑↑PTH, ↑Phosphate

& 24 hour calcium excretion

115
Q

Tx Hyperparathyroidism

A

1°
Parathyroid adenoma - surgical removal

Parathyroid hyperplasia - ALL 4 glands removed

2° & 3°
Treat the cause
–
If emergency :
> Rehydrate w/ 0.9% saline (to prevent STONES)
> Bisphosphonates after rehydration (prevents bone resorption - prevents painful BONES) e.g. IV Pamidronate

116
Q

What should a Patient with 1° Hyperparathyroidism avoid?

A

Thiazide diuretics
High Ca2+
Vitamin D intake

117
Q

Monitoring Hyperparathyroidism

A

Measure serum U&Es daily
?

118
Q

S/E of Cinacalcet

A

Myalgia
↓ Testosterone

119
Q

Associations with Hyperparathyroidism

A

MEN-1

120
Q

What should you check in ALL patients with HTN?

A

Ca2+
Bc could be hyperparathyroidism

121
Q

What are the complications of removing the adenoma or of ALL 4 hyperplastic glands to treat Hyperparathyroidism?

A

HYPOparathyroidism
Recurrent laryngeal nerve damage (∴ hoarse voice)

122
Q

Hyperparathyroidism :
Phosphate levels ↓ EXCEPT

A

In cases of renal failure

123
Q

What is the most likely cause of increased Ca2+?

A

Hyperparathyroidism

124
Q

What is Phaechromocytoma and where are they found?

A

RARE, catecholamine-producing tumours
Usually found in adrenal medulla, arise from paraganglia cells (which is a type of chromaffin cells)

Extra-adrenal tumours are even rarer - if found, usually at aortic bifurcation

125
Q

Signs / Symptoms Phaechromocytoma

A

Often all vague and episodic

CLASSIC TRIAD :
1. Episodic headache
2. Tachycardia
3. Sweating

↑ BP and ↑ glucose sometimes
Sx may be precipated by exercise, stress etc

Skin pallor
Cold peripheries

Suspect if BP is hard to control, accelerating or episodic !

126
Q

Ix Phaechromocytoma

A

↑Plasma/Urinary metanephines

(Should do 3 x 24 hour urine test for free metanephrine)

127
Q

Tx Phaechromocytoma

A

Phentolamine - alpha receptor blocker

SURGERY - remove tumour
If malignant, can also use chemo or radiotherapy

128
Q

Pathophysiology Phaechromocytoma

A

Neoplasia of adrenal medulla
Which secretes catecholamines

129
Q

Monitoring Phaechromocytoma

A

Monitor BP
Lifelong followup (bc malignant recurrence may present late!)

130
Q

Causes Hypoparathyroidism

A

1° - Gland failure
Congenital, auto-immune (Di George’s)

2° - Radiation, surgery (parathyroidectomy), magnesium def

131
Q

Causes Pseudoparathyroidism

A

Failure of target cells to respond to PTH

132
Q

Signs / Symptoms Hypoparathyroidism

A

SPASMODIC
Spasm - carpopdeal spasm, Trousseau’s sign, larynx spasm - obstructing airway, premature labour (uterus contractions)
Perioral/peripheral paraesthesia
Anxious, irritable
Seizures
Muscle tone ↑
Orientation impaired & confusion
Dermatitis
Impetigo herpetiformis
Chvostek’s sign / Cardiomyopathy / Cataracts
–
CATS go NUMB
Convulsions
Arrhythmias
Tetany
Spasms

NUMB fingers/hands

133
Q

Signs / Symptoms Pseudoparathyroidism

A

Short metacarpals (esp 4th & 5th)
Round face
Short stature
Calcified basal ganglia
Intellectual impairment

134
Q

Tx Hypoparathyroidism

A

Calcium supplements + Calcitriol (active vit D)
OR Synthetic PTH (SC, every 12 hours)

135
Q

Tx Hypercalcaemia

A

Rehydration w 0.9% saline
Then, bisphosphonates
Sometimes - loop diuretics e.g. furosemide

136
Q

Define hypercalcaemia

A

> 2.66 mmol/L Ca2+ in blood

137
Q

Causes Hypercalcaemia

A

MOST (90%) of cases are due to hyperparathyroidism OR malignancy (NHL, Myeloma, Bone mets, PTHrP)
–
CHIMPANZEES
Calcium supplements
Hyperparathyrodism
Iatrogenic drugs
Milk alkali syndrome
Paget’s disease of the bone
Addison’s & Acromegaly
Neoplasms
Zollinger-Ellison’s - MEN type 1
Excess Vit D
Excess Vit A
Sarcoidosis

138
Q

What is PTHrP?

A

Parathyroid Hormone relating peptide - mimics PTH, released in some kidney & lung cancer

139
Q

What is Milk Alkali syndrome?

A

TRIAD OF :
1. Hypercalcaemia
2. Metabolic alkalosis
3. AKI

140
Q

Why can cancer cause hypercalcaemia?

A

Unregulated bone breakdown
∴ ↑ Ca2+ in blood

141
Q

Signs / Symptoms Hypercalcaemia

A

Renal STONES, painful BONES, abdo GROANS, psychiatric MOANS

–
STONES - renal colic from renal stones (can lead to renal failure)
Biliary stones

BONES - painful bones
Usually osteotitis fibrosa cystitis

GROANS - GI symptoms
N+V, constipation, indigestion

MOANS - lethargy, fatigue, depression, memory loss, psychosis, insomnia, confusion

–
ALSO, thirst, polyuria, HTN, fractures & osteoporosis

142
Q

RF Hypercalcaemia

A

Typically affects older women

143
Q

Ix Hypercalcaemia

A

> ECG - Short QT, tented T waves

> 24 Urinary Calcium - check in young patients or if family history to test if familial hypocalcuric hypercalcaemia

> Bloods - Ca2+ & PTH
If PTH undetectable and Ca2+ is high, means NOT hyperparathyroidism ∴ reqs further investigation (could be tumour secreting PTHrP)

> Rule out possible causes - CXR (Myeloma, NHL), SynACTHen (Addison’s), US (1° hyperparathyroidism) etc

> DEXA

144
Q

Tx Hypercalcaemia

A

If Hyperparathyroidism, treat accordingly

IV saline - helps dilute Ca2+ in blood
Bisphosphonates - encourages osteoclasts to apoptosise so ↓bone breakdown

145
Q

Causes Hypocalcaemia
State whether they present with low or high phosphate

A

> Vit D def (low)
Hypoparathyroidism (high)
Pseudohypoparathyroidism -
Acute pancreatitis (low)
Osteomalacia (low)
CKD (high)
Drugs - Calcitonin, bisphosphonates

146
Q

Describe the mechanism of Vitamin D deficiency as a cause for Hypocalcaemia

A

Vit D = ↑ Ca2+ uptake

∴
Vitamin D deficiency causes ↓ Ca2+ uptake at GI tract & ↓ absorption in kidneys

147
Q

Describe the mechanism of Osteomalacia as a cause of Hypocalcaemia

A

Serum calcium low bc Ca2+ can’t be absorbed from blood

Parathyroid gland recognises this and produces PTH to suck calcium from kidneys and resorb bone ∴ low Phosphate

148
Q

Describe the mechanism of CKD as a cause of Hypocalcaemia
What might you find in tissues?

A

Poor uptake of Calcium in kidneys
Bc insufficient production of active vitamin D & renal phosphate retention

∴ might find microprecipitations of calcium phosphate in tissues

149
Q

Describe the mechanism of drugs as a cause of Hypocalcaemia

A

Calcitonin - ↓ Ca2+ and phosphate
Bisphosphonates - ↓ Osteoclast activity ∴ ↓ Ca2+

150
Q

Signs / Symptoms of Hypocalcaemia

A

SPASMODIC
Spasm - carpopdeal spasm, Trousseau’s sign, larynx spasm - obstructing airway, premature labour (uterus contractions)
Perioral/peripheral paraesthesia
Anxious, irritable
Seizures
Muscle tone ↑
Orientation impaired & confusion
Dermatitis
Impetigo herpetiformis
Chvostek’s sign / Cardiomyopathy / Cataracts
–
CATS go NUMB
Convulsions
Arrhythmias
Tetany
Spasms

NUMB fingers/hands

151
Q

What is Trousseau’s sign?

A

Carpopdeal spasm when BP cuff is inflated to 20mmHg above systolic blood pressure

Usually indicative of hypocalcaemia

152
Q

Ix Hypocalcaemia

A

ECG - long QT
Bloods - Ca2+ < 8.5mg/dL
Test PTH, Vit D, Albumin, Phosphorus and Mg levels

153
Q

Tx Hypocalcaemia

A

If mild, Adcal supplements (Calcium carbonate) OR cholecalciferol

If severe/acute, IV Calcium Gluconate
10ml of 10% solution over 10 mins
OR
IV Calcium chloride (but more likely to cause local irritation)

If persistent, Vitamin D supplements (50000 IU orally once a week for 8 weeks)

154
Q

Complications Hypocalcaemia

A

Seizure
Cardiac arrest
Long QT syndrome

155
Q

Define Hypokalaemia

A

< 3.5 mmol/L serum potassium level
If <2.5 mmol/L = Severe & medical emergency !!

156
Q

Explain the pathophysiology of Hypokaelaemia

A

If ↓ K+ in serum (ECF), creates a water conc gradient out of cells (ICF)

∴ ↑ Leakage from ICF
Causes hyper-polarisation of myocyte membrane
∴ ↓ Myocyte excitability

157
Q

Causes of Hypokalaemia

A

Essentially :
↓ Potassium intake
↑ Potassium entry into cells
↑ Potassium excretion (sweat, urine, GI etc)
Magnesium depletion
Hyperaldosteronism

–

If with ALKALOSIS, causes might include : Vomiting, Thiazide & Loop diuretics, Cushing’s, Conn’s

If with ACIDOSIS, causes might include : Diarrhoea, Renal tubular acidosis, Acetazolamide, Partially treated DKA

158
Q

Why does hyperaldosteronism cause Hypokalaemia?

A

Aldosteronism stimulates K+ excretion

159
Q

Signs / Symptoms Hypokalaemia

A

Usually asymptomatic !!

Muscle weakness
Cramps
Tetany
Palpitations
Light headedness
Constipation
Arrhythmias

160
Q

Ix Hypokalaemia

A

ECG
U have no pot (K+) and no tea but you have a long PR and a long QT

> Prominent U waves
Inverted/Small T waves
Long PR interval
Long QT
Depressed ST

–
Metabolic panel
Urine electrolytes - helps to differentiate between renal/non-renal causes

161
Q

What is a U wave?

A

> 0.5mm deflection after the T wave

162
Q

Tx Hypokalaemia

A

If mild (3-3.4 mmol/L), Oral replacement -> Sando-K
Consider IV

If severe (<2.5 mmol/L), IV replacement KCL
40 mmol KCL in IL 0.9% NaCl

163
Q

Complications Hypokalaemia

A

CVS - Chronic HF, acute MI, arrhythmias
Muscle - weakness, depression of deep tendon reflexes, rhabdomyolysis

164
Q

What is rabdomyolysis?
How does it present?

A

When damaged skeletal muscle breaks down rapidly
Tea-coloured urine & irregular heartbeat

165
Q

Define Hyperkalaemia

A

Serum K+ > 5.5 mmol/L

166
Q

Pathophysiology of Hyperkalaemia

A

When ↑ K+ :
↓ Difference in electrical potential between cardiac myocytes and outside cell
∴ ↓ Threshold for action potential
∴ Abnormal action potentials
∴ Arrhythmias
∴ Cardiac arrest

167
Q

Causes Hyperkalaemia

A

Essentially :
↑ Intake
↑ Production
Redistribution
↓ Excretion

–
XS consumption very quickly e.g. IV fluids
↓ Aldosterone in kidneys - adrenal insufficiency
AKI

DRUGS - ACE-i, Spironolactone, Heparin, NSAIDs, Ciclosporin

168
Q

Why does low aldosterone (e.g. adrenal insuffiency) cause Hyperkalaemia?

A

Aldosterone stimulates K+ excretion

169
Q

How do ACE-i cause hyperkalaemia?

A

Blocks aldosterone binding to receptors

170
Q

How does spironolactone cause hyperkalaemia?

A

Potassium-sparing diuretics

171
Q

How does AKI cause hyperkalaemia?

A

Decreased filtration rate
∴ more K+ maintained in blood

172
Q

Signs / Symptoms Hyperkalaemia

A

Muscle weakness
Rapid, irregular pulse
Impaired neuromuscular transmission
Flaccid paralysis
Chest pain
Light-headedness
Tachycardia
KUSSMAUL’S SIGN

173
Q

Ix Hyperkalaemia

A

ECG - small P waves, tall tented T waves, wide QRS complex, sine wave, ventricular fibrillations

U&E (>5.5mmol/L = HYPERkalaemia)
If ≥ 6.5 mmol/L = medical emergency!

Urine analysis
Metabolic panel

174
Q

Describe the gradual ECG changes in Hyperkalaemia

A
175
Q

Tx Hyperkalaemia

A

CIGS
Calcium gluconate - stabilise myocardial cells
Insulin
Glucose - Dextrose
SABA - as alternative to I+G

176
Q

How do loop diuretics e.g. furosemide help treat Hyperkalaemia?

A

↑ K+ excretion

177
Q

How does insulin & dextrose help treat Hyperkalaemia?

A

Drives K+ into cells
Short-term shift of potassium from ECF to ICF

178
Q

How does Polystyrene sylphonate resin help treat Hyperkalaemia?

A

Binds K+ in gut
∴ ↓ Uptake

179
Q

How does Calcium gluconate stabilise the myocardium?

A

↓ Excitability of cardiac myocytes
&& ↓ VF risk !

180
Q

Further management Hyperkalaemia

A

Stop exacerbating drugs - ACEi
Treat underlying cause - AKI
Lower body K+ - loop diuretics etc

181
Q

What is Carcinoid Syndrome?

A

When carcinoid tumour (made of enterochromaffin cells) is present and producing serotonin (5-hydroxytrytamine) (5HT)

182
Q

Where do carcinoid tumours most commonly arise?

A

GI TRACT
then liver, lungs, ovaries, thymus

MC GI site = appendix
then ileum, rectum

80% of tumours mets - usually from ileum to LIVER
(treat all as malignant)

183
Q

Signs / Symptoms Carcinoid Syndrome

A

Initially very few symptoms
But when liver mets, hormone released into circulation & liver dysfunction
–
Bronchoconstriction (asthma/wheezing)
Paroxysmal flushing - upper body
Diarrhoea
HF - pulmonary stenosis, triscupid incompentence bc 5HT fibrosis
Abdo cramps

184
Q

Ix Carcinoid Syndrome

A

1st line - 24 hour urine 5-hydroxyindoleacetic acid ↑

If liver mets not found/to find 1° tumour : CXR and chest/pelvic MRI & CT

185
Q

Tx Carcinoid Syndrome

A

SURGERY !!! - resection of tumour is only cure !! ∴ VITAL to find 1°tumour

Somatostatin analogues - Octreotide!

To ↓ Sx - debulking, embolisation, radiofrequency ablation

186
Q

How does octreotide help treat Carcinoid Syndrome ?

A

Blocks release of tumour mediators
Counters peripheral effects

187
Q

Median survival of Carcinoid syndrome?

A

5-8 years
BUT can survive ~20 years!
so don’t give up

188
Q

Complications Carcinoid Syndrome

A

CARCINOID CRISIS
If tumour outgrows blood supply/tumour handled too much in surgery, tumour mediators flood out into circulation

Sx - Vasodilation, HYPOtension, tachycardia, bronchoconstriction, hyperglycaemia

Tx - HIGH dose Octreotide, careful management of fluid balance

189
Q

Epidemiology T1DM

A

Young < 30 years, usually juvenile but can be any age
Lean
North European - e.g. Finland

190
Q

RF T1DM

A

FHx of autoimmune disease (HLA-DR3/DR4)
Personal Hx of autoimmune disease

191
Q

Signs / Symptoms T1DM

A

2-6 week history
Weight loss
Polyuria
Polydipsia
Glycosuria
MIGHT PRESENT W DKA

192
Q

Why do T1DM patients present with weight loss?

A

Fluid depletion & breakdown of fat/muscle bc of insulin deficiency

193
Q

Why do T1DM patients present with polyuria?

A

Osmotic diuresis, occurs when BG is higher than renal tubular absorptive capacity (/renal threshold)

194
Q

Pathophysiology of T1DM

A

Autoimmune destruction of pancreatic B cells
Autoantibodies directed against insulin & islet cell antigens

195
Q

Ix T1DM

A

Fasting plasma glucose ≥ 7.0 mmol/L
Random plasma glucose ≥ 11.1 mmol/L

If symptomatic, 1 abnormal value
If asymptomatic, at least 2 abnormal values
–
Can also explore :
> Ketosis
> Rapid weight loss
> Age of onset < 5 years old
> BMI < 25 kg/m2
> Personal/FHx of autoimmune disease

196
Q

Tx T1DM

A

Basal - Long acting insulin
SC insulin
Once a day usually

Bolus - Short acting insulin
Soluble or analogues
Faster onset, shorter duration
Given ~30 mins before meals
–
Patient education is vital !!!!
–
Lifelong insulin

197
Q

Name the macrovascular complications of DM
Why do these occur?

A

Usually occur bc DM is a RF for atherosclerosis

Cerebrovascular events - MI/Stroke
Peripheral vascular disease

198
Q

How much more common is MI in a DM Px?

A

4 times

199
Q

How much more common is stroke in a DM Px?

A

2 times

200
Q

Name some microvascular complications of DM

A

Neuropathy - Diabetic foot
Nephropathy - Renal failure
Retinopathy - glaucoma, blindness

201
Q

Why does diabetic neuropathy occur?

A

Occlusion of vasa nervosum & accumulation of fructose/sorbitol in vessels supplying peripheral nerves
∴ impaired function of peripheral nerves

202
Q

Signs / Symptoms Diabetic Neuropathy

A

> Numbness or ↓Ability to feel pain and/or temperature - usually in fingers/toes or glove/stocking distribution
Tingling/burning sensation
Sharp cramps/pains
Hypersensitivity - even a bedsheet can ouch
Muscle weakness
Hyporeflexia
Loss of balance/coordination
DIABETIC FOOT

203
Q

How might diabetic foot first present?

A

↓ Sensation to vibration, temp, pin-prick
Signs of vascular disease in lower leg i.e. thin skin, no hair, blue discolouration

204
Q

How might neuropathy result in diabetic foot and amputation?

A

Neuropathy causes a traume
∴ Ulcer forms
If ulcer fails to heal, causes severe infection
∴ Amputation is required

205
Q

Can you prevent diabetic foot?
If so, how?

A

YES !!!
Regular chiropody, daily inspection of feet
If trauma, seek early advice/Tx

206
Q

Management foot ulcers

A

Swab ulcers for culture & ∴ early Abx Tx
Good local wound care/surgical debridement
Reconstructive vascular surgery if artery occlusions

207
Q

Describe the pathophysiology of diabetic retinopathy

A

XS glucose in blood causes glucose uptake into lens
∴ blockage of retinal blood vessels
∴ eye tries to grow new vessels but don’t develop properly
∴ will leak !

208
Q

What are the 2 types of diabetic retinopathy?
&& QUICK! What are the differences?

A
  1. Proliferative - forms NEW blood vessels
  2. Non-proliferative - doesn’t
209
Q

What 3 big boi things happens in proliferative diabetic retinopathy?
Describe the pathophysiology behind them

A
  1. Damaged blood vessels close off
    ∴ new, abnormal vessels form
    ∴ leakage into vitreous humour
  2. Scar tissue forms bc of new vessels forming
    Can cause retina to detach from back of eye
  3. If new blood vessels interfere w/ normal fluid outflow, will ↑ pressure
    ∴ affects optic nerve
    ∴ Glaucoma
210
Q

Describe the pathophysiology of non-proliferative diabetic retinopathy

A

Walls of retinal vessels weaken
∴ leakage of microaneurysms into retina
Larger vessels dilate, become irregular in diameter
Retinal nerve fibre may swell
∴ Macular oedema

211
Q

Signs / Symptoms Diabetic Retinopathy

A

Spots/Floaters in vision
Blurred vision
Impaired colour vision
Dark/empty areas in vision
Vision loss (blindness)

212
Q

What might prevent blindness in retinopathy?

A

Aspirin

213
Q

Ix Diabetic Retinopathy

A

Fundoscopy - cotton wool spots & flare haemorrhages
(Will see if pre-proliferative)

214
Q

What is the earliest indicator of diabetic nephropathy?

A

Microalbuminuria
-> Can progress to intermittent albuminuria & persistent proteinuria

(Creatinine is normal! But once this stage has been reached, Px is usually 5-10 years away from end stage renal failure)

215
Q

What is microalbuminuria?
What does this indicate when put into context of Diabetic nephropathy?

A

When urine is -ve for protein but urine albumin:creatinine ratio (UCR) > 3mg/mmol
Indicates early renal risk & ↑ Vascular risk

If UCR > 3, should inhibit RAAS to protect kidneys even if BP isn’t high

216
Q

Tx Diabetic Nephropathy

A

Aggressive BP control
ACEi
If CI, Angiotension II antagonistis

217
Q

Other types of Diabetes

A

MODY - Mature onset diabetes of the young (rare autosomal dominant T2DM)
LADA - Latent autoimmune diabetes of adults (T1DM w/ slower progression)
1° Neonatal diabetes
Gestational diabetes - pregnancy, 3rd trimester

218
Q

What does SIADH stand for?

A

Syndrome of inappropriate secretion of ADH

219
Q

Causes SIADH

A

> Idiopathic
Malignancy - SCLC, pancreas, prostate, thymus, lymphoma
Major surgery!
Drugs - Opiates, chlorpropamide, carbamazepine, vincristine, SSRIs
Lung - pneumonia, TB, abscess, asthma, CF
Brain issues - head injury!, meningitis, tumour, stroke, haemorrhage, GB
Metabolic - Porphyria, alcohol withdrawal

220
Q

Signs / Symptoms SIADH

A

↓ GCS, confusion w/ drowsiness
Irritability
Headaches
Anorexia
Nausea
Concentrated urine
Muscle aches/cramps

If severe, seizures/loss of consciousness

221
Q

Ix SIADH

A

Usually diagnosis of exclusion
Must be distinguished from hyponatraemia
–
Clinical exam - euvolaemia
U&E - hyponatraemia
Serum osmolality - low
Urine Na+ & osmolality - high
Absence of hypokalaemia, hypovolaemia, hypotension
Normal renal, adrenal & thyroid function
–
Hyponatraemia is v common in elderly
∴ hard to distinguish
So test with 1-2L of 0.9% saline
If hyponatraemia, will respond. If SIADH, will not respond
–
Any type of imaging to find cause

222
Q

Pathophysiology of SIADH

A

XS ADH causes ↑ aquaporin 2 insertion
In turn, this causes :

1. ↑ Water retention
∴ dilution of blood plasma
∴ HYPONATRAEMIA

2. ↓ RAAS (↓aldosterone)
∴ ↑ secretion of Na+
The XS water is being secreted with Na+
i.e. body is removing Na+ from low Na+ concentrated blood

∴ NORMOVOLAEMIC & HYPONATRAEMIC

223
Q

Tx SIADH

A
  1. Treat cause & restrict fluid
    Might not need further treatment after this
  2. Demeclocycline

-
IF SEVERE : Loop diuretic (furosemide) +/- salts

IF CHRONIC (?) : Vasopressin receptor antagonist (vaptans) e.g. Tolvaptan

224
Q

How dose Demeclocycline work to treat SIADH?

A

Inhibits vasopressin action of kidneys
essentially causes nephrogenic DI

225
Q

Essentially, what is Diabetes insipidus?

A

Not enough ADH

226
Q

Pathophysiology DI

A

Cranial DI - Hypothalamus doesn’t produce ADH

Nephrogenic DI - Collecting duct of kidneys don’t respond to ADH

227
Q

Causes DI

A

CRANIAL :
Idiopathic
Congenital - defect in ADH gene
Tumour - craniopharyngioma, mets, pit tumour (might present as DI & hypopituitarism
Head trauma
Infiltrative disease - sarcoidosis, histiocytes
Surgery
Haemorrhage
Meningoencephilitis
–
NEPHROGENIC :
Drugs - Lithium, demeclocycline
↓ K+
↑ Ca2+
Sickle cell disease
CKD
Inherited (MC) - ADH receptor defect
Post-obstructive uropathy
–
NB. damage to hypothalamus-neurohyphysisial tract or post. pit does NOT cause ADH deficiency bc ADH can leak

228
Q

Signs / Symptoms DI

A

Polydipsia - uncontrollable & all-consuming!
Polyuria
Sx of hypernatraemia

229
Q

Ix DI

A

GS!! - Water Deprivation Test
Aim : to determine whether kidneys continue to produce dilute urine even when dehydrated
1. Restrict fluid
2. Measure urine osmolarity (if low = DI)
3. Desmopressin
(If osmolarity stays same = Nephrogenic, If increases = Cranial)
–
MRI Hypothalamus
Plasma biochemistry
Urine volume - to confirm polyuria
BG, Serum K+ & Ca2+ should be measured to exclude other causes of polyuria (DM)

230
Q

Tx DI

A

Cranial - desmopressin
Nephrogenic - Oral bendroflumethiazide & NSAIDs

231
Q

Describe how bendroflumethiazide & NSAIDs helps to treat nephrogenic DI

A

Bendroflumethiazide
Causes ↑ Na+ secretion in DCT
The increased water lost causes the body to ↓GFR
∴ diuretics are required

NSAIDs
↑GFR by inhibiting prostaglandin synthesis
Prostaglandins inhibit ADH action

232
Q

Complications DI

A

Severe hypernatraemia
(When treating, careful not to ↓ Na+ too quickly!!!)

233
Q

Pathophysiology Graves’

A

TSH-R autoantibodies formed
∴ Autostimulation of thyroid gland

234
Q

What is Hyperosmolar Hyperglycaemic State?

A

Life-Threatening emergency!!!!!!
Hyperglycaemia
Hyperosmolality
Usually no ketosis

235
Q

Signs / Symptoms Hyperosmolar Hyperglycaemic State

A

Fatigue, lethargy, N+V

Altered level of concious
Headaches
Papilloedema
Hyperviscosity
Dehydration
Hypotension
Tachycardia

236
Q

Ix Hyperosmolar Hyperglycaemic State

A

Severe Hyperglycaemia > 33mmol/L
Hypotension
Hyperosmolality > 320 mosmol/kg

No signif acidosis or ketosis

237
Q

Tx Hyperosmolar Hyperglycaemic State

A

Fluid replacement w 0.9% saline

VTE prophylaxis (high risk of dehydration) - LMWH e.g. enoxaparin

Insulin - only if ketones/glucose don’t decrease after fluid replacement

238
Q

Comps Hyperosmolar Hyperglycaemic State

A

Stroke
MI
PE

Insulin-related hypoglycaemia
Tx related Hypokalaemia

239
Q

Pathophysiology Hyperosmolar Hyperglycaemic State

A

↓ Insulin is enough to cause hepatic ketogenesis

BUT not enough to stop hepatic gluconeogenesis ∴ ↑glucose

Hyperglycaemia causes osmotic diuresis !! w assoc ↓Na+ and ↓K+

Severe vol depletion results in hyperviscosity of blood

240
Q

Typical Px for Hyperosmolar Hyperglycaemic State?

A

Elderly with T2DM

241
Q

Conn’s Types

A

1º- adrenal glands produce XS aldosterone

2º- XS renin stimulates adrenal glands to produce aldosterone

242
Q

Causes of 1ºConn’s

A

Bilateral adrenal hyperplasia - MC
Adrenal adenoma = Conn’s

243
Q

Signs / Symptoms Conn’s

A

Often ASx

HTN
Headaches
↓K+
Weakness, cramps, paraesthesia
Polyuria, nocturia, polydipsia!

No change in HR, glucose or skin colour

244
Q

Ix Conn’s

A
  1. FBC/U&E/LFT
    Plasma K+ might be low
    If aldosterone:renin is high = 1º

CT/MRI - locate adrenal lesion

GS = Selective adrenal venous sampling

245
Q

Tx Conn’s

A

Aldosterone antagonist - Eplerenone, Spironolactone

Tx underlying cause - surgery
e.g. Percutaneous renal artery angioplasty - via femoral artery to Tx renal artery stenosis

246
Q

Familial cause of phaeochromocytoma

A

Men 2a

247
Q

How to avoid hypertensive crisis in surgery with phaeochromocytoma?

A

Give Phentolamine - alpha receptor blocker

248
Q

Triad of DKA

A
  1. Polydipsia
  2. Polyuria
  3. Weight loss
249
Q

Where is aldosterone formed?

A

Zona glonerulosa in adrenal medulla

250
Q

Hypokalaemia ECG readings

A

Prominent U waves
Flattened T waves
Long PR
Long QT

251
Q
A

Phase 2 Quick (17 decks)

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