Endo Flashcards
Signs / Symptoms of DMT2
Polyuria
Polydipsia
Polyphagia
Glycosuria
Usually picked up on routine blood tests
Pathology of DMT2
Repeated, prolonged exposure to glucose results in insulin resistance
+
Pancreatic B cells become damaged from hyperglycaemia and produce less insulin
=
Chronic hyperglycaemia
Ix DMT2
-
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
- Blood tests
Random plasma glucose > 11.1 mmol/L
Fasting plasma glucose > 7 mmol/L - 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
Tx T2DM
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
Mechanism of Sulphonylurea
Stimulates pancreatic B cells to secrete insulin
S/E of sulphonylurea
Weight gain
Hyponatraemia
Hypoglycaemia
Examples of sulphonylurea
Glicazide
Glimepiride
Describe the mechanism of Metformin
Increases insulin sensitivity
Decreases hepatic gluconeogenesis
Side effects of Metformin
When is it CI?
GI upset
Lactic acidosis
CANNOT be used in Px with eGFR < 30ml/min AKA renal failure!!
Describe the mechanism of DPP4-inhibitors
Increase incretin levels
∴ ↓ Glucagon secretion
Side effects of DPP4-i
Usually not many side effects
But does increase risk of pancreatitis
Describe the mechanism of SGLT-2 inhibitors
Inhibits reabsorption of glucose in the kidney
Side effects of SGLT-2 inhibitors
UTI !!
& Weight loss
Example of SGLT-2 inhibitors
Glifazone
Example of DPP4-i
Sitagliptin
Signs / Symptoms of Cushing’s
Round, moon face
Truncal obesity
Abdominal striae
Buffalo hump
Acne
Hirsutism
Mood changes - depression, anxiety
Irregular periods - Amennorhoea
Proximal limb wasting
Define Cushing’s
Chronic, abnormal elevation of cortisol
Causes of Cushing’s
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
Investigations for Cushing’s
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
Describe how you can identify the cause of Cushing’s disease using the dexamethasone suppression test
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).
Treatment for Cushing’s
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
CUSHING
(acronym)
Cataracts
Ulcers
Striae
Hyperglycaemia or HTN
Increased risk of infection
Necrosis
Glycosuria
RF Acromegaly
MEN-1
Why are plasma GH levels not used as a diagnostic factor in Acromegaly?
Bc secretion is pulsatile
increases due to stress, pregnancy, puberty and during sleep
Signs / Symptoms Acromegaly
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”
Pathophysiology of Acromegaly
Hypothalamus secretes GHRH ∴ Ant. pit secretes GH
XS GH causes XS production of IGF-1
∴ inappropriate growth of soft tissue and bone
RF Acromegaly
MEN-1
Ix Acromegaly
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
Tx Acromegaly
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
S/E of Somatostatin analogues
Pain at injection site
Loose stool
Abdo cramps
↑ Gallstones
Impaired glucose tolerance
When would you use pegvisomant instead of somatostain analogues (SSA) ?
If intolerant or resistant to SSA
Monitoring Acromegaly
Yearly follow up - vascular assessment, visual fields, GH levels, BMI
Complications / Co-morbidities Acromegaly
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
RF Prolactinoma
Female
Peak incidence @ 20 - 40 years
Signs / Symptoms Prolactinoma
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
Pathophysiology Prolactinoma
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
Ix Prolactinoma
1st Line - Serum prolactin levels (ALSO GS!!! If high = prolactinoma)
2nd Line - Pituitary MRI (to detect adenoma)
Tx Prolactinoma
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)
Complications Prolactinoma
Infertility
Sight loss
↑ Intracranial pressure - bc adenoma growth
Quick! What is Addison’s?
Too little cortisol and too little aldosterone
What is the fun key phrase to remember for Addison’s?
Tanned, Toned (fit and ready), Tired, Tearful
Causes of Adrenal Insufficiency
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
Signs / Symptoms Adrenal insufficiency
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
Ix Adrenal Insufficiency
> 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
Tx Adrenal Insufficiency / Addison’s
STEROIDS!! - double dose if trauma, nightshift work, infection or surgery
Oral Hydrocortisone/Prednisolone - to replace cortisol
Fludrocortisone - to replace aldosterone
Which medication used to treat adrenal insufficiency corrects postural hypotension?
Fludrocortisone
Bc by replacing aldosterone, it ↑ Na+ and ↓ K+
What is an Addisonian crisis?
Medical emergency!! Sudden drop in aldosterone and cortisol
How does an Addisonian crisis present?
Hypotension and cardiovascular collapse
Fever
Hypoglycaemia
Hyponatraemia and hyperkalaemia
Hypovolaemic shock
Confusion
Fatigue
N+V
Abdo and back pain
Muscle cramps
How to treat an Addisonian crisis?
Fluid and IV Hydrocortisone
Describe the differences between 1°, 2° and 3° adrenal insufficiency
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)
When treating adrenal insufficiency, what is important to remember?
Double dose of steroids if infection, trauma, surgery or nightshift work
Causes Hyperthyroidism
GRAVES’ DISEASE (80%!!)
Toxic multinodular goitre
XS iodine consumption
De Quervain’s thyroiditis/Thyroiditis
Drug induced (iodine, amiodarone)
Pregnancy
Signs / Symptoms Hyperthyroidism
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
Ix Hyperthyroidism
- THYROID FUNCTION TEST
If 1° - ↓ TSH, ↑ T3/T4
If 2° - ↑ TSH, ↑ T3/T4 - THYROID AUTO-ANTIBODIES
Thyroid peroxidase Abs - more in hypothyroidism
Thyroglobulin Abs
TSH receptor Abs (TRAb) - ONLY Graves - THYROID ULTRASOUND
- 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
Tx Hyperthyroidism
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
What is a common S/E of Carbimazole when treating Hyperthyroidism?
Agranulocytosis
Contraindications of Radioiodine treatment in Hyperthyroidism
Pregnancy
Breast-feeding
Mechanisms for Hyperthyroidism
- Overproduction of thyroid hormone
- Leakage of pre-formed hormone from thyroid
- Ingestion of XS thyroid hormone
What are the 2 strategies when giving Carbimazole for hyperthyroidism?
- Titration - oral carbimazole for 4 weeks then reduce according to TFTs
- Block & Replace - oral Carbimazole and thyroxine (has a less risk of going hypo)
Complications of Hyperthyroidism
Congestive HF
Atrial Fibrillation
Osteoporosis
Graves’ opthalmopathy complications
Graves’ dermopathy - elephantitis
THYROID STORM
Comp of Radioiodine therapy when treating Hyperthyroidism
Could lead to HYPOthyroidism
Mechanism of Radioiodine therapy when treating Hyperthyroidism
Iodine taken up and local irradiation and tissue damage causes return to normal
function
What drugs must be adjusted alongside a thyroidectomy when treating hyperthyroidism?
Anti-thyroid drugs are stopped 10-14 days prior and replaced w/ oral potassium iodide
Complications of Thyroidectomy
Bleeding
Post-op infection
Hypocalcaemia
Hypothyroidism
Hypoparathyroidism
Recurrent laryngeal palsy - due to laceration
Recurrent hyperthyroidism
What is Thyroid Storm / Thyroid Crisis?
Rare, life-threatening condition
Rapid deterioration of thyrotoxicosis
Signs / Symptoms Thyroid Storm
Hyperpyrexia
Tachycardia
Extreme restlessness
Potentially delirium, coma and death
What is Thyroid Storm usually precipitated by?
Infection
Stress
Surgery
Radioactive Iodine therapy
How do you treat Thyroid Crisis/Thyroid Storm?
Large doses of Carbimazole
Propanolol
Potassium iodide - to acutely block release of thyroid hormone from gland
Hydrocortisone - inhibits peripheral conversion of T4 to T3
Causes Hypothyroidism
Post-partum
Autoimmune thyroiditis (Hashimoto;s)
Iodine deficiency
Drug-induced (Carbimazole, Lithium, interferon Amiodarone)
Iatrogenic (thyroidectomy or radioactive iodine therapy)
Congenital hypothyroidism
Signs / Symptoms Hypothyroidism
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 !!
Ix Hypothyroidism
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
Tx Hypothyroidism
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
Monitoring Hypothyroidism Tx
T4 half-life is ~7 days
∴ wait ~ 4 weeks to see new TSH levels after dose adjustment
Hashimoto’s Thyroiditis pathophysiology
Cell and antibody mediated autoimmune disease
Causes formation of anti-thyroid antibodies
∴ forming progressive fibrosis
What is Hashimoto’s thyroiditis associated with?
DMT1, Addison’s, Pernicious anaemia
RF Hashimoto’s Thyroiditis
Down’s syndrome
Turner’s
HLA-DR3
Graves’
Ix Hashimoto’s thyroiditis
1st Line = Thyroid Function Tests
↑ TSH, ↓T4
GS = Anti-Thyroid Peroxidase Antibodies
Tx Hashimoto’s thyroiditis
Levothyroxine
What is Diabetic ketoacidosis?
A life-threatening, medical emergency
Signs / Symptoms of DKA
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
What is the associated between DKA and DMT1?
Most common way children w/ DMT1 present is with DKA
Is DKA preventable?
YES, so preventable
Usually occurs when people w/ DMT1 stop insulin (bc of illness/vomiting)
Pxs SHOULD NEVER STOP INSULIN !!!!!!!!!!!
Causes DKA
Untreated DMT1 / Interruption of insulin therapy
Undiagnosed DM
Infection/Illness
Myocardial infection
What is Kussmaul’s breathing?
Deep, laboured breathing pattern at consistent pace
Often associated with severe metabolic acidosis
Ix DKA
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
DKA Pathology
↓↓↓ 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
Tx DKA
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
Why can insulin Tx for DKA cause hypokalaemia?
Why is this dangerous?
Bc insulin decreases K+ levels
K+ goes into cells bc ↑ Na+ pump activity
∴ Hypokalaemia
∴ can lead to arrhythmias etc
Monitoring DKA
Monitor BG closely
Bc therapy can lead to shift of K+ into cells
∴ hypokalaemia
Complications DKA
Cerebral oedema
Cell types of Thyroid Cancers
Papillary
Follicular
Medullary
Lymphoma
Anaplastic
Behaviour
Spread
Prognosis
for Papillary cell Thyroid Cancer
Affects young people
Local spread, followed by pulmonary/skeletal
Good prognosis
Behaviour
Spread
Prognosis
for Follicular Cell Thyroid Cancer
Affects middle aged people, 3x more common in Females
Pulmonary & skeletal (lung/bone)
Usually good prognosis if early but poorer than papillary
Behaviour
Spread
Prognosis
for Medullary Cell Thyroid Cancer
Often familial
Local and metastases (liver, lung, skeletal)
Poor prognosis - depends on age/stage
Behaviour
Spread
Prognosis
for Lymphoma Cell Thyroid Cancer
Variable
/
Usually poor prognosis
Behaviour
Spread
Prognosis
for Anaplastic Cell Thyroid Cancer
Aggressive, mean onset = 65years
Local spread
Very very poor prognosis (avg. survival = 3-8 months)
RFs Thyroid Cancer
Head & neck irradiation
Females
Signs / Symptoms Thyroid Cancer
Palpable thyroid nodule - increased size, hardness and irregularity
Dysphagia
Hoarseness of voice - if tumour presses on recurrent laryngeal nerve
DDx Thyroid Cancer
Goitre
Ix Thyroid Cancer
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
Tx Thyroid Cancer
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
Complications Thyroid Cancer
↑ Risk of recurrent laryngeal nerve damage OR hypoparathyroidism
Phases of De Quervain’s Thyroiditis
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
What is De Quervain’s Thyroiditis ?
Transient, self-limited inflammation of thyroid gland
Subacute granulomatous thyroiditis
Presents w/ hyperthyroidism
Probs viral
Ix De Quervain’s Thyroiditis
1st Line =
Total T4/T3
T3 resin uptake
Free thyroxine index
(all of above is elevated)
CRP = elevated
Tx De Quervain’s Thyroiditis
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
Complications De Quervain’s
Thyroid storm
Long term hypothyroidism
DDx De Quervain’s
Thyroid cancer!
Toxic multinodular goitre
Hashimoto’s
Graves’
How can you clinically detect recurrence with medullary thyroid cancer?
Calcitonin !
Medullary thyroid cancer often secretes calcitonin!
Causes Hyperparathyroidism
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
Describe the Ca2+, PTH and phosphate levels in 1°, 2°, 3° & Malignant Hyperparathyroidism
1° - ↑Ca2+, ↑PTH, ↓Phosphate
2° - ↓Ca2+, ↑PTH, ↑Phosphate
3° - ↑Ca2+, ↑↑PTH, ↑Phosphate
Malignant - ↑Ca2+, ↓PTH (bc PTHrP isn’t in assay)
Signs / Symptoms Hyperparathyroidism
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 !
Describe the 3 reasons that Hyperparathyroidism presents the way it does
1. ↑Ca2+
2. Bone resorption effects of PTH
3. ↑BP ( ∴ check Ca2+ in EVERYONE with HTN)
Ix Hyperparathyroidism
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
Tx Hyperparathyroidism
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
What should a Patient with 1° Hyperparathyroidism avoid?
Thiazide diuretics
High Ca2+
Vitamin D intake
Monitoring Hyperparathyroidism
Measure serum U&Es daily
?
S/E of Cinacalcet
Myalgia
↓ Testosterone
Associations with Hyperparathyroidism
MEN-1
What should you check in ALL patients with HTN?
Ca2+
Bc could be hyperparathyroidism
What are the complications of removing the adenoma or of ALL 4 hyperplastic glands to treat Hyperparathyroidism?
HYPOparathyroidism
Recurrent laryngeal nerve damage (∴ hoarse voice)
Hyperparathyroidism :
Phosphate levels ↓ EXCEPT
In cases of renal failure
What is the most likely cause of increased Ca2+?
Hyperparathyroidism
What is Phaechromocytoma and where are they found?
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
Signs / Symptoms Phaechromocytoma
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 !
Ix Phaechromocytoma
↑Plasma/Urinary metanephines
(Should do 3 x 24 hour urine test for free metanephrine)
Tx Phaechromocytoma
Phentolamine - alpha receptor blocker
SURGERY - remove tumour
If malignant, can also use chemo or radiotherapy
Pathophysiology Phaechromocytoma
Neoplasia of adrenal medulla
Which secretes catecholamines
Monitoring Phaechromocytoma
Monitor BP
Lifelong followup (bc malignant recurrence may present late!)
Causes Hypoparathyroidism
1° - Gland failure
Congenital, auto-immune (Di George’s)
2° - Radiation, surgery (parathyroidectomy), magnesium def
Causes Pseudoparathyroidism
Failure of target cells to respond to PTH
Signs / Symptoms Hypoparathyroidism
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
Signs / Symptoms Pseudoparathyroidism
Short metacarpals (esp 4th & 5th)
Round face
Short stature
Calcified basal ganglia
Intellectual impairment
Tx Hypoparathyroidism
Calcium supplements + Calcitriol (active vit D)
OR Synthetic PTH (SC, every 12 hours)
Tx Hypercalcaemia
Rehydration w 0.9% saline
Then, bisphosphonates
Sometimes - loop diuretics e.g. furosemide
Define hypercalcaemia
> 2.66 mmol/L Ca2+ in blood
Causes Hypercalcaemia
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
What is PTHrP?
Parathyroid Hormone relating peptide - mimics PTH, released in some kidney & lung cancer
What is Milk Alkali syndrome?
TRIAD OF :
1. Hypercalcaemia
2. Metabolic alkalosis
3. AKI
Why can cancer cause hypercalcaemia?
Unregulated bone breakdown
∴ ↑ Ca2+ in blood
Signs / Symptoms Hypercalcaemia
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
RF Hypercalcaemia
Typically affects older women
Ix Hypercalcaemia
> 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
Tx Hypercalcaemia
If Hyperparathyroidism, treat accordingly
IV saline - helps dilute Ca2+ in blood
Bisphosphonates - encourages osteoclasts to apoptosise so ↓bone breakdown
Causes Hypocalcaemia
State whether they present with low or high phosphate
> Vit D def (low)
Hypoparathyroidism (high)
Pseudohypoparathyroidism -
Acute pancreatitis (low)
Osteomalacia (low)
CKD (high)
Drugs - Calcitonin, bisphosphonates
Describe the mechanism of Vitamin D deficiency as a cause for Hypocalcaemia
Vit D = ↑ Ca2+ uptake
∴
Vitamin D deficiency causes ↓ Ca2+ uptake at GI tract & ↓ absorption in kidneys
Describe the mechanism of Osteomalacia as a cause of Hypocalcaemia
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
Describe the mechanism of CKD as a cause of Hypocalcaemia
What might you find in tissues?
Poor uptake of Calcium in kidneys
Bc insufficient production of active vitamin D & renal phosphate retention
∴ might find microprecipitations of calcium phosphate in tissues
Describe the mechanism of drugs as a cause of Hypocalcaemia
Calcitonin - ↓ Ca2+ and phosphate
Bisphosphonates - ↓ Osteoclast activity ∴ ↓ Ca2+
Signs / Symptoms of Hypocalcaemia
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
What is Trousseau’s sign?
Carpopdeal spasm when BP cuff is inflated to 20mmHg above systolic blood pressure
Usually indicative of hypocalcaemia
Ix Hypocalcaemia
ECG - long QT
Bloods - Ca2+ < 8.5mg/dL
Test PTH, Vit D, Albumin, Phosphorus and Mg levels
Tx Hypocalcaemia
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)
Complications Hypocalcaemia
Seizure
Cardiac arrest
Long QT syndrome
Define Hypokalaemia
< 3.5 mmol/L serum potassium level
If <2.5 mmol/L = Severe & medical emergency !!
Explain the pathophysiology of Hypokaelaemia
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
Causes of Hypokalaemia
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
Why does hyperaldosteronism cause Hypokalaemia?
Aldosteronism stimulates K+ excretion
Signs / Symptoms Hypokalaemia
Usually asymptomatic !!
Muscle weakness
Cramps
Tetany
Palpitations
Light headedness
Constipation
Arrhythmias
Ix Hypokalaemia
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
What is a U wave?
> 0.5mm deflection after the T wave
Tx Hypokalaemia
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
Complications Hypokalaemia
CVS - Chronic HF, acute MI, arrhythmias
Muscle - weakness, depression of deep tendon reflexes, rhabdomyolysis
What is rabdomyolysis?
How does it present?
When damaged skeletal muscle breaks down rapidly
Tea-coloured urine & irregular heartbeat
Define Hyperkalaemia
Serum K+ > 5.5 mmol/L
Pathophysiology of Hyperkalaemia
When ↑ K+ :
↓ Difference in electrical potential between cardiac myocytes and outside cell
∴ ↓ Threshold for action potential
∴ Abnormal action potentials
∴ Arrhythmias
∴ Cardiac arrest
Causes Hyperkalaemia
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
Why does low aldosterone (e.g. adrenal insuffiency) cause Hyperkalaemia?
Aldosterone stimulates K+ excretion
How do ACE-i cause hyperkalaemia?
Blocks aldosterone binding to receptors
How does spironolactone cause hyperkalaemia?
Potassium-sparing diuretics
How does AKI cause hyperkalaemia?
Decreased filtration rate
∴ more K+ maintained in blood
Signs / Symptoms Hyperkalaemia
Muscle weakness
Rapid, irregular pulse
Impaired neuromuscular transmission
Flaccid paralysis
Chest pain
Light-headedness
Tachycardia
KUSSMAUL’S SIGN
Ix Hyperkalaemia
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
Describe the gradual ECG changes in Hyperkalaemia
Tx Hyperkalaemia
CIGS
Calcium gluconate - stabilise myocardial cells
Insulin
Glucose - Dextrose
SABA - as alternative to I+G
How do loop diuretics e.g. furosemide help treat Hyperkalaemia?
↑ K+ excretion
How does insulin & dextrose help treat Hyperkalaemia?
Drives K+ into cells
Short-term shift of potassium from ECF to ICF
How does Polystyrene sylphonate resin help treat Hyperkalaemia?
Binds K+ in gut
∴ ↓ Uptake
How does Calcium gluconate stabilise the myocardium?
↓ Excitability of cardiac myocytes
&& ↓ VF risk !
Further management Hyperkalaemia
Stop exacerbating drugs - ACEi
Treat underlying cause - AKI
Lower body K+ - loop diuretics etc
What is Carcinoid Syndrome?
When carcinoid tumour (made of enterochromaffin cells) is present and producing serotonin (5-hydroxytrytamine) (5HT)
Where do carcinoid tumours most commonly arise?
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)
Signs / Symptoms Carcinoid Syndrome
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
Ix Carcinoid Syndrome
1st line - 24 hour urine 5-hydroxyindoleacetic acid ↑
If liver mets not found/to find 1° tumour : CXR and chest/pelvic MRI & CT
Tx Carcinoid Syndrome
SURGERY !!! - resection of tumour is only cure !! ∴ VITAL to find 1°tumour
Somatostatin analogues - Octreotide!
To ↓ Sx - debulking, embolisation, radiofrequency ablation
How does octreotide help treat Carcinoid Syndrome ?
Blocks release of tumour mediators
Counters peripheral effects
Median survival of Carcinoid syndrome?
5-8 years
BUT can survive ~20 years!
so don’t give up
Complications Carcinoid Syndrome
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
Epidemiology T1DM
Young < 30 years, usually juvenile but can be any age
Lean
North European - e.g. Finland
RF T1DM
FHx of autoimmune disease (HLA-DR3/DR4)
Personal Hx of autoimmune disease
Signs / Symptoms T1DM
2-6 week history
Weight loss
Polyuria
Polydipsia
Glycosuria
MIGHT PRESENT W DKA
Why do T1DM patients present with weight loss?
Fluid depletion & breakdown of fat/muscle bc of insulin deficiency
Why do T1DM patients present with polyuria?
Osmotic diuresis, occurs when BG is higher than renal tubular absorptive capacity (/renal threshold)
Pathophysiology of T1DM
Autoimmune destruction of pancreatic B cells
Autoantibodies directed against insulin & islet cell antigens
Ix T1DM
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
Tx T1DM
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
Name the macrovascular complications of DM
Why do these occur?
Usually occur bc DM is a RF for atherosclerosis
Cerebrovascular events - MI/Stroke
Peripheral vascular disease
How much more common is MI in a DM Px?
4 times
How much more common is stroke in a DM Px?
2 times
Name some microvascular complications of DM
Neuropathy - Diabetic foot
Nephropathy - Renal failure
Retinopathy - glaucoma, blindness
Why does diabetic neuropathy occur?
Occlusion of vasa nervosum & accumulation of fructose/sorbitol in vessels supplying peripheral nerves
∴ impaired function of peripheral nerves
Signs / Symptoms Diabetic Neuropathy
> 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
How might diabetic foot first present?
↓ Sensation to vibration, temp, pin-prick
Signs of vascular disease in lower leg i.e. thin skin, no hair, blue discolouration
How might neuropathy result in diabetic foot and amputation?
Neuropathy causes a traume
∴ Ulcer forms
If ulcer fails to heal, causes severe infection
∴ Amputation is required
Can you prevent diabetic foot?
If so, how?
YES !!!
Regular chiropody, daily inspection of feet
If trauma, seek early advice/Tx
Management foot ulcers
Swab ulcers for culture & ∴ early Abx Tx
Good local wound care/surgical debridement
Reconstructive vascular surgery if artery occlusions
Describe the pathophysiology of diabetic retinopathy
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 !
What are the 2 types of diabetic retinopathy?
&& QUICK! What are the differences?
- Proliferative - forms NEW blood vessels
- Non-proliferative - doesn’t
What 3 big boi things happens in proliferative diabetic retinopathy?
Describe the pathophysiology behind them
- Damaged blood vessels close off
∴ new, abnormal vessels form
∴ leakage into vitreous humour - Scar tissue forms bc of new vessels forming
Can cause retina to detach from back of eye - If new blood vessels interfere w/ normal fluid outflow, will ↑ pressure
∴ affects optic nerve
∴ Glaucoma
Describe the pathophysiology of non-proliferative diabetic retinopathy
Walls of retinal vessels weaken
∴ leakage of microaneurysms into retina
Larger vessels dilate, become irregular in diameter
Retinal nerve fibre may swell
∴ Macular oedema
Signs / Symptoms Diabetic Retinopathy
Spots/Floaters in vision
Blurred vision
Impaired colour vision
Dark/empty areas in vision
Vision loss (blindness)
What might prevent blindness in retinopathy?
Aspirin
Ix Diabetic Retinopathy
Fundoscopy - cotton wool spots & flare haemorrhages
(Will see if pre-proliferative)
What is the earliest indicator of diabetic nephropathy?
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)
What is microalbuminuria?
What does this indicate when put into context of Diabetic nephropathy?
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
Tx Diabetic Nephropathy
Aggressive BP control
ACEi
If CI, Angiotension II antagonistis
Other types of Diabetes
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
What does SIADH stand for?
Syndrome of inappropriate secretion of ADH
Causes SIADH
> 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
Signs / Symptoms SIADH
↓ GCS, confusion w/ drowsiness
Irritability
Headaches
Anorexia
Nausea
Concentrated urine
Muscle aches/cramps
If severe, seizures/loss of consciousness
Ix SIADH
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
Pathophysiology of SIADH
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
Tx SIADH
-
Treat cause & restrict fluid
Might not need further treatment after this - Demeclocycline
-
IF SEVERE : Loop diuretic (furosemide) +/- salts
IF CHRONIC (?) : Vasopressin receptor antagonist (vaptans) e.g. Tolvaptan
How dose Demeclocycline work to treat SIADH?
Inhibits vasopressin action of kidneys
essentially causes nephrogenic DI
Essentially, what is Diabetes insipidus?
Not enough ADH
Pathophysiology DI
Cranial DI - Hypothalamus doesn’t produce ADH
Nephrogenic DI - Collecting duct of kidneys don’t respond to ADH
Causes DI
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
Signs / Symptoms DI
Polydipsia - uncontrollable & all-consuming!
Polyuria
Sx of hypernatraemia
Ix DI
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)
Tx DI
Cranial - desmopressin
Nephrogenic - Oral bendroflumethiazide & NSAIDs
Describe how bendroflumethiazide & NSAIDs helps to treat nephrogenic DI
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
Complications DI
Severe hypernatraemia
(When treating, careful not to ↓ Na+ too quickly!!!)
Pathophysiology Graves’
TSH-R autoantibodies formed
∴ Autostimulation of thyroid gland
What is Hyperosmolar Hyperglycaemic State?
Life-Threatening emergency!!!!!!
Hyperglycaemia
Hyperosmolality
Usually no ketosis
Signs / Symptoms Hyperosmolar Hyperglycaemic State
Fatigue, lethargy, N+V
Altered level of concious
Headaches
Papilloedema
Hyperviscosity
Dehydration
Hypotension
Tachycardia
Ix Hyperosmolar Hyperglycaemic State
Severe Hyperglycaemia > 33mmol/L
Hypotension
Hyperosmolality > 320 mosmol/kg
No signif acidosis or ketosis
Tx Hyperosmolar Hyperglycaemic State
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
Comps Hyperosmolar Hyperglycaemic State
Stroke
MI
PE
Insulin-related hypoglycaemia
Tx related Hypokalaemia
Pathophysiology Hyperosmolar Hyperglycaemic State
↓ 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
Typical Px for Hyperosmolar Hyperglycaemic State?
Elderly with T2DM
Conn’s Types
1º- adrenal glands produce XS aldosterone
2º- XS renin stimulates adrenal glands to produce aldosterone
Causes of 1ºConn’s
Bilateral adrenal hyperplasia - MC
Adrenal adenoma = Conn’s
Signs / Symptoms Conn’s
Often ASx
HTN
Headaches
↓K+
Weakness, cramps, paraesthesia
Polyuria, nocturia, polydipsia!
No change in HR, glucose or skin colour
Ix Conn’s
- 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
Tx Conn’s
Aldosterone antagonist - Eplerenone, Spironolactone
Tx underlying cause - surgery
e.g. Percutaneous renal artery angioplasty - via femoral artery to Tx renal artery stenosis
Familial cause of phaeochromocytoma
Men 2a
How to avoid hypertensive crisis in surgery with phaeochromocytoma?
Give Phentolamine - alpha receptor blocker
Triad of DKA
- Polydipsia
- Polyuria
- Weight loss
Where is aldosterone formed?
Zona glonerulosa in adrenal medulla
Hypokalaemia ECG readings
Prominent U waves
Flattened T waves
Long PR
Long QT