Endocrinology Flashcards
DIABETIC FOOT DISEASE
- pathology (describe the 2 main mechanisms)? 2
- how do you screen for each of these two pathologies? 2 (who should have regular follow up at diabetes foot centre - ie more than just screening?)
- describe clinical presentation of each? 2 (nb not of complications!)
NEUROPATHY
- loss of sensation
- Warm, dry skin, foot pulses are palpable
= 10g monofilament test
PERIPHERAL ARTERY DISEASE
- diabetes is big risk factor for this
- Cool, pale foot with no palpable pulses
= palpate for dorsalis pedis + posterial tibial artery pulse (+/- ABPI)
need regular follow up at diabetic foot clinic:
* deformity or
* neuropathy or
* non-critical limb ischaemia
* previous ulceration or
* previous amputation or
* on renal replacement therapy or
* neuropathy and non-critical limb ischaemia together or
* neuropathy in combination with callus and/or deformity or
* non-critical limb ischaemia in combination with callus and/or deformity
BASICALLY ANYONE WITH ANYTHING MORE THAN A SIMPLE CALLUS!
Nb although diabetic foot is often described as ischaemic or neuropathic - if often an element of both
How to tell difference between venous, arterial and neuropathic ulcers?
incl location, pain etc
Venous ulcers
= shallow ulcers with a granulated base, often with other clinical features of venous insufficiency present
Neuropathic ulcers
= PAINLESS ulcers over areas of abnormal pressure (eg head of metatarsal bones or heal), often secondary to joint deformity in diabetics ALMOST ALWAYS on SOLE of feet!
Arterial ulcers
= found at distal sites, often with well-defined borders and other evidence of arterial insufficiency
DIABETIC NEUROPATHIC ARTHROPATHY:
- aka?
- describe pathology?
- describe presentation?
- management?
aka CHARCOT’S FOOT
The exact cause is unknown. Decreased pain and pressure perception, abnormal strain and weight distribution, as well as autonomic neuropathy that increases perfusion with a subsequent “washing out” of bone substance is suspected.
- Tarsus and tarsometatarsal joints most commonly affected
- Coexisting ulcers common
- Acute: swelling, warmth, erythema
- Chronic: painless bony deformities, midfoot collapse, osteolysis, risk of fractures
- specialist review for consideration of off-loading abnormal weight
- sometimes immobilisation of the affected joint in plaster
Management of complications of diabetic foot disease:
- how to prevent? 1
- imaging if any ulcers / deformities? 1
- management of diabetic foot ulcers?
- who to refer to if can’t feel pulses?
good glycaemic control prevents!
- also regular screening and self-inspection of feet
do x-ray to look for osteomyelitis / bone deformity - MRI if high clinical suspisiopn
NEUROPATHIC ULCERS
- regular chiropody
- surgical debridement if appropriate
- abx if become infected
- may need offloading to allow to heal!
- also dressing!
- last line = amputation!
if peripheral vascular disease - refer to vascular
GRAVES DISEASE
- what % of hyperthyroidism?
- other causes of primary hyperthyroidism? 3
- pathophysiology?
- gender + age most affected?
- what conditions associated with?
- common triggers? 3
66% of hyperthyroidism
- toxic multinodular goitre
- toxic adenoma
- too much levothyroxine
(nb can rarely get toxic thyroid tumours and also ovarian/testicular cancers which produce thyroid hormones)
also thyroiditis - eg caused by drugs, radiation etc can rarely cause hyperthyroidism - but norm cause hypo!
GRAVES
- circulating IgG auto-Ab bind to and activate G-protein thyrotropin receptors → smooth thyroid hyperplasia → ↑T3 production
= women aged 30-50
= a/w autoimmune conditions (eg vitiligo, type 1DM, Addison’s)
common triggers:
- infection
- child birth
- stress
What is meant by ‘subclinical’ hypo and hyperthyroidism?
how are these managed?
subclinical = T3/4 are normal but TSH is abnormal!
- Does NOT refer to presence or abscence of symptoms!
subclinical hyperthyroidism:
- norm T3/4
- low TSH
subclinical hypothyroidism
- norm T3/4
- high TSH
may or may not be symptomatic!
- if symptomatic treat the same as norm! (discuss w pt)
- if asymptomatic: norm just observe and repeat in few months!
THYROID ANTIBODIES
which condition out of:
- grave’s
- hashimoto’s
- thyroid cancer
- postpartum thyroiditis
are these most likely to be present in:
- TSH receptor antibodies (TRAb)
- Thyroid peroxidase antibodies (TPOAb or anti-TPO)
- Thyroglobulin antibodies (TgAb)
TSH receptor antibodies (TRAb)
= GRAVES (90%)
- may also be raised in hashimotos or multinodular goitre
Thyroid peroxidase antibodies (TPOAb or anti-TPO)
= HASHIMOTOS (90%)
= POSTPARTUM THYROIDITIS (>60%)
- graves (70%)
- can rarely be raised in thyroid cancer
Thyroglobulin antibodies (TgAb)
= HASHIMOTOS (80%)
- thyroid cancer (25%)
- other autoimmune diseases (40%)
^not great marker for diagnosis but important for thyroid cancer follow up / monitoring
GRAVES DISEASE
- describe palpation findings of the thyroid gland?
- additional signs / conditions found in graves disease? 4 (ie not found in other causes of hyperthyroidism)
Diffuse, smooth, non-tender goiter
1) THYROID EYE DISEASE (30%)
- Exophthalmos
- Opthalmoplegia (paralysis of muscles within or surrounding eye → diplopia)
- lid lag
- lid retraction
- hjigh risk for corneal ulcers + abrasions
2) PRETIBIAL MYXOEDEMA
- oedematous, discoloured swelling above lateral malleoli (see photos**)
3) THYROID ACROPACHY
- extreme manifestation with clubbing, painful finger + toe swelling,
- periosteal reaction in limb bones
4) THYROID BRUITS
- due to ↑vascularity in thyroid gland
nb not going to describe other symptoms / signs of hyperthyroidism as I’ve done them to death!!
- but remember get OLIGOMENORRHOEA in HYPER (menorrhagia in hypo!)
nb get hypertension with widened pulse pressure:
- Systolic pressure is increased due to increased heart rate and cardiac output
- Diastolic pressure is decreased due to decreased peripheral vascular resistance
SUSPECTED HYPERTHYROIDISM
- 1st line bloods? 2
- 2nd line bloods to do? 1
- other investigations to consider? 2
see investigation algorithm
1st bloods:
- TSH
- free T3/4
do thyroid antibody bloods 2nd (after know that hyperthyroid)
- TSH receptor antibodies (TRAb)
- Thyroid peroxidase antibodies (TPOAb or anti-TPO)
- Thyroglobulin antibodies (TgAb)
if cause of hyperthyroid unclear after antibodies endocrinologist can do:
- thyroid ultrasound with doppler
- radioactive iodine uptake scan
nb if TFTs show secondary hyperthyroidism - refer to endocrinologist for further tests
nb TFTs often normal in thyroid cancer!
nb don’t do radioactive iodine scan if woman is pregnant!
GRAVES DISEASE
- symptomatic mx? 1
- 1st line? 1 (what if pregnant? 1)
- options if relapse? 2
control symptoms: BETABLOCKERS - propranolol (until can start Carbimazole - can only be started by an encrinologist!)
nb if someone is unwell at diagnosis - admit them!
1ST line: CARBIMAZOLE
^Can give Carbimazole + Levothyroxine simultaneously (block and replace) – reduces risk of iatrogenic hypothyroidism
nb carbimazole is norm given for 6 weeks until euthyroid then keep at level and gradually reduce - most people are of drugs after 2 years!
if pregnant: PROPYLTHIOURACIL
IF RELAPSE
- Radioactive iodine
OR
- thyroidectomy
^will need levothyroxine for life after both of these!
nb can’t give radioactive iodine if:
- breastfeeding
- pregnant (or will becom ein next 6 months!)
CARBIMAZOLE
- main adverse effects? 3
- agranulocytosis
- teratogen (make sure on contraception)
- cholestatic jaundice (? is this one right? **)
THYROID EYE DISEASE
- biggest modifiable risk factor? 1
- symptoms / features?
- when to refer to opthalmology?
- management? 3
nb only get thyroid eye disease in graves - not in any other cause of hyperthyroidism
nb the patient may be eu-, hypo- or hyperthyroid at the time of presentation
SMOKING = biggest risk factor!
- Eye discomfort
- ↑tears
- photophobia
- ophthalmoplegia + diplopia
- ↓acuity
- afferent pupillary defect (optic N compression)
- Exophthalmos
- proptosis
- conjunctival oedema
- corneal ulcers
REFER ASAP!!!
- artificial tears
- high dose steroids (may need IV)
- surgical decompression
^also stop smoking!
THYROTOXIC CRISIS / STORM
- who gets it?
- triggers? 5
- clinical features? 4
- change in obs? 3
- typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature
- Iatrogenic levothyroxine excess does not usually result in thyroid storm
TRIGGERS
- thyroid or non-thyroidal surgery
- trauma
- infection (or intercurrent illness)
- acute iodine load e.g. CT contrast media
- stopping anti-thyroid meds suddenly
^basically anything that causes a big stress/adrenaline response!
- confusion + agitation
- nausea + vomiting
- heart failure
- abnormal liver function test (jaundice may be seen clinically)
- HTN (with wide pulse pressure)
- tachycardia (norm w AF)
- FEVER >38.5 deg
^also very sweaty!!
MANAGEMENT OF THYROID STORM:
- to reduce temp? 1
- to slow heart? 1
- anti-thyroid drug? 1 (be specific)
- other drugs? 2
- who to consider calling for help? 1
nb if lead to congestive heart failure, esmolol is the preferred beta blocker
1) PARACETAMOL
- bring temp down
2) IV PROPANOLOL
- reduce HR
- can use calcium channel blocker if B blocker CI
3) PROPYLTHIOURACIL
- anti-thyroid drug norm used in preg
- better than carbimazole in acute setting
4) POTASSIUM IODINE
- not sure how this works but they give it
- aka Lugol’s iodine
5) DEXAMETHASONE
- blocks the conversion of T4 to T3
ALSO treat UNDERLYING TRIGGER!
call ICU if need help!
BIGUANIDES
- example?
- brief mechanism of action?
- gain or loose weight?
- contraindications? 2
- adverse effects? 2
METFORMIN
- reduce glucose absorption (gut)
- reduce glucose production (liver)
- increase insulin secretion (pancreas)
- increase peripheral glucose uptake (fat + muscle)
weight LOSS
CONTRAINDICATIONS
- AKI
- eGFR < 30
ADVERSE EFFECTS
- GI symptoms
- lactic acidosis
OTHER ORAL MEDS FOR T2DM
for each:
- example?
- brief mechanism of action?
- gain or loose weight?
- Sulfonylureas
- Glitazones
- Gliptins
- GLP-1 mimics
- SGLT-2 inhibitors
SULFONYLUREAS
- eg gliclazIDE
= stimulates Beta cells in pancreas
- weight GAIN
GLITAZONES
- eg pioGLITAZONE
= reduces peripheral insulin resistance
- weight GAIN
GLIPTINS
- eg sitaGLIPTIN
= stop breakdown of the molecules that stimulate insulin secretion post-food (so insulin stays around longer)
- weight NEUTRAL
GLP-1 MIMICS
- eg exenaTIDE
= Increase insulin secretion, reduce glucagon secretion
- weight LOSS
= this is a SUB CUT injection!
SGLT-2 INHIBITORS
- eg dapaGLIFLOZIN
= Stop glucose being reabsorbed in kidneys (pee out sugar)
- weight LOSS
ADRENOCORTICAL INSUFFICIENCY:
- what two groups of hormones are deficient?
- what electrolyte effects does this have?
↓MINERALOCORTICOIDS (aldosterone) from z. glomerulosa → ↓stimulation of Na/K+ pump in kidney → ↑K+↓Na+; ↓water and ↓HCO3- (acidosis) reabsorption into blood
↓GLUCOCORTICOIDS (cortisol) from z. fasciculata →↓gluconeogenesis (formation of glucose from AA) → ↓blood glucose
nb also slight: ↓Androgens → ↓testosterone (mild, most produced in testes)
What does aldosterone (mineralocorticoid) do?
incl effect on BP, Na and K
Increases BP by retaining salt (and thus excreting K+)
What happens to:
- BP
- Glucose
- Sodium
- Potasium
in:
- Addisons
- Cushings
- Conns
ADDISONS
- BP: LOW
- Glucose: LOW
- Na: LOW
- K+: HIGH
CUSHINGS
- BP: HIGH
- Glucose: HIGH
- Na: HIGH
- K+: LOW
CONNS:
- BP: HIGH
- Glucose: norm
- Na: HIGH
- K+: LOW
Cushings looks like conns because, at high levels, corticosteroids start acting on mineralocorticoid receptors!
ADRENOCORTICAL INSUFFICIENCY:
- most common cause (of primary and overall)? (gender and age most affected?)
- other causes of primary? 5
- groups of secondary causes? 2
ADDISON’S (80%)
- autoimmune destruction of adrenal glands
= 30-50y
= females
= PMHx autoimmune conditions
other primary
- TB
- mets (eg bronchial Ca)
- meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
- HIV
- antiphospholipid syndrome
nb can also get through other causes of haemorrhage / infarction to adrenal glands (incl DIC)
secondary causes:
- pituitary disorders (e.g. tumours, irradiation, infiltration)
- long-term steroid therapy
ADDISON’S
- symptoms + signs?
- which sign is NOT present in secondary adrenal insufficiency
Lean + Tired:
- Anorexia, Weight loss
- Dizzy, Syncope, Postural hypoTN
Tanned:
- Bronze skin and pigmented palmar crease + buccal mucosa
Tearful + Weak:
- fatigue, depression, ↓self-esteem, psychosis
GI:
- Nausea, vomiting, abdo pain, diarrhoea or constipation (crave salty food!)
in women can get
↓Androgen symptoms (rarely affects men due to testis)
- ↓Sex drive
- ↓Pubic hair (women)
Primary Addison’s is associated with HYPERPIGMENTATION whereas secondary adrenal insufficiency is not
ADDISONS:
- initial blood test to do for screening? 1
- other bloods to do? 4
- diagnostic test? 1
- what can you do to exclude secondary causes? 1
1) 9am CORTISOL
Also:
- ACTH (high in addisons)
- Adrenal Auto-Ab (+ ve 80% in Addisons)
- U+Es (↑K+ ↓Na+ ↓HCO3-, mild ↑Ca2+)
- glucose (low)
DIAGNOSTIC TEST: Synacthen® ACTH stimulation test
- repeated blood tests (do in hosp)
AXR/CXR
- exclude secondary causes
- Identify past TB e.g. upper zone fibrosis or adrenal calcification
- Check for lung neoplasms
ADDISONS:
- two key meds for management?
- additional instructions to give for when pt is unwell?
nb usually managed by an endocrinologist
1) GLUCOCORTICOID REPLACEMENT
= norm hydrocortisone
- give blue steroid card
- tell not to stop abruptly
- DOUBLE dose in acute illness (give IM hydrocortisone pack to use if vomiting prevents oral meds)
2) HYDROCORTISONE REPLACEMENT
= fludrocortisone
(don’t need to double in illness)
nb can also give Androgen replacement: DHEA (Dehydroepiandrosterone)
ADDISONIAN CRISIS
- THREE main features?
- THREE key things for management? 3 (+ way to remember!)
norm cause:
Stress (e.g., infection, trauma, surgery) in a patient with underlying adrenal insufficiency
1) Pain in back, abdomen or legs (can resemble peritonitis)
2) Diarrhoea + Vomiting → Dehydration
3) ↓BP → Hypovolaemic shock →↓Consciousness → Death
(also often have fever)
3 Ss of Mx
1) SALT
- 0.9% saline (a lot!)
2) SUGAR
- 50% dextrose if hypo
3) STEROIDS
- IV hydrosortisone high doses
nb as well as someone with addisons getting this dt acute illness / surgery, can also get with:
- adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
- steroid withdrawal
HYPOTHYROIDISM
- most common cause of primary?
- other causes of primary? 7
- which of these have an initial hyperthyroid phase? 2/3
- medications which can cause hypothyroidism? 3
- most common cause of secondary hypothyroidism?
HASHIMOTOS THYROIDITIS = most common in UK
- may have initial hyper phase
Sub-acute de Quervain’s thyroiditis
= thyroiditis following viral infection → hyperthyroidism (phase 1) → euthyroid → hypothyroid (phase 3) = painful goitre
- self-limiting
Riedel’s thyroiditis
= fibrous replacement of thyroid parenchyma → painless goitre
Post-partum thyroiditis
= initial hyper phase -> prolonged hypothyroid phase
Iodine deficiency
= most common cause worldwide
drug-induced
- LITHIUM
- anti-thyroid drugs (eg carbimazole)
- AMIODARONE (can cause hyperthyroid)
post-hyperthyroid Mx
- following radioiodine ablation or thyroidectomy
Congenital
- can be sporadic or inherited
- very serious if not picked up!
secondary hypothyroid is rare!! - norm from pituatory failure
nb
Non-painful Goitre – Hashimoto and Riedel
Painful Goitre – De-Quevain
HASHIMOTO’S THYROIDITIS
- gender most affected?
- autoimmune conditions associated with? 3
- non-autimmune conditions associated with? 3
Female (5-10 times more common)
- type 1 DM
- addison’s
- perncious anaemia
- Down’s syndrome
- Turner’s syndrome
- coeliac disease
HYPOTHYROIDISM
- typical symptoms?
- typical signs?
- Weight gain despite loss of appetite
- Fatigue, Lethargy ↑Sleeping,↓Mood
- ↓Memory + ↓Cognition → dementia like symptoms
- Constipation
- MENORRHAGIA
- Hoarse voice
- Cold Sensitivity
- Myalgia + Cramps
- ↓Libido
- Dry skin + Hair loss/thinning + Cold Hands
(± loss of lateral eye brows) - ↓HR (bradycardia) ↑BMI
- ↓Reflexes
- Oedema (swelling in skin + soft tissue, typically lids, hands, face, tongue)
- Peaches + cream complexion + Round puffy face
may get Ascites, Pericardial or pleural effusion
may also get cerebellar ataxia
HYPOTHYROIDISM
- investigations? 3
- what used for monitoring? 1
- management? 1
- possible side effects of treatment? 4
- TSH (high in primary, low in secondary)
- T3/4 (low in both)
- autoantibodies (anti-TPO) - positive in hashimotos
?refer all to endocrinologist
TSH used for monitoring primary! (if secandary need T3/4 too)
LEVOTHYROXINE (T4)
- review every 3-4wks until stable TSH - then r/v 4-6 months
^if elderly or IHD then start very low dose and slowly build up!
SIDE EFFECTS:
- hyperthyroidism (over treatment)
- worsen angina
- worsen AF
- osteoporosis
nb if high TSH and norm T3/4 then norm means non-compliance with levothyroxine
nb Iron reduces absorption of levothyroxine – give at least 2hrs apart
MYXOEDEMA COMA
- who does this occur in?
- two main features? 2
- management? 4
poorly controlled hypothyroidism who undergo infection or surgery
- low GCS (or confusion)
- hypothermia
Mx
- IV thyroid replacement
- IV fluid (incl IV electorylte correction)
- IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)
- sometimes rewarming
SICK EUTHYROID SYNDROME
- what is it?
- what happens to TFTs?
- management?
aka non-thyroidal illness syndrome
no thyroid symptoms
- just abnormality in TFTs when someone is acutely unwell (esp in ICU)
NORM LOW T3
- T4 nd TSH are normal or low
Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed
HYPERPARATHYROIDISM:
- ways in which PTH increases blood calcium? 3
- describe difference between primary, secondary and tertiary hyperparathyroidism?
incl calcium and PTH levels
- COMMONEST cause of PRIMARY hyperparathyroidism?
PTH
- pulls calcium from bone
- decreased calcium loss in urine, loose more phosphate (and activate vit D)
- increased absorption of calcium from gut
PRIMARY
= Increased PTH secretion from PTH gland
= norm dt single parathyroid ADENOMA
- High PTH (or can be norm!), high Ca2+
- low phsophate, rasied ALP
SECONDARY
= Hypocalcaemia (norm dt CKD) -> reactive (and appropriate) increase in PTH
- High PTH, low (or norm) Ca2+
- high phosphate
- low Vit D
TERTIARY
= prolonged secondary → hypertrophy of PTH gland -> release PTH independent of Ca2+ levels
- Very high PTH, high Ca2+
- low or norm vit D
- low or norm phosphate
- high ALP
nb phosphate norm does opposite to calcium
so hypercalcaemic crisis may occur in primary or tertiary (but not secondary!
HYPERPARATHYROIDISM
- commonest cause of primary? 1
- other causes of primary? 3
- commonest cause of secondary? 1
- other causes of secondary? 3
PRIMARY
= PTH gland adenoma (85%)
- hyperplasia / multiple adenomas (15%)
- carcinomas (0.5%)
- MEN (multiple endocrine neoplasia) type 1 or 2
SECONDARY
= CKD
- malnutrition
- vit D deficiency (low sun, nutritional deficiency, liver cirrhosis)
- cholestasis (need bile to absorb fat-soluable vits like vit D)
nb parathyroid adenoma most common in post-menopausal/elderly women!
Symptoms of HYPERCALCAEMIA:
- stones? 1
- bones? 5
- abdominal groans? 5
- thrones? 1
- psych overtones? 4
- others? 3
which of these norm happen first? 2
what ECG abnormality can you sometimes see? 1
the MAJORITY of pts with primary hyperparathyroidism are ASYMPTOMATIC!
STONES
- renal colic
BONES
- bone, muscle + joint pain
- fragility fractures
- pseudogout
- Osteitis fibrosa cystica (cyst-like brown tumors)
- Skull: granular decalcification (salt-and-pepper skull)
ABDO GROANS
- anorexia
- nausea (+ vomiting)
- constipation
= gastric or duodenal ulcers (get dyspepsia 1st)
- pancreatitis
THRONES
= polydipsia + polyuria + dehydration (nephrogenic diabetes insipidus)
PSYCH OVERTONES
- Depression
- confusion
- hallucinations
- coma
OTHER
- hyporeflexia
- muscle weakness
- malaise
short QT interval (rarely seen)
can also get HYPERTENSION
if severe can also get: Osteitis fibrosa cystica (severe) – pts. w/ sub-periosteal resorption of distal phalanges, tapering of distal clavicle, salt and pepper skull, brown tumours of long bones
PRIMARY HYPERPARATHYROIDISM:
- bloods to do if suspect? 4 (+ findings)
- conservative management to lower calcium levels? 1
- which med to AVOID? 1
- definitive management? 1
- what is sometimes used if person is unfit for surgery? 1
BP will often be raised!
- Calcium = high
- PTH = high (or norm!!)
- phosphate = low
- ALP = high
can also do a DEXA scan to determine levels of osteoporosis/dystrophy
to lower Ca = LOTS of saline!!! (forces diuresis - may need to replace K and Mg as these will also lower, as well ac Calcium)
AVOID THIAZIDE diuretics! (will raise calcium further!)
(if really bad can have dialysis / haemofiltration)
definitive = TOTAL PARATHYROIDECTOMY (surgery)
if unfit for surgery: CINACALCET (calcimimetic) → ↑sensitivity of parathyroid cells to ca2+ levels → ↓PTH secretion
- may also use bisphosphonates if have osteoporosis
nb conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage AND asymptomatic!
Main differential for primary hyperparathyroidism?
how does it mimic?
Malignancy
parathyroid related protein is produced by SCC lung cancer (breast and renal too) → mimics PTH → high calcium!
Management of secondary hyperparathyroidism:
- main focus? 1
- additional meds that may be used? 2
TREAT UNDERLYING CONDITION (ie norm CKD)
- phosphate dietary restriction +/- phosphate binders
- activated vit D (if deficiency)
