Endocrinology Flashcards
(91 cards)
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
