Endocrinology Flashcards
HYPERTHYROID PRESENTATION
i) what would be seen in relation to weight and appetite?
ii) what may the patient be intolerant to?
iii) how may periods be affected? what type of mood may be seen?
iv) how may bowel habits be affected?
v) name two important things to ask about in the history
i) weight loss with increased appetite
ii) heat intolerant
iii) oligomenorrhoea (sparse/infrequent) with anxiety/panic
iv) diarrhoea or increased frequency
v) ask about pregnancy and family hx of thyroid disease
HYPERTHYROID - EXAMINATION
i) name two things that may be seen in the hands
ii) two things that may be felt in the pulse
iii) name two things seen in the neck? do you expect to see enlarged LNs?
iv) name four things that may be observed in the eyes? what is the one part for the eye that may not be inflammed?
i) see fine tremor / sweaty hands
ii) feel sinus tachy or AF in pulse
iii) neck - goitre that moves on swallow, bruit (graves), dont expect to see large LNs
iv) eyes - lid retraction, proptosis, diplopia, inflamm of everywhere apart from eye itself
THYROID FUNCTION TESTS - HYPERTHYROID
i) what TSH and FT4/3 levels would be expected in hyperthyroid?
ii) which antibodies should be tested for?
iii) what does the patient have if they have thyroid eye disease?
i) see low TSH and high FT4/3
ii) test for thyroid auto antibods (TRAB) > indicates graves thyrotoxicosis
iii) TED - graves thyrotoxicosis
HYPERTHYROID TREATMENT
i) give three broad options for treatment
ii) give two complications that may arise if not treated?
i) medical, radioactive iodine, surgery
ii) complications - dysrhythmias, osteoporosis
TOXIC MULTINODULAR GOITRE
i) will the patient be hypo or hyper thryoid?
ii) what treatment would be reccomended?
iii) what type of scan would be useful to diagnose?
i) hyperthyroid - nodules produce thyroid hormone
ii) radioiodine treatment
iii) thyroid uptake (isotope) scan
POST PARTUM THYROIDITIS
i) what is it? hat three phases are seen?
ii) is it usually self limiting?
iii) does it respond to anti thyroid drug therapy?
iv) is it suitable for radio iodine therapy
i) transient thyrotoxic phase then hypothyroid phase, then euthyroid
ii) usually self limiting
iii) does not respond to anti thyroid drug therapy
iv) not suitable for RI therapy
HYPOTHYROID - HISTORY AND EXAMINATION
i) what weight change may be seen?
ii) what may they be intolerant to?
iii) give three other symptoms
iv) what heart rate may be seen if prolonged/severe?
v) how may reflexes be affected?
i) weight gain
ii) cold intolerance
iii) tiredness, constipation, menorrhagia
iv) bradycardia
v) slow relaxing reflexes - upstroke of reflex normal but long to relax
HYPOTHYROID - INVESTIGATIONS AND TX
i) what antibody may be investigated for?
ii) what is the treatment? in which two groups of patients would you start on a lower dose?
iii) how long should be waited before repeating thyroid function tests if the patients symptoms are not improving?
i) look for thyroid auto antibody (TPO)
ii) treat with thyroxine (T4) - start on 100ug
- if very elderly/ischaemic heart disease - use lower dose (25ug)
iii) wait 6 months before repeating TFTs, even if the patient doesnt feel better (there can be a lag phase before patients feel better)
HYPERCALCAEMIA
i) what symptoms are usually seen in mild/mod disease? how is it usually detected?
ii) what symptoms may be seen in severe disease? (stones, bones, abdo gorans, psychic moans)
iii) how may the PT gland be acting in hypercalc?
i) mild/mod = usually no symptoms
- detected on routine blood testing
ii) severe - stones (kidney stones), bones (bone pain), abdo groans (GI symptoms), psychic moans (lethargy, depression, confusion)
iii) primary hyper parathyroidism (autonomous function of PT gland)
HYPERCALCAEMIA - FURTHER INVESTIGATIONS
i) what may you screen for with US? what condition can be screened for with a DEXA scan?
ii) what group of people is surgery reserved for?
iii) what is 1st, 2nd and 3rd line methods for pre op localisation of a parathyroid adenoma?
iv) would a mild/mod case with no symptoms or end organ damage be treated?
v) what calcium levels would indicate treatment is needed?
i) screen for end organ damage eg renal stones and osteoporosis
ii) surgery for young people (under 50)
iii) pre op loc - 1st line neck US, 2nd line isotope (sestamibi) scan, 3rd line 4D neck CT
iv) no treatment if mild/mod with no symptoms
v) calcium concentration >2.85
HYPERCALCAEMIA TREATMENT
i) what is the only curative option?
ii) what two things should be monitored in surveillance?
iii) what can be used to monitor bone mineral density?
iv) what should be recommended for - fluid intake? calcium intake? vitamin D intake?
i) surgery is only curative option
ii) monitor calcium and renal function every 12 months and do a DEXA scan 2 yrly
iii) use DEXA to monitor bone mineral density
iv) good fluid intake to reduce risk of kidney stones, normal dietary calcium intake (dont restrict), vit D supplements to protect the bones
HYPERCALCAEMIA AND MALIGNANCY
i) what type of patients is this usually seen in?
ii) what type of malignancy is it seen in?
iii) what is it usually due to?
iv) what PTH levels will be seen?
i) usually seen in very unwell patients
ii) metastatic malignancy
iii) usually due to PTHrP (PTH related protein - paraneoplastic peptide)
iv) see supressed levels of PTH
OTHER CAUSES OF HYPERCALC
i) give three others causes of hypercalcaemia
ii) what levels of PTH may be seen? (2)
i) granuloamtous disease/lymphoma/multiple myeloma/familial hypocalcuria (mut in calcium sensing receptor)
ii) PTH may be low or inappropriately normal
OSTEOMALACIA
i) what calcium levels will be seen?
ii) what is lacking in OM? how can this be tested?
iii) what could be a DD?
iv) how is it treated?
i) low calcium levels
ii) lack of vitamin D (from skin/dietary) - can they get up from a chair without using arms? eg is there proximal myopathy
iii) DD - malabsorptive eg coeliac
iv) treat with calcium and vitamin D replacement
HYPONATREMIA
i) what medication should be checked for in patients presenting with hyponat?
ii) what is the main thing you look for on examination? what would be seen in each case?
iii) name four further tests you would order
i) look to see if patient is on diuretics
ii) O/E - is the patient hypo/eu/hypervolaemic
- hypovol = tachycardia, orthostatic HTN
- hypervol - oedema, ascites, raised JVP
iii) further tests - plasma osmolality, urine osmolality, urine Na+, TFTs, 9am cortisol
T1DM
i) what is it? what is the genetic concordance in twins? when does it usually present?
ii) name three presenting features? what blood glucose is seen? how may it present acutely? how is it dx? does C peptide and auto ABs confirm dx? when should the patient not be screened?
iii) what may be seen on bloods? name three other RF? what should be done if the patient is symptomatic (weight loss)? (3) name three auto antibodies that may be positive?
iv) what treatment should be offered first? what is first line insulin treatment? what is second line? how often should glycaemic control be checked?
i) autoimmune/idiopathic destruction of panc beta islet cells, low genetic concordance in twins
- Usually presents in childhood/puberty
ii) polydipsia, polyuria, weight loss, ketosis,
* Raised venous glucose (>7mmol/L fasting or >11.1mmol/litre random),
* May present acutely with DKA
- Dx on clinical grounds - what is the pt presenting with?
* C peptide & diabetes auto Abs (doesn’t confirm dx)
iii) Hyperglycaemia, ketosis, rapid WL, age <50yrs, BMI <25, family history of AI disease
* May be positive for auto Abs (ICA, IAA, GAD, IA-2A)
* Microalbuminuria, decreased renal function
* Random venous >11mmol/l
* Fasting plasma glucose >7mmol/L
* 2 hour post OGTT >11.1mmol
* HbA1c >48mmol/mol
* dont screen during asymptomatic phase
IF PT IS SYMPTOMATIC (weight loss)
* Random plasma glucose, Fasting plasma glucose, 2 hour plas glucose (2hrs post OGTT) and HbA1c
iv) 1) Offer lifestyle advice - diet/exercise
2) Treat with insulin - basal bolus (first line) or mixed regimen (second)
3) Review glycaemic control annually (HbA1c <48mmol is ideal)
4) Follow up for eye/foot/nerve complications
COMPLICATIONS OF DIABETES MELLITUS
i) name three acute complications? which type does gastropariesis present with? how is it treated? (2)
ii) which CV conditions are pts more predisposed to? (3) what other dysfunction may they get?
iii) what three things can it predispose to in the kidney? what levels should be monitored annually? (2) what medication should be offered to any pts with nephropathy?
iv) what type of eye disease is seen? name two components of this? what three types of retinopathy can occur? what is maculopathy? name another eye pathology it can pre dispose to
v) what can neuropathy lead to? how does it result in toxic metabolite build up? what distribution does peripheral neuropathy have? name two other manifestations
i) Acute > DKA, HHS/HONK, Hypoglycaemia
- Gastroparesis > T2DM with erratic gluc control/unexplained gastric bloating or vomiting
- Tx with metoclopramide or domperidone
ii) CV > More predisposed to ACS, angina, periph artery disease, 4x likely MI, 2x likely to have stroke
- also get Erectile dysfunction
iii) Nephropathy > Can predis to pap necrosis, renal fail & UTI
- Monitor annually for microalbuminuria (small inc inc in albumin excretion by kidneys, indep risk factor for complicats) - use early am albumin:creatinine ratio (ACR)
- monitor annually for proteinuria (ACR >30mcg)
- Optimise risk factors and offer ACEi therapy to any pts with nephropathy, prot/microalbuminuria, T1DM
iv) Eye disease - microvascular retinal disease > retinal ischaemia & new vessel formation (VEGF)
- Can cause retinopathy - non prolif (mild, microaneursym), moderate (microan, blot haemm, venous bleed), severe (widespread haemm, severe intraretinal abnorm)
- Maculopathy - decrease in vis acuity, macular oedema, retinal thickening, hard exudates
- Cataracts/rubeous iridis (neovasc over iris = red)/glaucoma
v) Neuropathy > major cause of foot ulcers
- Microvasc damage & ischaemmia to vasa vasorum > tox metab bup
- periph sensorimotor neuropathy (glove stocking)
- painful neuritis, amyotrophy (prox lower limb musc weak and wasting), autonomic, mononeuropathy
T2DM
i) what is it? what is the twin concordance? what is the precursor?
ii) which group of patients does it commonly present in? (4) is it usually symptomatic? name three symptoms? what is random and fasting glucose levels? HbA1c?
iii) what is first line tx? what is second line? what is given in HbA1c is 58? what if it is >58?
i) Decreased insulin secretion with or without Insulin resistance, high concordance in twin studies
- Progresses from impaired glucose tolerance/impaired fasting glucose tolerance
ii) Usually presents in older patients, obese, poor diet, sedentary lifestyle
- Usually asymptomatic but can present with complications eg MI
- can px with Polydipsia, polyuria, High BP and lipid levels
- random >11mol/l, fasting >7mmol/l, HbA1c >48mmol
iii) Individualised care plan
1) Lifestyle mod (diet, weight control, exercise, BP control)
2) Monotherapy (metformin - GI SEs)
3) HbA1c = 58 = dual therapy (Met + DDP4/pioglitazone/SU/SGLT-2i)
* HbA1c >58mmol = triple therapy or insulin
HYPOGLYCAEMIA
i) what is it defined as? what is the most common cause? name the causes in non diabetics? (EXPLAIN)
ii) name four autonomic symptoms that may be seen? name three neuroglycopaenic symptoms? what are the three criteria for dx? (whipples triad)
iii) what should be thought about if insulin levels are high? (2) what cause could be responsible if low insulin/no excess ketones? (2) low insulin and high ketones? (2)
iv) what can be given if episodes are often? what needs to be reviewed? name two ways glucose can be given if concious? how is it given if unconcious? (2)
i) Plasma glucose <3mmol/L
Emergency
* Fasting hypo - most common cause is insulin/sulphonyurea tx
* Non diabetics - EXPLAIN
Exogenous drugs, Pit insuffic, Liver fail, Addisons, Islet cell tumours, Non panc neoplasms
ii) Autonomic - sweating, anxiety, hunger, tremor, palp, dizzy
Neuroglycopenic - confusion, drowsy, visual change, seizure, coma
Three criteria for dx (whipples triad) -
1) hypoglycaemia
2) Symptoms indicative of hypo
3) Resolution of symptoms post treatment
iii) If hyperinsulinaemia - think insulinoma, SUs, insulin injection (no inc in C peptide, only secreted with endog ins)
* If low insulin/no excess ketones - non panc neoplasm or anti insulin receptor antibodies
* low insulin & high ketones - alcohol, pit insuff, addisons
iv) If episodes are often - small high starch meals
* rationalise insulin therapy in DM
* oral/liquid glucose or buccal glucogel if concious
* if unconcious - 125ml 20% dextorse or 250ml of 10% dextrose or 1mg glucacgon by IM injection
DKA
i) what is it? what is it provoked by? (3) what is ketoacidosis? what does DKA occur in relation to excess glucose?
ii) what are the three main signs? name four other symptoms a patient may present with?
iii) what four bloods should be done? name two bedside tests? what imaging?
iv) what two things need to be replaced? what should be given if systolic BP <90? what should be added into fluids? when should K+ replacement start? what type of insulin is given? how often should cap glucose and ketones be checked?
v) name four complications? what type of insulin can patient be put on once eating and drinking?
i) Medical emergency 2nd to abso insulin defic/resistance
* Provoked by poor tx adherence, infection, trauma, illness
* Ketoacidosis = alt metab pway used in starvation states > prod acetone
* DKA = excess glucose but no ins so cant be taken into cells > body in starvation state
ii) 1) Acidaemia (blood pH <7.3/HCO3 <15)
2) Hyperglycaemia (blood gluc >11)
3) Ketoneaemia (>3mmol)/ketoneuria ++
* gradual drowsy, vomiting, dehy (T1), vom, abdo pain, polydip/uria, ketotic breath, coma
iii) Urine: ketones and glucose, MCS, Cap glucose and ketones, VBG: acidosis + ↑K, Bloods: U+E, FBC, glucose, cultures, CXR: evidence of infection
iv) Replace volume and correct metabolic defects
* Give K+ replacement (K+ shuttled for H+)
* Large bore cannula - fluid (1L 0.9% saline if systolic BP <90) more until SBP >90
- Then: 1L over next 2h, 1L/2h, 1L/4h, 1L/4h, 1L/6h
- Add 10% dextrose 1L/8h when glucose <14mM
- Start Potassium Replacement in 2nd Bag of Fluids
* Add fixed rate insulin infusion (actrapid)
* Check cap glucose & ketones hourly
v) Cerebral oedema
* aspiration pneumonia
* hypokalemia
* hypomagnesia
* hypophosphatemia
* thromboemolism
- patient can be transferred to sub cut insulin once eating and drinking
HYPEROSMOLAR HYPERGLYCAEMIC STATE
i) how is it characterised? (3) what type of DM does it typically occur with? name three things that ppt it? what is pH/ketones/insulin levels? why are they profoundly dehydrated? which group of patients does it commonly present in?
ii) name two key symptoms? what will the patients volume status be? name four other symptoms?
iii) what will blood glucose be? what will be seen in the urine? (2) what will serum osmolality be?
iv) what is the main aim of treatment? how is this done? what is given to prevent clots? how is insulin given? when should K+ replacement be given?
v) what levels of glucose/plasma osmolal are seen once resolved? what else is improved? what insulin is given to pt before weaning off IV insulin?
i) characterised by profound hyperglycaemia (glucose >30 mmol/L hyperosmolality , and volume depletion in the absence of significant ketoacidosis (pH >7.3 and bicarbonate >15 mmol/L)
- Typically occurs as complication of T2DM - ppt by disease state/illness
* can be first presentation of DM
* pH remains above 7,3 and ketones are absent low (no acidosis/ketosis)
* there is some insulin but not enough
* hypergly > wee out glucose > pull water with it = profound dehy
* Patients are often elderly
ii) Dehydration & profound hyperglycaemia (>33)
* Hyperosmolality (due to hypergly)
* Hypovolaemia in absence of ketoacidosis
- also get Muscle cramps and confusion, profound weakness, weight loss, polydip/uria
iii) Very high blood glucose
* Urine - glucose with low/absent ketones
* serum osmolality = high (usually very tight control)
iv) Main aim of tx is to correct profound dehydration (IV 0.9% NaCl/dextrose when gluc less 15)
* Give LMW heparin ro prev clots
* IV Actrapid insulin - fixed rate
* K+ replacement if <5.5
v) Resolved : Gluc <16.7, plasma osmolal <315, improved mental status
* Give subcut insulin before eweaning patient off IV insulin
SIADH
i) what is it? name four causes? what two things does it result in? why is there no oedema?
ii) what sodium status is seen? what is the osmolality of urine? what is plasma osmolarity?
iii) what will serum sodium levels be? name two other causes for this?
iv) what ultimately needs to be treated? what should be done in relation to fluid intake? what drug should be considered if there is no improvement? what other drug may be given?
i) Pathological processes causing inapprop ADH secretion
* Due to malignancy (ectopic ADH prod from neoplastic cells), SCLC, meningitis, surgery
* results in h2o retention + hyponatremia (no oedema due to urinary excretion of Na+)
ii) Hyponatremia (dilutional due to excess water retention) - mild is usually asymp and severe is confusion/drowsy
*Hyperosmolar urine
* Plasma hypo-osmolarity / urine hyper osmolarity
iii) Serum sodium levels will be low - (<135, often incidental finding)
* Other hyponat causes - thyroid/adrenal insuff
* urine osmolality (elevated), urinary Na (>40)
iv) Treat any underlying causes
* Fluid restrict - will help correct hyponat by inc serum sodium
* If no improvement - consider demeclocycline (abx but reduces efficacy of ADH at CD as a SE)
* Consider V2 receptor antagonists in CD (prev ADH working eg conivaptan)
CUSHING SYNDROME
i) what is overproduced? name three conditions associated with a higher incidence? what is a common cause? what are 80% caused by? what type of cancer may it be associated with?
ii) name five characteristic signs? how may the skin be affected? (3) how may psych be affected? (2) what BP may be seen? what is there increased risk of? how may periods be affected?
iii) which test is done? when is cortisol tested? what other cortisol test can be done? what do low or high ACTH levels indicate?
iv) what is done if the cause is a pituitary adenoma? what is done if adrenal adencoma? what if given if surgery cant be done?
i) Pathological over production of cortisol
* higher incidence if diabetes, HTN, osteoporosis
* Steroid therapy is a common cause
* 80% caused by pit adenoma secreting excess ACTH
* 10% caused by a cortisol secreting adrenal adenoma
* ACTH secreting tumours can be assoic, assoc with SCLC
ii) Suprascapular fat pads, abdo striae, depression, truncal obesity, easy bruising
* Moon face, buffalo hump
* Skin - thin, fragile, acne, hirsutism
* Psych - depress, anx, irritable, decreased lib
* Vasc - new or worse high BP
* increased risk of fractures
* Reprod - irreg/absent periods, erectile dysf
iii) 1g overnight Dex supress test - test cortisol at 8am and if not supressed then CS
* 24hr free urine coirtsol - three collections but can be difficult
* Low ACTH levels = adrenal pathology
* High ACTH levels = do high dose (8g) dex test if >50% supress with high dex = CS pit source, if <50% supress = ACTh secreting tumour
iv) If pit adenoma (80%) - trans-sphenoidal sx resection + GC support
* if ectopic tumour (adrenal adenoma) - adrenalectomy w GC support
* If cant do sx - use steroidgenesis inhibitor (mifepristone) less effective than sx
ADDISONS DISEASE
i) what is it? what is it usually caused by? what is most common cause worldwide? how may it present acutely? explain
ii) name three symptoms? what is it often associated with? (3) what electrolyte levels are seen - sodium, glucose, calcium, potassium? how is skin pigmentation affected?
iii) what may be seen on U&Es? (3) what hormone test should be done early in the morning? what is a short synacten test? what will it show in AD? what plasma ACTH levels are seen?
iv) name two things that need to be replaced? how is this done? what needs to be given in minor illness/surgery to avoid crises?
i) Primary adrenal insufficiency (usually due to AI destruction of the gland)
* TB is most common cause worldwide
* Can present acutely w addisonian crisis - ppt event eg illness > inc demand for MC/GC = shock and hypogly
ii) Fatigue, weight loss, depression
* Assoc with other AI conditions eg vitiligo, pernicious anaemia, hashimotos
* Electrolyte imbalance - hypnonat, hypogly, hypocalc but hyperkal (in primary insuff)
*Hyperpigmentation - espec in buccal mucosa & palmar creases
iii) U&E - hyponat/calc/gly but hyperkal
* Early am serum cortisol - <100-500ml = further investigation (if >500 probs not adrenal insuff)
* Short synacthen test (analog of ACTH) - ig adrenal insuff then cortisol levels don’t rise
* Plasma ACTH - ACTH levels are high but cortisol is low
iv) Replace GC/MCs - give hydrocortisone/fludrocortisone
* Hydrocortisone doses inc 2-3x IM/IV in minor illness/surgery to avoid crises
