diabetes and endocrinology phase 3 revision day - bma your career... · diabetes and endocrinology...
TRANSCRIPT
Aims
‐ Provide a quick reference guide for important endocrine topics (hence why the slides are so dense!)
‐ Highlight high yield facts that can help you out in MCQs
‐ Flag up potential MCQ pitfalls
‐ Practice some MCQs
Plan
‐ Diabetes ‐ Diagnosis‐ Treatment‐ Primary and secondary prevention ‐ DKA‐ Hypos
‐ Endocrine‐ Thyroid disease‐ Addisons
A 55 year old man presents to your for a check‐up, his BMI is 29 and his Blood pressure is 163/80. His examination is otherwise normal. You check a U and E, Random venous glucose and Lipid profile. His bloods return normal except his random glucose is elevated at 11.9 mmol/l. You telephone him to discuss his results ‐ he tells you he has been feeling increasingly tired recently but denies polyuria, polydipsia or any visual disturbance.
Which of the following is true?A. This patients is symptomatic with a blood sugar in the diabetic range ‐
he has type 2 diabetesB. An HbA1c would not be useful in helping to diagnose this man with
diabetesC. This gentleman has impaired fasting glucoseD. This gentleman should be started on MetforminE. A second venous glucose reading (ideally fasting) is needed to confirm
diabetes
Diagnosing diabetes
‐ Fasting BG ‐ >7.0 (IFG – 6.1‐7 mmol/l)‐ Random BG ‐ >11.1‐ HbA1c > 48 mmol/ml (6.5%)‐ If asymptomatic need a repeat reading
‐ OGTT ‐ >11.1 (IGT – 7.8 ‐11.1)
Diagnosing diabetes
‐ An 8 year old girl with weight loss, polyuria and ketonuria‐> 1 random plasma venous glucose sufficient
‐ A southeast asian man with a BMI of 35 ‐> Two Hba1c readings or two fasting plasma glucose readings
‐ Hba1c should not be used in CKD, EPO use, high or low Hb, haemaglobinopathies, HAART, Chronic alcoholism, High lipids, Pregnancy
‐ A normal HbA1c cannot rule out DM
Diagnosing diabetes – who to test?
‐ Clinical suspicion of diabetes
‐ Demographic factors that make T2D more likley‐ As part of CVD risk assessment ‐ High BMI/Large waist‐ Non white European descent‐ Family history of Type 2 diabetes‐ Age 50 and up‐ Male
Managing diabetes
‐ Education ‐ DAFNE (T1D) ‐ DESMOND (T2D)
‐ Lifestyle changes
‐ Anti‐hyperglycemic agents
‐ Primary and secondary prevention
‐ Multi‐disciplinary care
Managing diabetes ‐ Glycemic control
‐ T1 diabetes‐ HbA1c ‐ <6.5%
‐ Offer basal bolus regimen
‐ T2 diabetes‐ HbA1c ‐ <6.5% in most individuals
‐ <7% if on drugs associated with Hypos (SUs and combined therapy)
‐ Consider higher targets based on age, co‐morbidities, consequences of hypos
Complications of diabetes
Multi‐factoral Glycemic controlStatins, anti‐platelets Early detectionGlycemic control, BP and interventionSmoking, Exercise BP
A 33 year old gentleman with Type 1 Diabetes attends his annual Diabetes review. His HbA1c is 7%/53 mmol/L He has a early morning urine sample sent for ACR ‐ it comes back indicating microalbuminuria (3.7 micrograms/milligrams). What is the most appropriate management?
A. Ask him to return tomorrow to repeat the testB. Start an ACE inhibitorC. Optimize glycemic controlD. Prescribe Trimethoprim 200 mg BD for one weekE. Ask him to return in 1 month to repeat the test
Complications of diabetesRetinopathy ‐ annual fundus photography for all >12yo
‐ Pan‐retinal photocoagulation ‐ Anti‐VEGF for Diabetic maculopathy
Nephropathy ‐ Annual early morning ACR test ‐ Early nephropathy eGFR is normal(>60)‐ ACR ‐ an index of glomerular damage‐ Need another ACR >1 week later‐ Control BP with ACEi or ARB
Complications of diabetesFeet ‐ 10g monofilament screening annually or
vibration sense‐ Assess for deformity, ulcers, pulses, ischemic changes, check ABPI
‐ Foot care education ‐ If at high risk more regular review and
intensify educationMacrovascular DM BP Target Lipid lowering
therapyBP exceptions
Type 1 135/85* CVD rfs, >40yo, Nephropathy,FH, DM>10yrs
*Albuminuria, metabolic syndrome (130/80)
Type 2 140/80* As per rest of population
*Eye, renal or Cerebrovasc(130/80)
Diabetic Ketoacidosis
Definition ‐ Glucose >11.1 mmol/l or known diabetes‐ Ketones ++ on dipstick or >3 mmol/l‐ pH<7.3 ‐ venous gas sufficient or HCO3‐<15mmol/l
Causes ‐ T1D ‐ omission of long acting insulin‐ Illness ‐ Can be common presenting feature‐ Stress ‐ trauma, surgery, MI, pregnancy
Clinical features ‐ Hx suggestive of above, dehydrated, nausea, abdo pain and vomiting, ketones
on breath, Kussmaull’s, decreased GCS, headache, often raised K+ and low Na+
Diabetic Ketoacidosis‐Management
Read local guidance!ABCDE ‐ treat shock if present.Investigations Fluids ‐ 0.9% saline ‐ 1L first hour, 2L next four hours,
2L next eight hours, 1L next 6 hours
Insulin ‐ 0.1U/Kg/Hr ‐ Fixed Rate Insulin Infusion ‐ continue long acting insulin during Rx‐ add glucose once <14mmol/l‐ continue insulin until pH normal and
ketones <0.6mmol/l
Potassium ‐ Add 40 mmol KCL/Litre of Saline after first litre givenprovide K+ is normal
‐ If K+ >5.5 omit KCL from fluids‐ If K+<3.5 stop insulin and get senior help
Diabetic Ketoacidosis‐Management
Read local guidance!ABCDE ‐ treat shock if present.Investigations Fluids ‐ 0.9% saline ‐ 1L first hour, 2L next four hours,
2L next eight hours, 1L next 6 hours
Insulin ‐ 0.1U/Kg/Hr ‐ Fixed Rate Insulin Infusion ‐ continue long acting insulin during Rx‐ add glucose once <14mmol/l‐ continue insulin until pH normal and
ketones <0.6mmol/l
Potassium ‐ Add 40 mmol KCL/Litre of Saline after first litre givenprovide K+ is normal
‐ If K+ >5.5 omit KCL from fluids‐ If K+<3.5 stop insulin and get senior help
Diabetic Ketoacidosis‐Management
Regular assessment ‐ Assess clinical condition‐Monitor U and E, BM, Venous gas, ketones
1‐2 hourly
Search for and treat cause ‐ ?infection, insulin omission, trauma, surgery, pregnancy, MI
Education ‐ Ensure understanding of sick day rules, that long acting insulin should never be stopped and
when to seek help
Risks of DKA management ‐ Cerebral Oedema‐ Hypokalemia‐ Hypoglycemia
Hypoglycemia
Definition ‐ <4 mmol/L ‐ practical definition for diabetes‐ >3.5 mmol/L is technically normoglycemic‐ For people with diabetes make 4 the floor
Causes ‐ Insulin ‐miscalculation, double dose, lumpy sites‐ Sulfonylureas‐ Exercise ‐ Alcohol ‐Missed meal/Fasting
Symptoms ‐ Autonomic ‐ Hunger, Sweating, Tachycardia..‐ Neuroglycopenic ‐ Drowsy, LOC, Seizure….
You are an F1 doctor working a night shift in general medicine. A nurse contacts you about a patient with type 2 diabetes treated with metformin and Gliclazide whose BM is 3.0 mmol/L. The nurse feels he would be able to eat or drink if asked. What is the most appropriate management option?
A. Get IV Access and give 150‐200 ml 10% glucose StatB. Inject 1mg Glucagon IMC. Give fruit juice and chocolate and recheck BM in 15 minutesD. Give a high glucose drink and recheck BM in 5 minutesE. Give a high glucose drink and recheck BM in 15 minutes
Hypoglycemia ‐Management
Depends on level of consciousness
If co‐operative and able to swallow 15‐20g of quick acting carbohydrate (glucose best)
‐ 90‐120 ml lucozade‐ sweets, glucotabs etc
If uncooperative but able to swallow‐ squeeze glucogel/hypostop into mouth, rub into gums
If unconscious ‐ If IV access 150‐200 ml of 10% Dextrose‐ If no IV access 1mg Glucagon IM ** If fasting glucagon may not work
Re‐check BM 10‐15 minutes later, if low repeat action
Hypoglycemia ‐ Follow‐up
Eat next meal or a snack with slow‐release carbs to keep blood sugars up
Take history ‐ Establish cause ‐ Enquire about warning signs ‐Was the person able to treat hypo themselves ‐ if not, this is defined as a severe hypo
Educate on how to treat, carrying monitor and carbohydrate and wearing ID bracelet
Driving ‐ Severe hypo ‐ no driving for 12 months
Thyroid Physiology
TSH
Thyroid
T3,T4
Pituitary AdenomaOther SOLPituitary surgeryShockBleedingGranulomatous
Hashimoto’sAtrophic auto‐immuneIatrogenicPost‐partum thyroiditisSubacute ThyroiditisIodine deficiencyDeQuervain’s
Inhibitoryfeedback
Rare
Grave’s diseaseToxic multinodularGoitreFunctioning adenomaSub‐acute thyroiditisPost‐partum thyroiditisDeQuervain’siodine intakeIatrogenic
Other ‐ Struma ovarii, choriocarcinoma
You are asked to see a young female who has been complaining of heat intolerance, palpitations and insomnia. Her TFTs are: FT4 75 pmol/L (7.6‐19.7) TSH is undetectable (0.5‐5 mu/l). What is the diagnosis?
A. Tertiary hyperthyroidismB. Secondary hypothyroidismC. Primary hyperthyroidismD. Secondary hypothyroidismE. Grave’s disease
Thyroid function tests ‐ quick guide
High T4, SUPPRESSED TSH ‐ Primary hyperthyroidism
High T4, High TSH ‐ Secondary Hyperthyroidism ‐ Rare
Raised TSH, Low T4 ‐ Primary hypothyroidism
Low (‐normal) TSH, Low T4 ‐ Secondary hypothyroidism
High TSH, normal T4 ‐ subclinical hypothyroidism
Sick Euthyroid ‐ deranged TFTs in acute illness, but clinically euthyroid
Hyperthyroidism ‐ Distinguishing features
Grave’s Disease ‐most common‐ Auto‐immune mediated primary hyperthyroidism ‐ Stimulatory Anti‐TSH antibodies drive thyroid hormone production (Anti‐
TPO also present)‐ Diffuse goitre‐ Associated dermopathy ‐ Finger clubbing and hyperkeratosis)‐ Grave’s Ophthalmopathy ‐ (Present with dry sore eyes, bulging eyes,
diplopia due to tethering)‐Smoking and Radio‐iodine exacerbate ‐ Use Glucocorticoids if severe or if starting RAI
Toxic Multinodular Goitre‐ Multinodular goitre‐ Usually starts euthyroid and then acquires autonomy
Toxic Adenoma‐ Single nodule‐ Dx on Radio‐iodine scan as ‘Hot nodule’
Hyperthyroidism ‐ManagementBeta‐Blocker ‐ control symptoms, lipophillic BB like propanolol
Carbimazole‐ Pro‐drug converted to methimazole‐ Inhibits thyroid peroxidase‐ 18 months therapy and trial of withdrawal (50% relapse)‐ Block versus block and replace ‐ SE: Rash, hepatotoxicity, agranulocytosis ‐ warn of fever, sore throat if concerned go to hospital to get check FBC
‐ Use propylthiouracil in first trimester of pregnancyRadio‐iodine
‐ Unsuitable in pregnancy, small children, Grave’s ophthalmopathy‐ Often hypothyroid
Surgery‐ If radio‐iodine unsuitable and symptom control difficult or Large goitre +/‐Obstructive symptoms
Thyroid Physiology
TSH
Thyroid
T3,T4
Pituitary AdenomaOther SOLPituitary surgeryShockBleedingGranulomatous
Hashimoto’sAtrophic auto‐immuneIatrogenicPost‐partum thyroiditisSubacute ThyroiditisIodine deficiencyDeQuervain’s
Inhibitoryfeedback
Rare
Grave’s diseaseToxic multinodularGoitreFunctioning adenomaSub‐acute thyroiditisPost‐partum thyroiditisDeQuervain’siodine intakeIatrogenic
Other ‐ Struma ovarii, choriocarcinoma
Primary Hypothyroidism ‐ Distinguishing features
Hashimoto’s‐ Goitorous auto‐immune thyroiditis‐ Anti‐TPO antibodies‐ Also Blocking TSH antibodies (cf grave’s ‐ stimulatory)‐ Associated with a variety of other auto‐immune conditions‐ Also atrophic autoimmune thyroiditis
Iatrogenic‐ Radio‐iodine‐ Surgery‐ Drugs eg too much Anti‐thyroid
Thyroiditis ‐ all are transient‐Sub‐acute painless‐DeQuervain’s ‐ painful
Primary Hypothyroidism ‐Management
Repeat T3/T4 in 2‐12 weeks to exclude transient forms
Thyroid hormone replacement with levothyroxine‐ Replace so TSH is suppressed to mid‐low normal range and asymptomatic‐ In auto‐immune forms Rx lifelong ‐ Excessive thyroid hormone ‐ risk of osteoporosis and AF‐ Start low and titrate up ‐ particularly important in elderly ‐ Once stable follow‐up not necessary until pregnancy
Be vigilant for the development of other auto‐immune diseases
NB ‐ subclinical hypothyroidism ‐ Treat if high TSH (>10)
Secondary Hypothyroidism ‐Management
Secondary hypothyroidism presents with Low TSH and low T4 ‐ Pituitary controls levels of lots of hormones in body‐ Thus assessment of pituitary function BEFORE t4 replacement is essential‐ Ask about symptoms of pituitary adenoma‐ Short synacthen test, FSH, LH, prolactin ‐MRI brain
If adrenal insufficiency is present this must be treated before replacing thyroid hormone or else you may precipitate adrenal insufficiency which may be fatal if unrecognised
Surgical/radiotherapy for pituitary adenoma
Adrenal Physiology
ACTH
AdrenalCortex
CortisolAng II Aldosterone
Androgens
Pituitary AdenomaOther SOLPituitary surgeryGlucocorticoid withdrawalShockBleedingGranulomatous
Auto‐immune destructionNeoplastic destructionGranulomatous diseaseSurgeryDrugs HaemorrhageEnzymatic defects
Inhibitoryfeedback
Functioning adenomaPituitary hyperplasia
GlucocorticoidsFunctioning adenomasAdrenal hyperplasiaAdrenal carcinoma
Other ‐ Paraneoplastic ‐ usually lung cancerPseudo‐cushings ‐ alcoholism, depression, obesity
Isolated high aldosteroneCause of Endocrine HTNConn’s ‐ adenomahyperplasia
Tests for assessing adrenal function
Short synacthen ‐ IV or IM synthetic ACTH ‐measure cortisol produced ‐deficiency
AM cortisol ‐ deficiency
Midnight cortisol ‐ excess
24 hour urinary cortisol ‐ excess
Overnight dexamethasone supression test ‐ excess
Low dose dexamethasone suppression test ‐ excess
High dose dexamethasone suppression test ‐ if pituitary or ectopic cushings
You are asked to see a 19 yo female who was brought to A and E by her sister because she was drowsy, disorientated and speaking incoherently. They mention she has lost lots of weight in the past few months and had fainted once today. O/E her BP is 80/40, she is tachycardic and has a weak thready pulse. Her blood glucose is 2.1 mmol/L and her U and E and bone profile shows the following: Na+ 125 (135‐145), K+ 5.7 (3.5‐5), Urea 8 (2.5‐9) Creatinine 90 (40‐110). Her sister states she has hypothyroidism
What is the most likley diagnosis
A. Type 1 diabetesB. Dehydration C. Myxedema comaD. Diuretic abuseE. Hypoadrenalism
Hypoadrenalism
Presenting features‐ Lethargy‐ Low mood‐ Postural hypotension‐ poor appetite‐Weight loss‐ Increased pigmentation**‐ Other autoimmune disease ‐ female, vitiligo, hashimoto’s, T1D‐ Addisonian crisis!
Ix ‐ U and E, Bone profile, Short synacthen, Adrenal autoantibodies, imaging
**POMC ‐ ACTH precursor ‐ ‐ > ACTH is made by cutting up POMC‐ also makes Melanocyte stimulating hormone which increases
a melanin production and pigmentation‐ in primary hypoadrenalism ACTH rises and therefore high POMC
and MSH‐ so pigmentation indicates primary disease (ie adrenal problem) rather than
secondary
Addisonian Crisis ‐ recognition‐ Acute exacerbation of clinical condition caused by a relative or absolute deficiency of cortisol
‐May be presenting feature, may be precipitated by illness, trauma, surgery, burns, pregnancy, MI, poor compliance
‐ Classic presentation is syncope, hypoglycemia, n + v with characteristic U and E ‐ Hyponatraemia‐ Hyperkalemia (mild) ‐ loss of aldosterone‐Mild metabolic acidosis (normal anion gap) ‐ loss of aldosterone‐ Raised Urea ‐ dehydration‐ Hypercalcaemia
Addisonian crisis ‐managementABCDE ‐ Fluid bolus, treat hypoglycemiaInvestigations ‐ random cortisol, definitive tests should not delay Rx
Five S’s‐ Support ‐ ABCDE‐ Sugar‐ Saline‐ Steroids ‐ hydrocortisone** at stress doses (100mg 6 hourly)‐ Search for cause
Patient Education to prevent recurrence
**Dexamethasone may be used as an alternative as it will not affect cortisol levels in short synacthen test (4mg IV)
Look over!Endocrine hypertension ‐ renal causes are way more common cause of secondary hypertension, know that headache, sweating and palpitations in an MCQ = phaeochromacytoma, be wary of a person with hypertension with hyponatremia and hypokalemia +/‐metabolic alkalosis (hyperaldosteronism/conn’s syndrome)***
Know sick day rules for addisons and diabetes (OSCE mainly)
Understand that in hypercalcemia PTH should be suppressed not normal!
Diabetes drugs ‐ Pioglitazone and SGLT2 inhibitors are very topical!
***This could also be Cushing’s but these features will accompany classical cushingoid symptoms/signs
