Endocrine Flashcards

Question

Pheochromocytoma: definition, features?

Answer 1

(phios – dusky, chromo – colour, cytoma – growth of cells) • Definition: Adrenaline producing tumour ``` • Features: o EPISODIC Headache (80%) o Palpitations (70%) o Profuse sweating (60%) o Tremor o HTN (sustained in 60%, paroxysmal in 40%) ``` Might be associated with: MEN type II, neurofibromatosis and von Hippel-Lindau syndrome (10%)

Answer 2

o First: Urinary metanephrines (97% sens, more specific) o Positive Urine: MRI adrenals • Treat: A-blocker: PHaeochromocytoma - give PHenoxybenzamine before beta-blockers otherwise hypertensive crisis lABetalol- blocks both alpha & beta receptors if not above regimen. Surgery: 10 days after Medical Rx

Answer 3

• Type 1 o Background:  No insulin production  Insulin autoantibodies can be detected as early as 6-12mo of age  Initiates with precipitating event (e.g. infection)

Answer 4

o Diagnosis: Use the American Diabetes Association (ADA) criteria  DIAGNOSE: Random BG ≥11.1 OR fasting BG ≥7 OR HbA1C >6.5% (48) • If BG 6-6.9 (impaired fasting glucose): 75g OGTT (test 2hr after) o Diabetes: BG ≥11.1 o Impaired Glucose Tolerance (IGT): BG 7.8-11 Anti-Islet cell + Anti-GAD (75% each)

Answer 5

``` • Treat: o First: Insulin S/C  Types: • Short-acting (e.g. novorapid) o Ultra-short acting o Rapid acting • Intermediate (e.g. isophane) • Long-act (e.g. glargine, levemir) ```  Best regimen: 1 Long-acting OD + 1 Ultra-short acting at meal time o Second: Insulin pump o Third: Islet cell transplant • Follow-Up: o HbA1C o Diabetic log

Answer 6

• Background: o Insulin resistance, but still producing insulin • Diagnosis: Same as T1DM

Answer 7

• Treat: o First: Diet + Exercise + Educate if >6.5% or 48mmol/mol (target to reduce to 6.5% or 48mmol/mol. o Second: Metformin (biguanide) If patient has HbA1c of >6.5% or >48mmol/mol & wants to try metformin:  Start people on lifestyle + metformin unless mild and patient NOT overweight  Lactic acidosis  Diarrhoea/N+V (reduce in severity as Rx goes on, worse at beginning of Rx)  Contraindicated if poor renal function  No risk of hypos, no risk of weight gain (in fact causes weight LOSS)   ONLY oral hypoglycaemic proven to reduce stroke + MI   Reduced mortality  The modified release variant of metformin appears to have a better gastrointestinal side effect profile and is recommended in patients experiencing those side effects as a second-line treatment. It’s given once daily rather than the immediate release which can be given TDS. o Third – HbA1c still >6.5%: after 6 months. Increase Metformin dose to maximum tolerated dose e.g. His HbA1c is 51 mmol/mol (6.8%). You increase his metformin from 500mg bd to 500mg tds and reinforce lifestyle factors Fourth: already on on drug but HbA1c risen to >7.5% or >53mmol/mol= add Second drug either Sulfonylurea (e.g gliclazide), Gliptins, or SGLT2 inhibitors, pioglitazone. Each has pros/cons so chosen for the right patients needs. Sulfonylurea (e.g. gliclazide)  Weight gain  Risk of hypo so e.g. can’t be given to lorry drivers Gliptins- DPP4 inhib when BMI <35 but probably the least effective drug and should only be used if there is no better alternative. Sodium-glucose transport protein 2 (SGLT2) inhibitor (the 'gliflozins')-improve cardiovascular outcomes and reduce the admission rates for patients with heart failure - an extra benefit in this case. They do carry a small hypoglycaemia risk, but much less so than gliclazide. Glitazone/Thiazolidenidiones (pioglitazone) usually given as last resort e.g. third drug.  Weight gain  Abnormal LFTs  Fluid retention  Contraindicated in heart failure  Bladder cancer (RR 2.64)  Pathological fractures  No risk of hypos Fifth: If this fails, NICE recommends triple therapy with either: Metformin + gliclazide + gliptin/glifozin/pioglitazone or Metformin + pioglitazone + glifozin or Insulin +/- other drug (not if significantly overweight and has already struggled with hypos) o Sixth: Incretins (GLP-1 analogue [Exenatide]  GLP-1 when BMI >35 achieve an 11 mmol/mol (1%) reduction in HbA1c AND 3% weight loss in the first 6 months in order for it to be continued. o Last: Insulini

Answer 8

``` • Diabetic Ketoacidosis/DKA (Type 1) o Definition (Amer Diab Assoc):  BG >11-13.8  pH <7.3  Ketones + ``` o Presentation:  Young (teens)  Abdominal pain, Vomiting, Confusion/Low GCS, SOB (Kussmaul breathing)  Polyuria o Diagnose: Criteria as above  Blood sugar  Urine dip  VBG

Answer 9

• Treat: o First:  Fluid  Insulin  Dextrose?  Potassium? The osmolar gradient caused by the high blood glucose in DKA results in water shift from the intracelluar fluid (ICF) to the extracellular fluid (ECF) space and contraction of cell volume. Correction with insulin and intravenous fluids can result in a rapid reduction in effective osmolarity, reversal of the fluid shift and the development of cerebral edema.“ Or simply: Insulin clears up glucose + fluid = low osmolality (ECF) = water moves from low to high osmolality in the brain (ICF) = cerebral edema Young patients need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment but can be present at any time. If any suspicion, request a CT head and call senior immediately.

Answer 10

o Features:  Very high blood glucose (often >30-40)  Normal ketones (or small amount only)  Normal pH (>7.3 at least, unless combined with AKI)  Dehydrated/polyuria (massive – biggest problem) ``` o Diagnose:  High blood sugar  Normal pH  Normal ketones  High serum osmolality ``` o Treat:  IV Fluid (vigorous; 0.9% NS)  Insulin  ± K+

Answer 11

o Microvascular  Neuropathy  Nephropathy  Retinopathy o Macrovascular  MI, Stroke, PVD...

Answer 12

Hypoglycaemia*** (<3.0... however <2.5 = pathological) • Definition: Whipple’s Triad: o ↓glu o Symptoms of hypoglycaemia (tachycardia, confusion, sweating...) o Reversal with sugars • Cause: o Fasting/starving o Liver failure, adrenal failure (Addison’s) o Endogenous insulin  Insulinoma o Exogenous insulin  Factitious/Drugs:  Insulin  Sulfonylureas

Answer 13

• Mx: o First:  Not unwell (conscious): • Oral sugar x3 (10-20g) • Complex carb to prevent subsequent hypo  Unwell (unconscious): IV dextrose (100mL of 20%) – check BM 15min later, and continue as necessary • If IV access not available: Glucagon 1mg IM/SC/IV o Second – Ongoing Mx: 10% dextrose infusion + hourly glucose monitoring  Particularly important in sulphonylurea overdose as effects may continue

Answer 14

• Features: Lethargy, confusion, seizures, stroke-like syndrome, coma • Complication: Prolonged hypoglycemic coma o Cause: Cerebral oedema

Answer 15

Definition: High aldosterone secretion. Causes: 1-Primary (Conn's): high Aldosterone, low renin due to- adrenal adenoma or bilateral adrenal hyperplasia. Secondary: high aldosterone & high renin. Due to-Renovascular hypertension, juxtaglomerular cell tumors, oedema (cirrhosis, HF, Nephrotic disease).

Answer 16

Hypernatraemia, Hypokalaemia, Hypertension, Metabolic alkalosis -Lethargy, headaches, muscle cramps.

Answer 17

1-U&E's for electrolytes imbalances + any renal secondary causes. 2-Aldosterone:Renin ratio- high=p Conn's Normal= Secondary. *stop spironolactone & diuretics 6w before. 3-ECG 4-CT adrenals + adrenal venous sampling. Mx: Conn's- 1-Adrenalectomt if adrenal adenoma. 2-Aldosterone antagonists: Spironolactone, eplerenone or amiloride if bilateral hyperplasia. Secondary: Treat underlying cause.

Answer 18

Metformin (biguanide): MOA: increase insulin sensitivity, increase glucose uptake, reduce liver gluconeogenesis. SE:  Lactic acidosis  Diarrhoea/N+V (reduce in severity as Rx goes on, worse at beginning of Rx)  CI: poor renal function Positives:  No risk of hypos, no risk of weight gain (in fact causes weight LOSS)  ONLY oral hypoglycaemic proven to reduce stroke + MI  Reduced mortality Sulfonylurea (e.g. gliclazide) MOA: Insulin secretors- 1- stimulate pancreas to secrete Insulin by blocking K-channel= release insulin. SE:  Weight gain  Risk of hypo CI: Liver impairment Glitazone/Thiazolidenidiones (pioglitazone) PPAR gamma agonists: MOA: increases insulin sensitivity by reducing peripheral insulin resistance. SE:  Weight gain  Abnormal LFTs  Fluid retention ``` CI: heart failure  Bladder cancer (RR 2.64)  Pathological fractures Positives:  No risk of hypos ``` Incretins (GLP-1 analogue [Exenatide]: MOA: Inhibits glucagon production in pancreas which stimulates cells of pancreas to release insulin. SE: headaches, weight loss, pancreatitis. DPP-4 inhibitor [Sitagliptin]) MOA: Inc. levels of GLP-1. SGLT-2 inhibitor (sodium glucose transport protein 2) e.g. Dapagliflozin, canagliflozin, empagliflozin. MOA: Helps kidney lower blood glucose levels (stops reabsorption of glucose back to blood). SE: normoglycaemic ketoacidosis (CI IN T1DM!!) Increased risk of lower-limb amputation: feet should be closely monitored CI: frequent UTI's & thrush infections. o Last: Insulin

Answer 19

Two conditions account for 90% of cases of hypercalcaemia: 1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients 2. Malignancy: the commonest cause in hospitalised patients. This may be due to number of processes, including; bone metastases, myeloma, PTHrP from squamous cell lung cancer ``` Other: sarcoidosis* vitamin D intoxication acromegaly thyrotoxicosis Milk-alkali syndrome drugs: thiazides, calcium containing antacids dehydration Addison's disease Paget's disease of the bone** TB histoplasmosis ```

Answer 20

TSH- the therapeutic goal is 'normalisation' of the thyroid stimulating hormone (TSH) level. Cardiac disease, severe hypothyroidism or patients over 50 years the initial dose = 25mcg od Other patients initial dose = 50-100mcg od Hypothyroidism in pregnancy= dose increased 'by at least 25-50 micrograms