Endo Flashcards
Outline the pathology between TI and TII DM
Type I:
Autoimmune destruction of the pancreatic islet cells leading to rescued insulin
Low C-peptide
Type II:
Hyper secretion of insulin by depleted beta cell mass. Increasing insulin resistance.
C-pepetide high
Physiology of the pancreas in response to glucose
Alpha cells = glucagon Beta cells = Insulin Glucose enters the beta cells via the GLUT-2 pathway. Insulin is released Binds to the insulin receptor on muscles Moblises GLUT -4 to memebrane, glucose can enter the cell. Suppression of - Gluconeogenesis - Lipolysos - Proteolysis - Ketogenesis
A patient presents to the GP surgery complaining of polydipsia, polyuria and recurrent infections.
You suspect DM. What investigations will you run?
Urine dip Fasting plasma glucose Random plasma glucose HbA1c FBC
Note
- Symtomatic + one elevated FPG (≥7.0) or RPG (≥11.1)
- HbA1c FPG OGTT (2hr)
Normal: ≤ 5.6% <5.6 <7.8
Prediabetes: 5.7-6.4 5.6-7 7.8-11.0
Diabetes: ≥6.5% ≥7 ≥11.1
Outline the cut offs for the diagnosis of DM for the following readings
- HbA1c
- FPG
- OGTT
HBa1C
- normal: <56%
- prediabetes: 5.7-6.4%
- diabetes: >6.5%
FPG
- normal: <5.6
- prediabetes: 5.6 - 7
- diabetes: >7
OGTT
- normal: <7/8
- prediabetes: 7.8- 11.0
- diabetes: >11.1
List the complications associated with diabetes
NEUROPATHY
- Lipid preoccupation of myelin
- Glove and stocking distribution
NEPHROPATHY
- Mesangial expnasion and thickening of glomerular BM
- Narrowing of the efferent renal artery
- Glomerular sclerosis and thickening of the BM
- Increased gaps in the podcytes and hyperfilteration.
- Rx ACEi/ARB
RETINOPATHY
- Occlusion
- Leakage (loss of parasites
- Rx photocoagulation
CV
- Increase risk
- BP control and statins
- QRISK
ERECTILE DYSFUNCTION
INFECTION
Discuss the risk factors for diabetic foot
PAD Peripheral neuropathy Callus Smoking HTN Hypercholestrolaemia
Presentation and features of diabetic foot
Ulcers
- painless punched out
- loss of pulses
- charcot foot
Neuropathic joints
Loss of sensation
Chronic
- Rockerbottom sole
- Claw toes
- Loss of transverse arch
List the problems associated with diabetic eye disease
Cataracts
Retinopathy
Maculopathy
Glaucoma
Features of diabetic eye disease
Painless, gradual reduction of central vision.
Microaneurysm Hard exudates Haemorrhages ( small dots, blots or flame) Cotton wool spots Neovascularisation
Dx on slit lamp test
Rx Laser photocoagulation
Classify the types of diabetic eye disease
Background retinopathy
- Dots
- Blots
- Hard exudates (yellow lipid patches)
Pre-proliferative
- Cotton wool spots (infarcts)
- Venous bleeding
- Dark haemorrhages
- Intra retinal microvascular abnormalities
Proliferative
- New vessels
- Pre-retinal or viterous haemorrhage
- Retinal detachment
Maculopathy
- caused macula oedema
- reduced acuity
- hard exudates w/i one disc width of the macula
Outline the criteria for metabolic syndrome
- Truncal obesity
- HTN
- High triglycerides
- Fasting glucose >6.1mmol/L (prediabetes)
List the medications that can cause gynaecomastia
Digoxin Isoniazid Spironolactone Cimetidine Oestrogen Steriods Finasteride
Conditions linked with gynaecomastia
Androgen resistance
Klinefleters
Mumps
Renal disease
Causes of hypothyroidism
PRIMARY
- atrophic thyroiditis
- hashimotos thyroiditis
- post de quervains (painful qoitre raised ESR)
- iodine deficiency
- drugs ( carbimazole, amiodarone, lithium)
POST SURGICAL
SECONDARY
- hypopituitarism
Features of atrophic thyroiditis
Thyroid abs +ve, anti TPO, anti TSH
Atrophy no goitre
Assoc pernicious anaemia, vitiligo, endocrinopathies
Features of hashimotos
TPO+ve anti TG +ve
Atrophy and regeneration = goitre
Initial thyroidtoxicosis phase
A patient presents to you complain of feeling tired all the time, heavy period and constipation. She says it is getting her down.
O/E you notice she feels cold to touch, with a decrease HR, and slow reflexes.
What is your working dx?
What test will you order?
What will they show?
- Hypothyroidism
- TFT
- Increase TSH
- Decreased T3/T4
- ? normochromic anaemia and increased MCV
- SIAD ( if secondary)
- Increase CK if myopathy
- Abs: TPO, TSH
Treatment of hypothyroidism
Levothyroxine
- titre to normalise TSH
- 2 wks before improvement
- beware of other autoimmune disease
Features of myxoedema coma
Hypothermia Hypoglycaemia Heart failure (bradycardia with raised JVP) Coma Seizures
Triggers for a myxoedema
Radioiodine Thyroidectomy Pituitary surgery Infection Trauma
Treatment of a myxoedema coma
- Bloods
- TFTs, FBC, U+E, glucose, cortisol - Give T3/T4 IVI slowly
- Hydrocortisone 100mg IV
Causes of hyperthyroidism
- Grave’s disease
- Toxic multinodular goitre
- Toxic adenoma
- Toxic phase of thyroiditis
- Drugs
Features specific to Grave’s disease
Opthalmopathy
- exophthalmos
- ophthalmoplegia
- eye discomfort/ grittiness
- photophobia
- decreased acuity
- chemosis
Dermopathy
- pre-tibial myoxedema
Thyroid acropachy
Diffuse goitre
A patient presents to his GP surgery complain of weight loss despite an increased appetite, feeling sweaty and anxious with palpitations. She is worried she has got bad menopausal symptoms a she has not had a period in three months.
What do you suspect is the dx?
What investigations would you do?
TFTs
- decreased TSH, increased T3/T4
- abs: TSH receptor, TPO
- increased Ca
- increased LFTs
Eye screening
Radioiodine uptake scan
Treatment of patients with hyperthyroidism
Two methods
- Block and replace
- Dose titration
MEDICAL
Symptom relief: Beta blockers ( propanolol 40mg/6hr)
Block: Carbimazole (inhibits TPO)
(Graves disease treat for 12-18mnth and then withdraw and check if remission)
BEWARE OF AGRANULOCYTOSIS
RADIO-IODINE
- often become euthyroid
SURGERY
- thyroidectomy
Features of thyroid storm
Increase temp Agitation, confusion, coma Tachycardia AF Acute abdomen Heart failure
Treatment of thyroid storm
- Fluid resuscitation + NGT
- Bloods: TFT’s + cultures if infection suspected
- Propranolol PO/IV
- Digoxin
- Carbimazole ( must give lug’s Iodine 4h later to inhibit the thyroid)
- Hydrocortisone
- Rx cause
Presentation of hyperparathyroidism
(same as hypercalcaemia) Stone - renal stones - polyuria/ polydipsia - nephrocalcinosis
Bones
- Bone pain
- pathological #
Moans
- Depression
Groans
- Abdo pain
- n/v
- Constipation
- Pancreatitis
Causes of hyperparathyroidism
Primary
- Solitary adenoma
- Hyperplasia
- Pathyroid Ca
- Association with MEN 1/2
Secondary
- Vit D deficiency
- Chronic renal failure
Outline the biochemical pictures seen in both primary and secondary hyperparathyroidism
PRIMARY Increased Ca Increased PTH Increased ALP Decreased PO4
ECG: bradycardia, decreased QTc (1st degree block)
DEXA: osteoporosis
SECONDARY Increased PTH Decreased Ca Increased Po4 Increased ALP Decreased Vit D
Treatment of primary hyperparathyroidism
General
- increase fluid intake
- avoid dietary Ca2+ and thiazides
Surgical excision of the adenoma
Treatment of secondary hyperparathyroidism
Correct the causes Phosphate binders - with Ca: calcite - w/o : sevelamer Vitamin D: calcitriol ( active) Cinacalcet: increased PTH Ca sensitivty
Clinical features of hypoparathyroidism
(SPASMODIC) Spasms Perioral paraesthesia Anxious Seizures Muscle tone increase Orientation impaired Dermatitis Impetigo herpetiformis (Ca + pustules) Chovsteks, cardiomyopathy ( Increased QTc)
Causes of hypoparathyroidism
Autoimmune Congenital: DiGeorge - Cardiac abnormality - Abnormal facies - Thymic aplasia - Cleft palate - Hypocalcaemia - Chr 22
Iatrogenic
- Surgery
- Radiation
Treatment of hypoparathyroidism
Calcium and Vit D supplement
Recombinant PTH
Discuss pseudohypoparathyroidism
Failure of the target organ to response to PTH Present with symptoms of hypocalcaemia Low calcium High PTH Rx with calcium and calcitrol