Endo Flashcards
Treatment for Graves disease
- Carbimazole, either titrated to effective dose or given concurrent with
thyroxine to prevent iatrogenic hypothyroidism - Beta-blockers (eg. propanolol) for rapid symptom control
- Radioiodine
Where is cortisol produced
Adrenal cortex - zona glomerulosa
Describe the pathophysiology of a phaeochromocytoma
Neoplasia of adrenal medulla
-Which secretes catecholamines (NAd, Adr)
Biochemical investigation for pheochromocytoma
Plasma (and urinary) metanephrines (will be raised)
How to avoid hypertensive crisis in surgery
Give phentolamine (an Alpha receptor blocker)
Hypothyroidism diff
Primary
* thyroid gland dysfunction (1 mark)
so have high TSH but low T3 and T4 / thyroid hormone (1 mark)
Secondary
pituitary gland dysfunction (1 mark)
so have so have high TRH low TSH and low T3 and T4 / thyroid hormone (1 mark)
Tertiary
hypothalamic dysfunction (1 mark)
so have low TRH low TSH and low T3 and T4 / thyroid hormone (1 mark)
Name 1 primary and 1 secondary cause of nephrogenic diabetes insipidus
Primary (1 mark)
inherited / genetic mutation
Secondary (1 mark)
Polycystic kidney disease
Hydronephrosis
Fanconi syndrome
Renal amyloidosis
Hypercalcemia
HIV infection
Iatrogenic - drug or surgery induced
Name 1 cause of cranial diabetes insipidus
Brain tumor
Head injury
Meningitis or encephalitis
Sarcoidosis
Aneurysms
Sickle cell anaemia
Sheehans syndrome
Iatrogenic - drug or surgery induced
Pathology of coeliac
In coeliac disease, auto-antibodies are created in response to exposure to gluten that target the epithelial cells of the intestine and lead to inflammation. There are two antibodies to remember: anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA). These antibodies relate to disease activity and will rise with more active disease and may disappear with effective treatment.
Inflammation affects the small bowel, particularly the jejunum. It causes atrophy of the intestinal villi. The intestinal cells have villi that help absorb nutrients from the food passing through the intestine. The inflammation causes malabsorption of nutrients and the symptoms of the disease.
Coeliac gold standard
Biopsy of the duodenum showing :
Raised intraepithelial lymphocytes
Crypt hyperplasia
Villous atrophy
Acute pancreatitis has a range of complications of variable likelihood. Clinicians must be aware of the complications of acute pancreatitis and how likely they are to occur. Name 3 complications of acute pancreatitis and label their likelihood of occurrence as high medium low
Acute renal failure = high
Sepsis = medium
Acute respiratory syndrome = medium
Pancreatic pseudocyst = low
Pancreatic abscess = low
Ascites/ pleural effusion = low
Enteric fistula = low
Chronic pancreatitis = low
Abdominal compartment syndrome = low
Sarah is a 44 year old lady with a family history of sarcoidosis. She is chatting to the nurse about the disease and wants to know what signs and symptoms to look out for are. Name the triad present in sarcoidosis and give 3 clinical features of the triad
Lofgren’s triad (1 mark)
erythema nodosum (1 mark)
bilateral hilar lymphadenopathy (1 mark)
polyarthralgia / pain in more than 1 joint (1 mark)
Describe the steps of old RBCs being excreted starting with haemolysis of the old RBCs
Haemolysis = RBC destruction - no marks
(Producing protoporphyrin ring / biliverdin) which then becomes unconjugated bilirubin (which is lipid soluble)
Unconjugated bilirubin entres hepatocytes and at hepatocytes its conjugated via uridine glucuronyl transferase (UGT)
Conjugated bilirubin leaves the hepatocytes via bile canaliculi / then bile ducts / then bile ducts / then hepatic ducts / then common hepatic duct into gall bladder where its concentrated. Gallbladder releases the conjugated bilirubin into the duodenum via the common bile duct
Bacterial proteases convert conjugated bilirubin into urobilinogen
90% of this is excreted making stool dark brown
10% is reabsorbed and then excreted by the kidneys
There are 4 main patterns of MS. Briefly describe relapsing remitting MS and progressive relapsing MS
Relapsing remitting = have an autoimmune attack / flare which causes a rapid development in symptoms followed by a period of remission / remyelination where symptoms improve and return to a constant level but this new baseline has more disability than before
Progressive relapsing = a steady increase in disability with flares superimposed. After each flare there is a period of remission / remyelination where symptoms improve but they return to a level of steady increase in disability
Charcot’s neurological triad
Used for multiple sclerosis
dysarthria
Nystagmus
Intention tremor
Hormones anterior pituitary
Main feature of U&E detection
hyperkalaemia
Clinical examination of hypocalcaemia
Chvostek’s sign - tap over the facial nerve causes spasm of the facial muscles
Trousseau’s sign - inflate the blood pressure cuff to 20mmHg above systolic for 5 minutes and the
hand should form a claw.
Role of PTH
PTH increases bone remodelling and turnover. PTH stimulates osteoclasts to reabsorb bone mineral
which liberate calcium into blood (breaks down bone).
* PTH increases the amount of calcium reabsorbed in the kidney which means that less is excreted in
urine.
* PTH decreases phosphate reabsorption in the kidney.
* PTH decreases phosphate reabsorption in the kidney, increasing the amount excreted.
* PTH increases absorption of Ca2+ in the gut.
What does carbimazole
Blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin, this
leads to decreased thyroid hormone production.
Options for blocking GH
Dopamine agonists (bromocriptine)
Somatostatin analogues (ocreotide)
GH antagnoists (pegvisomant)
Key Signs in Cushing
Abdominal Striae
Moon Face
Buffalo Hump
Thinning of skin
Acne
G.S for acromegaly
Oral glucose tolerance test (GTT)
The effects of superantigens?
A molecule that causes non-specific polyclonal T-cell activation