BRS MOCK 1 - pancreatitis, CVD disorders, urological disorders, control of heart function Flashcards
What does the pancreas look like in acute pancreatitis?
Inflamed.
What does the pancreas look like in chronic pancreatitis?
Lots of fibrosis.
Common cause of acute pancreatitis?
Alcohol and gallstones.
What procedure can cause acute pancreatitis?
Endoscopic retrograde cholangio pancreatography
What drugs can cause acute pancreatitis?
S - Sulphonamides and steroids
A - Azothioprine
N - NSAIDS
D - Diuretics
How do gallstone cause acute pancreatitis?
Gallstone gets stuck in the ampulla and bile can’t leave and so you get bile reflux. You also get pressure build up of pancreatic juice as it can’t leave the ampulla. Reflux of activated enzymes from duodenum if gall stone leaves ampulla into duodenum.
How does alcohol cause acute pancreatitis?
Increased permeability of pancreatic duct epithelium and so enzymes diffuse into periductal interstitial tissue. Alcohol can precipitate proteins in the ducts that obstruct the duct and result in upstream pressure.
How does premature, intracellular enzyme activation occur in pancreatitis?
Proenzymes and lysosomal proteases incorporated into same vesicles resulting in trypsin being activated and pancreatic enzymes being activated intracellularly.
What does extracellular/intracellular activation of trypsin in pancreatitis result in?
Activation of elastase which causes vessel destruction and islet necrosis leading to bleeding and hyperglycemia. Activation of complement also causes vessel destruction. Activation of prothrombin leads to thrombosis which leads to ischaemia. Activation of phospholipase A2 leads to fat necrosis which leads to hypocalcemia. Activation of kallikrein leads to vasodilation and plasma exudation that can lead to shock.
Types of acute pancreatitis?
Oedematous pancreatitis. Haemorrhagic pancreatitis. Necrotic pancreatitis.
Why is necrotic pancreatitis dangerous?
Can get infected.
Biomarkers for acute pancreatitis?
Raised amylase. Raised lipase.
Local complications of acute pancreatitis?
Pancreatic necrosis, pancreatic pseudocyst, haemorrhage, thrombosis.
Chronic pancreatitis mechanism?
Alcohol abuse leads to a decrease in citrate and lithostatin concentration which result in calcium precipitation which leads to calcium deposition. This leads to epithelial lesions which leads to enzyme activation.
What can cause heart failure?
Cardiac damage (ischaemia), hypertension and valve disease.
What biomarker for heart failure?
Elevated brain natriuretic peptide (BNP).
What would you see on an xray of a patient with heart failure?
Cardiomegaly.
Treatment for heart failure?
ACE inhibitors, beta blockers.
What might you see in an ECG for a patient with heart failure?
Enlarged QRS complex.
What can be seen in the ventricles in patients with reduced ejection fraction?
Dilated ventricles.
What can be seen in the ventricles in diastolic heart failure?
Thickened ventricular muscle.
What causes Wolff-Parkinson-White syndrome?
Additional accessory conduction pathway (the bundle of Kent) between the atria and ventricles.
ECG findings in atrial fibrilation?
Absent p-waves & ‘irregularly irregular’ rhythm.
ECG findings in Wolff-Parkinson-White syndrome?
QRS pre-excitation & biphasic T wave.
Treatments for atrial fibrilation?
Cardioversion, anti-arrhythmics.
NSTEMI ECG reading?
ST-depression.
STEMI ECG reading?
ST-elevation.
What biomarker is present in STEMI and NSTEMI?
High troponin levels.
How do you treat angina?
Vasodilators.
How do you treat NSTEMI or STEMI?
Coronary stents, antiplatelets.
How does kidney dysfunction cause anaemia?
Kidneys produces EPO which stimulates production of erythrocytes.
How does kidney dysfunction lead to secondary hyperparathyroidism?
Kidneys have enzyme 1 alpha hydroxylase to convert 25(OH)D3 into calcitriol. Calcitriol inhibits PTH release and so without calcitriol you will have high amounts of PTH in blood.
What is inflammation of the bladder called?
Cystitis
What is the most common pathogen for inflammatory urological disorders?
Bacteria.
What are the key features of nephritic syndrome?
Haematuria, proteinuria.
Tests for nephritic syndrome and nephrotic syndrome?
Urine dipstick, urine microscopy, urine protein : creatinine ratio.
Blood tests : kidney function and immunological tests.
What test would confirm an IgA nephropathy?
Kidney biopsy and immunohistochemistry.
What is the first line treatment for nephropathy?
ACE inhibitor or angiotensin receptor inhibitor.
How does an ACE inhibitor treat nephropathy?
Reduces hypertension. Reduce proteinuria by lowering the intraglomerular pressure, reducing hyperfiltration.
In good pasture syndrome what is targeted?
Alpha 3 chain of type IV collagen in Glomerular basement membrane and alveolar basement membrane.
Autoimmune conditions that can cause nephropathy?
Goodpasture’s disease, systemic lupus erythematosus and vasculitis.
Autoantibody for vasculitis?
Anti-neutrophil cytoplasm antibody.
Urine markers for diabetic nephropathy?
Microalbuminuria and proteinuria.
Treatments for diabetic nephropathy?
ACE inhibitor, Angiotensin receptor inhibitor and SGLT2 inhibitor.
What histological features in diabetic nephropathy?
Thickened glomerular basement membrane. Deposition of extracellular matrix in the glomerulus (fibrotic tissue).
Key features of nephrotic syndrome?
Peripheral oedema, severe proteinuria, low serum albumin.
Treatment for nephrotic syndrome?
Corticosteroid, cyclophosphamide, tacrolimus. Diuretics. Anticoagulants.
What is seen in the kidney biopsy of minimal change glomerulopathy when using an electron microscope?
Flattened podocyte foot processes.
Treatment for kidney stones?
Shockwave lithotripsy, ureteroscopy, percutaneous nephrolithotomy.
What medications is used to treat polycystic kidney disease? What kind of drug is it? How does it treat?
Tolvaptan - vasopressin receptor 2 antagonist. Slows down formation of cysts.
In a nodal cell action potential what causes the prepotential phase?
Sodium influx.
In a nodal cell action potential what causes the upstroke phase?
Calcium influx.
Plateau in cardiac muscle action potential is caused by what?
Calcium influx.
Depolarisation/upstroke in cardiac muscle action potential is caused by what?
Sodium influx.
What receptor on the heart do parasympathetic nerves act on?
M2 receptor.
What receptor on the heart do sympathetic nerves act on?
Beta 1 receptor.
How does sympathetic nervous system act on the kidneys to increase blood volume?
Acts on alpha one adrenoreceptor to cause vasoconstriction of afferent arteriole that enters glomerular capsule. Decrease in glomerular filtration which results in decreased sodium excretion. Increase in blood volume.
What receptor do sympathetic nerves act on to secrete renin?
Beta 1 adrenoreceptor.
Where are pressure sensors in the cardiovascular system?
Aortic arch and afferent arterioles in the kidney.
Local vasodilators?
Nitric oxide and prostacyclin.
Local vasoconstrictors?
Thromboxane A2 and endothelins.
Systemic vasodilators
Kinins (stimulate NO synthesis) and atrial natriuretic peptide (ANP).
What receptor does vasopressin bind to cause vasoconstriction?
V1 receptor.
When is atrial natriuretic peptide released?
Secreted from the atria in response to stretch
