final to learm Flashcards
Lead in: How do Statins worK? Options:
A 52 year old man, presents to his GP, from working out his QRISK assessment score it is 15%, and he is offered lipid modification therapy. He asks how does this work?
A
PCSK9 inhibition
B
Competitive inhibition of HmG-CoA Reductase
C
Non-competitive inhibition of HmG-CoA Reductase
D
Inhibition of NPC1L1 transporter
E
Activation of nuclear transcription factor PPARα
Answer: B – Competitive inhibition of HmG-CoA reductase
A 72 year old female patient presents with feeling like her heart is racing all the time, on examination her pulse is irregularly irregular, her HR is 120 and she is haemodynamically stable.
She is diagnosed with new onset-atrial fibrillation due to valvular heart disease following an Echocardiogram
Before she can be started on Apixaban her bleeding risk needs to be assessed.
Lead in: What score is used to assess her bleeding risk?
HAS-BLED
Lead in: What is the most likely drug causing this presentation? Options:
A 53 year old male presents with a resting tremor, rigidity, bradykinesia, postural instability, cognitive changes.
He had started a new medication to treat nausea.
A
Chlorpromazine
B
Co-careldopa
C
Rasagaline
D
Rotigotine
E
Entacapone
Answer: A - Chlorpromazine
Rationale : (A) – Antiemetic often used to treat nausea + vomiting which blocks D3 receptors in the brain, which can worsen Parkinson’s symptoms which the patient is now presenting with, (B,C,D,E – are all treatments for Parkinson’s Disease) (B) = L-DOPA plus peripheral DOPA Decarboxylase inhibitor, (C) Monoamine oxidase B inhibitor (D) – Dopamine Receptor Agonist, (E) – COMT inhibitors
28 year old female, who has been diagnosed with SLE (systemic lupus erythematous) has been struggling to control her disease and has recurrent flares.
She has tried NSAIDs, corticosteroids and hydroxychloroquine
The Rheumatologist wishes to start Azathioprine.
A
TPMT levels
B
U&E
C
FBC
D
LFTs
E
TFTs
TMPT levels
TPMT levels/activity need to be checked before patients receive thiopurine drugs, as the enzyme thiopurine methyltransferase metabolises these drugs.
If there is low activity there is increased risk of myelosuppression, as there is greater concentration of the active metabolite 6-Mercaptopurine which ↓ RNA synthesis and ↓ DNA synthesis
A 65 year old male is having a left total hip replacement due to osteoarthritis.
The anaesthetist is discussing general anaesthetic options with the patient.
A
Halothane
B
Isoflurane
C
Propofol
D
Ketamine
E
Barbiturates
ketamine
The General anaesthetics which act on the NMDA R to inhibit glutamate potentiation = slow induction of anaesthesia = Xenon, Nitrous Oxide, Ketamine
The GA which act on GABAA Receptors = mediate chloride ion conductance = reducing action potential transmission = leading to rapid indiction of anaesthesia = Halothane, Deslurance, Isoflurane, Sevoflurane, Propofol, Barbiturates
A 32 year old female who has had epilepsy since age 12, is thinking of trying for a baby with her partner.
Her current Medications are;
Phenytoin & Oral Contraceptive Pill
What would be a safe anti-epileptic drug to take during pregnancy?
A
Amlodipine
B
Carbamazepine
C
Phenytoin
D
Sodium Valproate
E
Ethosuximide
Answer: B – Carbamazepine
Carbamazepine, Lamotrigine and Levetiracetam are known to be safe during pregnancy + folic acid 5mg supplementation;
A
Anterior dislocation of hip
B
Fractured mid-shaft of femur
C
Posterior dislocation of hip
D
Fractured pelvic rami
E
Fractured neck of femur
Posterior dislocation of the hip
posterior dislocation = shortened, internally rotated and adducted
anterior dislocation= shortened and externally rotated
What is a microvascular complication of diabetes?
A
Heart Attack
B
Peripheral Vascular disease
C
Stroke
D
Retinopathy
E
Carotid Artery Disease
Retinopathy
Rationale : (D) – Retinopathy, Nephropathy and neuropathy are microvascular complications of diabetes; (A, B, C, E) are macrovascular complications of diabetes, which come under the umbrella term of cardiovascular disease due to the hyperglycaemia resulting in atherosclerosis.
A 38 year patient presents to A & E with severe RUQ pain, fever and nausea. She has a Hx of abdominal pain which got worse after eating takeways but is the worst shes felt now.
On examination she is jaundiced, with a positive Murphy’s sign.
Blood tests show deranged LFTs, (↑ ↑ ALP, ↑ ALP, ↑ ↑ Bilirubin), ↑ ↑ CRP, ↑ γ-GT
A
Biliary Colic
B
Acute Cholecysitis
C
Acute ascending Cholangitis
D
Acute pancreatitis
E
Ruptured peptic ulcer
Answer: C – Acute Ascending Cholangitis
Acute Ascending cholangitis= Triad of RUQ pain + Fever + Jaundice (+ positive Murphys sign, + Hx of abdo pain worse after eating fatty foods = hx of biliary colic + gallstone disease)
Biliary colic= would just be the RUQ pain worse after eating, no fever, no nausea, no jaundice, negative murphys sign
Acute cholecysitis = RUQ pain + fever = no jaundice, positive murphys sign
Acute pancreatitis= epigastric pain radiating to the back, this is a complication of gall stone disease, + vomiting, may notice on examiantion Grey Turner’s and Cullen’s sign, + ↑ ↑ LIPASE / Amylase levels
Ruptured peptic ulcer = epigastric pain, vomiting, nausea, ± haematemesis (if ruptured a blood vessel), no deranged LFTs, no raised gamma-GT levels
Biliary colic
Gall stones happily sitting within gall bladder, but can cause sudden onset of RUQ pain typically a few hours after eating a fatty meal
Due to cholecystokinin (CCK) release after meal, which causes the gall bladder contract and push a gallstone up against the neck of the gall bladder- temporary obstruction of biliary duct
Constant pain- can last for a long time and then ease for a while
Treatment- pain relief and removal
Acute cholecystitis
RUQ pain- caused by full impaction of stone in cystic duct
Inflammatory features
Positive Murphy sign place a hand on right side of the patients stomach and ask them to take a deep breathe in- will push gall bladder down and cause them to take a sharp breathe in pain (wont happen on left hand side)
Treatment- pain relef and Ab, will need to be removed
Ascending cholangitis
Statis due to blockage of CBD by stone
Infection of biliary tree
Charcots triad- Inflammation, RUQ pain, jaundice (when stone reaches common bile duct)
GalphaQ
G-αq stimulates the phospholipase C pathway. PIP2 is cleaved into secondary messengers IP3 and DAG. IP3 binds to receptors on SR to increase intracellular Ca2+ concentration. DAG stimulates protein kinase C
GalphaI
inhibits adenylate cylase (AC)
inhibits cAMP
no activation of second messengers
GalphaS
stimulates adenylate cyclase
increases cAMP
cAMP stimualtes PKA
