clinical scenarios 3

Question 1

STEMI MANAGEMENT

Answer 1

300mg Aspirin Immediately (to continue indefinitely)

For Repercussion therapy (primary PCI or fibrinolysis)

Drug therapy after PCI
prasugrel with aspirin if not on oral anticoagulant
aspirin and clopidogrel if on anticoagulant

Cardiac rehabilitation and secondary prevention

Question 2

when is PCI / fibrinolysis

Answer 2

Angio/PCI - with 120 minutes of symptoms
Consider if > 12 hours after symptoms and continuing myocardial ischaemia or cariogenic shock
radial access in preference to femoral access

Fibrinolysis if presenting in 12 hours of symptoms and PCI not possible in 120 minutes

Question 3

NSTEMI management

Answer 3

300mg aspirin and continue indefinitely
fondaparinux unless immediate angiography

Use GRACE score to predict 6 month mortality of cardiovasular event

If low risk - Conservative management - DAPT

Immediate or higher risk 0 offer angiography within 72 hours, if unstable - offer immediate angiography

Cardiac rehab and secondary prevention

Question 4

secondary prevention ACS

Answer 4

ACE inhibitor
DAPT for up to 12 months
Beta blocker
Statin

Question 5

Anti platelet therapy post ACS

Answer 5

If on anticoagulant - offer clops for 12 months after PCI

If no PCI - continue aspirin for up to 12 months if on anticoagulation

Question 6

initial management of NSTEMI?

Answer 6

MONABASH = Morphine, Oxygen, Nitrates, Antiplatelets, Beta-blockers, ACE-inhibitors, Statins, Heparin.

Question 7

what are high risk features that would support patients having early angio and revasc in NSTEMI?

Answer 7

Risk factors include:

Poor LV systolic function
Previous CABG/PCI (in last 6/12)
Patients with other comorbidities
Patients with high-risk features of NSTEMI/UA
Recurrent angina
Recurrent ischaemic ECG changes despite optimal medical therapy
Elevated troponin
Tachyarrythmias post MI

Question 8

common complications post MI?

Answer 8

DARTH VADER:

Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm
Dressler’s syndrome
Embolism
Re-infarction.

Question 9

what is Dressler’s syndrome?

Answer 9

Also described as autoimmune pericarditis, it occurs 2-10 weeks post MI. In fact, simple pericarditis post-MI is more common than Dressler’s syndrome and presents within 2-4 days post MI.

You would manage this patient as you would any with acute chest pain. Remember the ABCDE approach. An ECG will be important and may show widespread diffuse saddle-shaped ST elevation across multiple leads. An echocardiogram may show pericardial effusion. The management of this condition is with non-steroidal anti-inflammatory medication. If there is a significant effusion it can be aspirated.

Question 10

History in Diarrhoea?

Answer 10

any abdo pain
PR bleeding
Night sweats weight loss
vomiting
anything similar previously
any travel
eaten anything differently
any family history
anyone have similar symptoms

Question 11

Differentials for Diarrhoea?

Answer 11

Infective causes – This could be viral or bacterial gastroenteritis
Irritable bowel syndrome, anxiety
Malabsorption – coeliac disease, pancreatic insufficiency
Inflammatory bowel disease – Crohn’s disease or Ulcerative Colitis
Metabolic causes – Hyperthyroidism causing increased bowel motility.

Question 12

Investigations for Diarrhoea?

Answer 12

FBC
U&E
CRP
TFTs
Calcium
Phosphate
VBG - to measure lactate
ECG and CXR
Stool sample - for culture
Faecal calprotectin
FIT test
Endoscopy
XR if indicated to look for colonic dilatation

Question 13

What clinical signs on examination may suggest at an underlying diagnosis of IBD?

Answer 13

I would look for extra-intestinal manifestations of IBD:

Aphthous ulcers
Erythema Nodosum
Pyoderma gangrenosum
Peripheral arthropathy
Sacroiliitis
Ankylosing spondylitis
Eye complications – uveitis, conjunctivitis, episcleritis

Question 14

What suggests severe attack of IBD?

Answer 14

> 6 bloody stools a day
Systemically unwell: pyrexia and tachycardia
Hb <10 g/dL
Albumin <30g/L
Toxic dilatation

Question 15

How would you manage an acute flare of IBD ?

Answer 15

Fluid Resuscitation
Monitor for electrolyte derangement
If severe - discuss with surgical colleagues
Send sample to exclude infective colitis

Corticosteroid can be used
NICE recommends that IV corticosteroids should be considered for people admitted to hospitals with severe IBD. If I were considering this, I would discuss this decision with my senior registrar or the gastroenterology team.

Question 16

colonoscopy signs of Crohn’s vs UC?

Answer 16

UC - only affects the colon - rectumis always affected. Inflammation is uniform and confide to the mucosa, granulomas are absent

Crohns - any part of the gastric tract, has skip lesions, rectum is often spared, the bowel wall is thickened and has cobblestone appearance due to deep ulcers and swellings
On histology there will be granulomas with inflammation extending through the mucosa and muscle of the bowel

Question 17

Does Surgery have a role in the management of IBD?

Answer 17

Around 30% of patients with UC will require a colectomy at some stage. Colonic perforation, uncontrollable bleeding, toxic megacolon and fulminating disease require urgent proctocolectomy.

Surgery in Crohn’s disease is not curative and is only indicated for perforation, obstruction, abscess formation and fistulae. There is a high recurrence rate after surgery.

Question 18

New Jaundice - what questions do you want to ask?

Answer 18

is it acute or chronic
any associated symptoms - RUQ pain, vomiting, pruritis
Fever or diarrhoea, dark urine and pruirtis are seen in obstruction of biliary flow
weight loss fevers might sweats may indicate malignancy
bronzed skin - and signs of DM - suggestive of haemochromatosis

PMH - gallstones, history of fatty liver disease, PBC, PSC, alpha 1- antitrypsin deficiency

abx
regular paracetamol

FH - There are various familial conditions that cause jaundice: Gilbert’s; Haemochromatosis; Wilson’s disease; sickle cell disease; hereditary spherocytosis

SH - alcohol, drug use, unprotected sex, recent travel, tattos, vaccination history

Question 19

Signs of Chronic liver Disease?

Answer 19

Finger clubbing; leukonychia; palmar erythema
Ecchymosis
Jaundice
Spider naevi
Gynaecomastica
Testicular atrophy
Hepatomegaly (the cirrhotic liver may be small or enlarged. In most cases a cirrhotic liver is small and shrunken, but in cases where it is due to alcohol or NAFLD, hepatomegaly may be present)

Question 20

Causes of Liver Cirrohis s

Answer 20

Alcohol
Viral causes: Hep B and Hep C
Autoimmune causes: Primary biliary cirrhosis Primary sclerosing cholangitis Autoimmune hepatitis
Metabolic Non-alcoholic steatohepatitis, Haemochromatosis, Alpha-1 antitrypsin deficiency, Wilson’s disease, Cystic fibrosis
Drugs
Methotrexate
Isoniazid
Amiodarone

Question 21

Investigations for Jaundice?

Answer 21

FBC – to check for anaemia and platelet count
Liver enzymes and serum bilirubin levels. ALT and AST are often very high in acute viral hepatitis.
ALP may be raised if the jaundice is due to bile flow obstruction. (ALP is released from damaged biliary epithelial cells).
GGT – raised in isolation after recent alcohol consumption.
Amylase – if raised is suggestive of pancreatic pathology.
Clotting studies. Prothrombin time should be measured if liver pathology is suspected – deranged PT is an early marker of compromised liver function.

Blood film - ? anaemia
BBV screen
Autoimmune screen - ANA/AMA.
Ferritin
Serum copper
Ascitic tap and send for culture and microscopy
USS abdomen

Question 22

jaundice, confused, hypotension, tachycardia - what is the cause?

Answer 22

Based on the previous presentation to clinic and his current sudden deterioration, this likely represents decompensation of chronic liver failure with hepatic encephalopathy.

Question 23

Causes of acute decompensation of acute liver failure

Answer 23

Infection - SBPl, pneumonia
Acute GI haemorrhage
Additional Hepatotoxic insult - alcoholic binge, acute viral hepatitis, hepatotoxic drugs

Drugs - diuretics, sedative, narcotic
Metabolic derangement - hypoglycaemia, electrolyte disturbance

Question 24

What is hepatic encephalopathy?

Answer 24

This is a neuropsychiatric disturbance of cognitive function in a patient with acute on chronic liver disease. Clinically there is altered conscious level, asterixis, abnormal EEG, impaired psychometric tests, and an elevated arterial ammonia concentration.

Hepatic encephalopathy may be seen in liver disease of any cause. The aetiology is not fully understood but is thought to include excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut.

Question 25

How is hepatic encephalopathy graded?

Answer 25

Grade 1 – Insomnia/reversal of day/night sleep pattern

Grade 2 – Lethargy/disorientation

Grade 3 – Confusion

Grade 4 - Coma

Asterixis may be present at any stage.

Question 26

how is hepatic encephalopathy managed?

Answer 26

The aim of treatment is to improve morbidity

Exclude other causes of confusion
Identify and correct the precipitating cause
Give lactulose. This alters faecal pH and nitrogen utilisation by bowel flora.
Phosphate enemas help to purge the large bowel.

Question 27

why does lactulose help encephalopathy

Answer 27

Lactulose acidifies the gastrointestinal tract, which reduces the amount of ammonia produced by bacteria

Question 28

Long term management of liver Cirrhosis?

Answer 28

Treat underlying cause - stop drinking, antiviral in viral hepatitis and immune suppression in autoimmune hepatitis

Abstinence from alcohol improves prognosis in viral hepatitis and chronic liver disease.

6 monthly abdominal USS and AFP to monitor for hepatoma

All patients should undergo endoscopy as surveillance for oesophageal varices

Following an episode of spontaneous bacterial peritonitis, prophylactic antibiotics are indicated.

Question 29

when should a patient be recommend for liver transplantation?

Answer 29

A transplant centre should take this decision. The selection for transplantation is taken based on the severity of the underlying liver disease against the presence of any co-morbidities. Some conditions should be considered for transplant irrespective of disease severity such as PBC or recurrent cholangitis in PSC.

Question 30

precipitating factors of hepatic encephalopathy?

Answer 30

Precipitating factors
infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)

Question 31

features of hepatic encephalopathy ?

Answer 31

Features
confusion, altered GCS (see below)
asterixis: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
constructional apraxia: inability to draw a 5-pointed star
triphasic slow waves on EEG
raised ammonia level (not commonly measured anymore)

Question 32

What is Wernicke’s encephalopathy?

Answer 32

Wernicke’s encephalopathy is a neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics. Rarer causes include persistent vomiting, aոοrеxiа nervosa, stomach cancer, and dietary deficiency.

Question 33

Classic Triad of symptoms in Wernicke’s encephalopathy and other symptoms?

Answer 33

A classic triad of ophthalmoplegia/nystagmus, ataxia and encephalopathy may occur.

Features
oculomotor dysfunction
nystagmus (the most common ocular sign)
ophthalmoplegia: lateral rectus palsy, conjugate gaze palsy
gait ataxia
encephalopathy: confusion, disorientation, indifference, and inattentiveness
peripheral sensory neuropathy

Question 34

what happens if wernike’s encephalopathy is not treated?

Answer 34

If not treated Korsakoff’s syndrome may develop as well. This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of antero- and retrograde amnesia and confabulation in addition to the above symptoms.

Question 35

differentials for Wernicke’s?

Answer 35

Delirium Tremens - DT occurs in a similar population as WE and is associated with rapid onset confusion, shaking which may be confused with ataxia, and tachycardia.
DT is associated with hyperthermia rather than hypothermia, however, and is usually associated with a history of having significantly reduced alcohol intake in the prior 5 days.
High doses of parenteral thiamine are rapidly administered to both DT and WE patients so precise discrimination is not always required.

Hepatic Encephalopathy

Stroke

Normal Pressure Hyrdocephalus - Normal-pressure hydrocephalus presents with Hakim’s triad of mental state changes, gait instability and urinary incontinence, highly similar to the triad of mental state changes, ataxia and ocular movement abnormalities associated with WE.

Question 36

Korsakoff’s syndrome?

Answer 36

Overview
marked memory disorder often seen in alcoholics
thiamine deficiency causes damage and haemorrhage to the mammillary bodies of the hypothalamus and the medial thalamus
in often follows on from untreated Wernicke’s encephalopathy

Features
anterograde amnesia: inability to acquire new memories
retrograde amnesia
confabulation

Question 37

SOB differential?

Answer 37

seconds to minutes – Acute asthma attack, anaphylaxis, Pneumothorax (+ Tension), Inhaled foreign body, Pulmonary Embolism
Hours to Days – Pneumonia, Heart Failure, Pleural Effusion
Weeks to Months – Worsening COPD, Chronic Asthma, Heart Failure, Pulmonary Fibrosis, Anaemia, Pulmonary HTN, Obesity.

Question 38

what is a history for SOB would help you differentiate the cause?

Answer 38

Time and Onset
Alleviating or aggravating factors - worse when lying flat , worse of exertion
associated features - cough, wheeze, chest pain, pleuritic pain? weight loss or night sweats

PMH and drug history
any recent changes to drugs
Any Allergies
Have they been admitted to hospital before , have they ever been admitted to ITU

Do they smoke

Occupational History

Question 39

Investigations for SOB and wheeze?

Answer 39

Bedside - observations, peak flow, ECG, ABG

Bloods - FBC, U&E’s CRP

CXR

Question 40

What treatments for acute asthma attack?

Answer 40

State the patient is having SEVERE asthma attack if not able to finish sentences

• sit the patient up in bed
• high flow oxygen
• salbutamol nebulisers - these can be given back to back
• Steroid - IV or oral
• Add nebulised ipratropium if response to beta 2 agonist is poor
• monitor patient with serial peak flows before and after nebuliser. Repeat ABG if no improvement
• IV abx if signs of infection
• IV fluid resuscitation
• IV magnesium sulphate if no response
• IV aminopylline - best to get support before dong this
• of making no progress - get urgent support 2222 or ITU

Question 41

what are the signs that a patient having asthma attack are deteriorating?

Answer 41

Explain that acute asthma attacks can be split into acute severe asthma and life-threatening asthma.

The markers for a life-threatening asthma attack include:

PEF <33% best or predicted
Soft breath sounds or silent chest
Feeble respiratory effort
Exhaustion, drowsiness, decreasing GCS
Hypotension SBP <100
Arrhythmia – suggest haemodynamic compromise
Signs of cyanosis
Hypoxia SpO2 <90% or PaO2 <8kPa despite 60% FiO2
Rising PaCO2 – this is the most important as it indicates ‘near-fatal’ asthma

Any of these signs would prompt me to put out an arrest call as they all suggest the patient is approaching respiratory arrest

Question 42

Long term management of asthma?

Answer 42

Initially managed on a short course of steroid

They can be safely discharged once they are off of regular nebulisers and PEF is >75% of best.

The patient should be started on an inhaled Corticosteroid (if not on one already). This dose should be titrated up to response. A short acting Beta-2 agonist is required for symptomatic control.

A long acting Beta-2 agonist can be added following an observed response to the inhaled corticosteroid.

Patient education is always important prior to discharge and should include observation of inhaler technique and PEF record keeping.

Follow up arranged with GP

smoking Cessation