Practice Paper 4 Flashcards
Whats the mx of pulmonary embolism?
Primary Prevention
Compression stockings
Heparin prophylaxis for those at risk
Good mobilisation and adequate hydration
If haemodynamically stable O2
Anticoagulation with heparin or LMWH *
Switch over to oral warfarin* for at least 3 months
Maintain INR 2-3 Analgesia
If haemodynamically UNSTABLE (massive PE) Resuscitate
O2
IV fluids
Thrombolysis with tPA* may be considered if cardiac arrest is imminent
Surgical or radiological
Embolectomy
Recognise the signs of pulmonary embolism on physical examination
Recognise the signs of pulmonary embolism on physical examination
Severity of PE can be assessed based on associated signs:
SMALL - often no clinical signs.
There may be some tachycardia and tachypnoea
MODERATE Tachypnoea Tachycardia Pleural rub Low O2 saturation (despite O2 supplementation) **
MASSIVE PE Shock Cyanosis Signs of right heart strain ** Raised JVP ** Left parasternal heave Accentuated S2 heart sound **
MULTIPLE RECURRENT PE
Signs of pulmonary hypertension
Signs of right heart failure
35yo woman presents with a rash under the axilla
Its dark and velvety texture
pmh of diabetes
Acanthosis Nigricans
(sign of severe insulin resistance) - velvety thickening and hyperpigmentation of the skin of the axillar or neck
Which score is used to asses the risk of an adverse outcome following an upper GI bleed
Rockall score
o Scores the severity after a GI bleed
o Score < 3 carries good prognosis
o Score > 8 carries high risk of mortality
64yo male presents to a&e with large rectal bleed left sided abdominal pain long history of constipation and is febrile and tachycardic
diverticulitis
What’s the aetiology of diverticula?
There is hypertrophy of the muscles resulting in high intraluminal pressure
This leads to herniation of the mucosa at potential sited of weakness in the bowell wall ie: points of entry of blood vessels.
LAZ:
• Aetiology:
o A low-fibre diet leads to loss of stool bulk
o This leads to the generation of high colonic intraluminal pressures to propel the stool out
o This, in turn, leads to the herniation of the mucosa and submucosa through the muscularis
What classification is used for acute diverticulitis?
Hinchey Classification of Acute Diverticulitis:
• Ia: phlegmon
• Ib and II: localised abscesses
• III: perforation and purulent peritonitis
• IV: faecal peritonitis
What’s the pathogenesis of diverticulitis
• Pathogenesis:
o Diveticulae are most commonly found in the sigmoid and descending colon
o However, they can also be right-sided
o Diverticulae are NOT found in the rectum
o Diverticular are found particularly at sites of nutrient artery penetration
o Diverticular obstruction by thickened faeces can lead to bacterial overgrowth, toxin production and mucosal injury
o Which can then lead to diverticulitis, perforation, pericolic phlegmon, abscess, ulceration and fistulation or stricture formation
Summarise the epidemiology of diverticular disease
- Diverticular disease is VERY COMMON
- 60% of people living in industrialised countries will develop colonic diverticulae
- Rare < 40 yrs
- RightMsided diverticulae are more common in Asia
Recognise the presenting symptoms of diverticular disease
• Often ASYMPTOMATIC (80M90%)
• Complications can lead to symptoms such as:
o PR bleeding
o Diverticulitis (causing LIF and lower abdominal pain and fever)
o Diverticular fistulation (causing pneumaturia, faecaluria and recurrent UTI)
Identify appropriate investigations for diverticular disease
Identify appropriate investigations for diverticular disease
BLOODS:
o FBC: increased WCC, increased CRP
o Check clotting and crossMmatch if bleeding
BARIUM ENEMA (with or without air contrast):
o Shows presence of diverticulae (saw-tooth appearance of lumen) **
o This reflects pseudohypertrohy of circular muscle
o IMPORTANT: barium enema should NOT be performed in the acute setting because there is a high risk of perforation
FLEX SIG AND COLONOSCOPY
o Diverticulae can be visualised and other pathology (e.g. polyps and tumours) can be excluded
ACUTE SETTING:
CT scan for evidence of diverticular disease and complications may
be performed
How do diverticulae present on barium enema scans?
saw tooth apearance of lumen
What’s the mx plan for diverticulitis?
• Diverticulitis: o IV antibiotics o IV fluid rehydration o Bowel rest o Abscesses ma be drained by radiologically sited drains
Generate a management plan for asymptomatic diverticular disease
o Soluble high-fibre diet (20M30 g/day)
o Some drugs are under investigation for their use in preventing recurrent flares of diverticulitis (such as probiotics and anti-inflammatories)
Identify the possible complications of diverticular disease
- Diverticulitis
- Pericolic abscess
- Perforation
- Faecal peritonitis
- Colonic obstruction
- Fistula formation (bladder, small intestine, vagina)
- Haemorrhage
Define haemochromatosis
• An autosomal recessive disease in which increased intestinal absorption of iron causes accumulation of iron in tissues, which may lead to organ damage.
Typical haemochromatosis presentation
Bronze (tan) skin pigmentation
Hepatomegaly
Diabetes mellitus background
Explain the aetiology/risk factors of haemochromatosis
Explain the aetiology/risk factors of haemochromatosis
• Autosomal recessive
• Caused be a defect in the HFE gene (used to screen family members)
What are the late symptoms of haemochromatosis?
o Diabetes mellitus ** o Bronzed / tan skin ****** o Hepatomegaly ** o Impotence o Amenorrhoea o Hypogonadism o Cirrhosis o Cardiac - arrhythmias* and cardiomyopathy o Neurological and psychiatric problems
Identify appropriate investigations for haemochromatosis
HAEMATINICS***
serum ferritin (HIGH),
transferrin (LOW),
transferrin saturation (HIGH),
TIBC (LOW)
o NOTE: serum ferritin is NOT very specific because it is an acute phase protein
o Serum iron concentration and transferrin saturation do NOT accurately reflect total body iron stores
Patient in post op ward presents with
vomiting, small pupils and respiratory depression
what are you thinking
opiate use/withdraw
Effects: euphoria nausea and vomiting constipation anorexia hypotension respiratory depression* pinpoint pupils* tremor erectile dysfunction
What is given as an antidote for opiate withdraws?
Naloxone
What are the effects of opiate WITHDRAWS?
dilated pupils* lacrimation sweating diarrhoea insomnia tachycardia abdominal carmp like pains* nausa and vomiting
How is opiate dependance managed
methadone
buprenorphine
Whats the difference regarding pupil presentation in opiate USE and opiate WITHDRAW?
opiate use = pinpoint
opiate withdraws = dilated
What does GTN spray do ?
It causes peripheral vasodilatation reducing afterload and resting her myocardium
What are you thinking for a pt with “sob on exertion” with normal ecg normal bloods normal xray.
stable angina
Which AB are contraindicated for pregnancy?
Ciprofloxacin - quinolone - development of arhtropathy in a child
Trimethoprim - folate antagonist - risk of teratogenicity
Which AB can be used in pregnancy?
Co-amoxiclav
Penicillins
What does a pansystolic murmur indicate?
Mitral regurgiation - left ventricular dilatation
What do you expect to find on an ECG for left ventricular hypertrophy?
o Hypertrophic
• LeftMaxis deviation
• Signs of left ventricular hypertrophy
• Q waves in inferior and lateral leads
What is polycystic kidney disease
Autosomal dominant inherited disorder characterised by the development of multiple renal cysts that gradually expand and replace normal kidney substance, variablyas
What are the genetics of PKD?
85% caused by mutations in PKD1 on chromosome 16
This is a membrane-bound multidomain protein involved in cell-cell and cell-matrix interactions
15% caused by mutations of PKD2 on chromosome 4
Whats the pathophysiology of PKD?
Pathophysiology
Proliferative/hyperplastic abnormality of the tubular epithelium
Early on, the cysts are connected to the tubules from which they arise and thefluid content is glomerular filtrate
When cyst diameter >2 mm, they detach from the tubule and the fluid content isderived from secretion of the lining epithelium
With time, the cysts enlarge and cause progressive damage to adjacent functioning nephrons
Summarise the epidemiology of polycystic kidney disease
MOST COMMON inherited kidney disorder
Responsible for 10% of end-stage renal failure
Recognise the presenting symptoms of polycystic kidney disease
Present at 30-40 yrs*
20% have no family history
May be asymptomatic
Flank Pain - may result from cyst enlargement/bleeding, stone, blood clot migration,infection
Haematuria*
Hypertension
Associated with berry aneurysms and may present with subarachnoid haemorrhage
Recognise the findings OE for PKD
Abdominal distension
Enlarged cystic kidneys - palbable masses in flanks
Palpable liver Hypertension
Signs of chronic renal failure (at late stage)
AAA signs
Identify appropriate IX for PKD
US or CT
Multiple cysts bilaterally
Liver cysts
What’s the treatment of status epilepticus?
IV lorazepam (or PR) and repeat every 10
then
IV phenytoin
then consider GA
What is a classic status epilepticus presentation?
Homeless alcoholic found seizing for more than 30 mins
What’s the antidote for paracetamol?
N-acetylcysteine
Recognise the signs of paracetamol overdose on physical examination
- 0-24 hrs - no signs
- 24-72 hrs - liver enlargement and tenderness
- 72+ hrs - jaundice, coagulopathy, hypoglycaemia, renal angle tenderness
What’s the first line treatment of massive PE?
dose of LMWH then warfarin
then consider thrombolysis (if the pt has no haemorrhagiv risk
Whats the treatment for H Pylori? And for how long
TRIPLE THERAPY:
PPI
Metronidazole
Clarithromycin
for 1-2 weeka
What is Zollinger-Ellison syndrome?
RARE cause of ulcer disease
A condition in which a gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas cause overproduction of gastric acid, resulting in recurrent peptic ulcers
What differs between pc of duodenal and gastric ulcer?S
Symptoms have a variable relationship to food intake:
o Gastric - pain is worse SOON after eating
o Duodenal - pain is worse SEVERAL AFTERS HOURS eating
What ix do you do for H pylori
• Testing for H. pylori:
o C13-urea breath test :
• RadioMlabelled urea is given by mouth
• C13 is detected in the expelled air
o Serology:
• IgG antibody against H. pylori confirms exposure to H. pylori but NOT eradication
o Campylobacter-like organism (CLO) test:
• Gastric biopsy is placed with a substrate of urea and a pH indicator
• If H. pylori is present, ammonia is produced from the urea and there is a colour change from yellow to red
Pt comes in following a fall He is a smoker o2 sats 76% ABG: ph normal, po2 low, pco2 high, hco3 high. What are you thinking?
Smoker = suggests COPD
high paco2 and low po2 = type 2 resp failure
which can lead to respiratory acidosis
which is then compensates by hco3 (thats why ph is normal)
