Laz - make a medic / MLA Flashcards

1
Q

define achalasia

A

A disease characterised by intermittent dysphagia due to failure of relaxation of the lower oesophageal sphincter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

pathophysiology of achalasia?

A

Occurs due to degeneration of ganglion cells of the myenteric plexus in the oesophagus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

symptoms of achalasia - how does it present ?

A

Intermittent dysphagia involving solids and liquids

Regurgitation

Heartburn

Weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ix for supsected achalasia ?

A

barium swallow - you would see Birds’ beak

CXR you would see widened mediastinum

Manometry: shows increased pressure at the lower oesophageal sphincter

Endoscopy: exclude malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how to manage achalasia ?

A

Medical (aims to relax the lower oesophageal sphincter)

Nitrates

Calcium Channel Blockers (e.g. Nifedipine)

Surgical

Pneumatic dilation

Peroral endoscopic myotomy (POEM)

Botulinum toxin injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

path of coeliac disease

A

Inflammatory immune response to the gliadin component of gluten within the small bowel, resulting in intestinal malabsorption.

The presence of gluten within the duodenum triggers an immunological reaction resulting in a number of cellular and architectural changes within the lining of the duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

characteristic changes of GI in coeliac - and what part of GI?

A

duodenum:

Subtotal villous atrophy

Crypt hyperplasia

Increased intraepithelial lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does coeliac present ?

A

Chronic diarrhoea

Malabsorption of nutrients → Failure to thrive, weight loss

Tiredness

Abdominal discomfort

Itchy elbows (dermatitis herpetiformis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ix for coeliac disease

A

FBC (anaemia)

iron and folate

Anti-tissue transglutaminase antibodies: positive

NOTE: This is an IgA antibody. Patients should also have their serum IgA levels measured as patient with selective IgA deficiency (relatively common in the population) would have a false negative anti-tTG result.

Anti-Endomysial Antibodies (IgA and IgG)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

vaccine in coeliac disease ?

A

Patients with coeliac disease often have a degree of functional hyposplenism

For this reason, all patients with coeliac disease are offered the pneumococcal vaccine

Coeliac UK recommends that everyone with coeliac disease is vaccinated against pneumococcal infection and has a booster every 5 years

Currrent guidelines suggest giving the influenza vaccine on an individual basis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how does crohns present ?

A

Chronic diarrhoea (may be bloody)

Abdominal pain

Malaise

Weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ix for crohns

A

Bloods

FBC: anaemia

CRP/ESR: raised

Imaging

CT Scan: inflammation of the bowel wall

Barium Follow-Through: identify strictures

Other

OGD/Colonoscopy and Biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

management for crohns

A

Inducing Remission

Initial Agents

Glucocorticoids

E.g. prednisolone, methylprednisolone, IV hydrocortisone

Consider enteral nutrition as an alternative to steroids in:

Children and young people with concerns about growth and side-effects

Consider budesonide in people with:

One or more of distal ileal, ileocaecal or right-sided colonic disease

AND
Conventional steroids are not appropriate (e.g. not tolerated)

Consider aminosalicylates if steroids are not tolerated (e.g. mesalamine/mesalazine or sulfasalazine)

Add-Ons

Consider adding azathioprine or mercaptopurine to steroid treatment if:

2 or more exacerbations in 12 months

Glucocorticoid dose cannot be tapered

WARNING: assess thiopurine methyltransferase (TPMT) levels before starting azathioprine or mercaptopurine

Consider methotrexate as a second-line add-on if azathioprine or mercaptopurine are not tolerated

Biologics

Consider infliximab or adalimumab for adults with severe active Crohn’s disease who have not responded to conventional therapy (immunosuppressants)

Maintaining Remission

Avoid smoking

NOTE: smoking makes Crohn’s worse and ulcerative colitis better

Offer azathioprine or mercaptopurine as monotherapy

Consider methotrexate if:

Needed methotrexate to maintain remission

Azathioprine and mercaptopurine not tolerated or contraindicated

Do NOT offer glucocorticoids to maintain remission

Maintaining Remission Post-Operatively

Consider azathioprine with metronidazole

Surgery

Consider surgery early on in the disease if it is mainly confined to the terminal ileum

Consider surgery in children and young people who have refractory disease or a growth impairment despite maximal medical treatment

Strictures

Consider balloon dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which biologics for crohns ?

A

infliximab or adalimumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which bacteria give you bloody diarrheoa gastroenteritis ?

A

Blood diarrhoea

More commonly associated with ‘CHESS’ bacteria (Campylobacter, Haemorrhagic E.coli, Entamoeba histolytica, Salmonella, Shigella)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ix for gastroenteritis

A

Bloods

U&E: assess extent of dehydration

Stool

Faecal microscopy and culture

Faecal C. difficile toxin assay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how to manage gastroenteritis ?

A

Usually managed conservatively with oral fluid rehydration as the disease is normally self-limiting

Correct electrolyte imbalances

Antibiotics may be considered in severe infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

risk factors for GORD ?

A

Obesity

Pregnancy

Hiatus Hernia

Alcohol excess

Smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does GORD present ?

A

Epigastric pain

NOTE: check for triggers (e.g. spicy food)

Abnormal taste in mouth

Dysphagia

Chronic cough (worse at night and when lying down)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ix for GORD ?

A

Largely a clinical diagnosis

Bloods

FBC: anaemia may be suggestive of a bleeding ulcer/malignancy

Other

ECG (always consider cardiac causes of chest/epigastric pain)

24 hour oesophageal pH monitoring

Upper GI endoscopy (exclude malignancy)

Helicobacter pylori breath test and stool antigen

NOTE: 2 week washout period following PPI treatment must be observed before testing for H. pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Explain H pylori breath test ?

A

H pylori express Urease enzyme

patient swallows pill containing urea with carbon-13/14 isotope. If H pylori present, then CO2 is produced with the isotope. Therefore if labelled CO2 is detected by the analyser, then H pylori is present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

GORD management

A

Conservative

Weight loss

Avoid precipitants (e.g. alcohol, spicy food)

Stop smoking

Sleep propped up

Uninvestigated Dyspepsia

Offer empirical high-dose PPI therapy for 4 weeks for people with uninvestigated dyspepsia

Offer H. pylori ‘test and treat’

Offer histamine antagonist (e.g. nizatidine) if there is an inadequate response to the PPI

Gastro-oesophageal Reflux Disease

Offer full-dose PPI for 4-8 weeks

If symptoms recur after initial treatment, offer long-term PPI at lowest dose possible that achieves symptom control

Offer histamine antagonist if the response to the PPI is inadequate

Referral to gastroenterologist for persistent/refractory GORD

Surgical

Nissen fundoplication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is zollinger-ellison syndrome ?

A

Zollinger-Ellison syndrome is a rare condition where a duodenal or pancreatic tumour secretes excessive quantities of gastrin.

Gastrin is a hormone that stimulates acid secretion in the stomach. Therefore, there is excess production of stomach acid, resulting in severe dyspepsia, diarrhoea and peptic ulcers.

Gastrin-secreting tumours (gastrinomas) may be associated with multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant genetic condition, which can also cause hormone-secreting tumours of the parathyroid and pituitary glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

how does IBS present ?

A

Bloating

Abdominal discomfort (often relieved by defecation)

Constipation and diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
ix for IBS ?
Often a diagnosis of exclusion Tests to Exclude Other Causes Coeliac Disease: FBC, anti-tTG antibodies IBD: faecal calprotectin, endoscopy
26
how to manage IBS ?
Conservative Advice and reassurance Encourage identification of precipitants Stress management (exercise, mindfulness, gut-directed hypnotherapy) Medical If predominantly diarrhoeal symptoms: Reduce intake of insoluble fibre If predominantly symptoms of constipation: Try soluble fibre supplements (e.g. ispaghula) or foods high in fibre Consider bulk-forming laxatives or loperamide depending on nature of symptoms If complaining of abdominal pain: Consider antispasmodic (e.g. mebeverine hydrochloride or hyoscine butylbromide) Consider trial of low-dose tricyclic antidepressant (e.g. amitriptyline) Consider trial of SSRI Consider referral to dietician for specialised diet (e.g. FODMAP)
27
who gets a mallory weiss tear ?
Alcohol excess Bulimia
28
how does mallory weiss tear present ?
Epigastric discomfort Recent history of severe vomiting Haematemesis Melaena
29
ix and mx for mallory weiss tear
Usually does not require active investigation and management Bloods FBC: microcytic anaemia Other OGD (looking for varices) Management Heals spontaneously the majority of the time Consider PPIs Interventional Endoscopy and sclerotherapy
30
causes / risk factors for peptic ulcer disease ?
Helicobacter pylori Drugs (NSAIDS, steroids, bisphosphonates, SSRIs, aspirin) Smoking Alcohol Excess
31
pathophysiology for peptic ulcer disease ?
Development of ulcers within the gastric and duodenal mucosa due to increased exposure to stomach acid. Aetiology and Risk Factors Occurs due to excessive acid and pepsin activity and insufficient mucosal defence systems
32
how does peptic ulcer disease present ?
Epigastric pain Gastric: may occur whilst eating food Duodenal: may occur hours after eating food Melaena
33
pain characteristics gastric vs duodenal ulcer and why ?
gastric = pain often worsens by eating as food stimulates acid production in stomach duodenal = pain worse when hungry/empty stomach or at night. No food to neutralise the acid. pain is relieved by eating.
34
ix for peptic ulcer disease
FBC: microcytic anaemia U&E: raised urea may be suggestive of upper gastrointestinal bleed Other Endoscopy and Biopsy Required urgently in patients with dysphagia, significant acute gastrointestinal bleeding or those aged 55 years or older with unexplained weight loss and symptoms of upper abdominal pain, reflux or dyspepsia Urease Breath Test (non-invasive detection of H. pylori) CT Scan (in cases of perforation)
35
management of peptic ulcer disease
Management Lifestyle changes (e.g. smoking cessation) Review drug history, consider reducing/substituting NSAIDs Offer H. pylori eradication therapy (three treatments, twice daily for 7 days) if tested positive for H. pylori PPI (e.g. omeprazole) Amoxicillin Clarithromycin OR Metronidazole NOTE: clarithromycin can be given with metronidazole in penicillin-allergic patients, other options include levofloxacin and tetracyclines Offer patients with an ulcer and H. pylori a repeat endoscopy 6-8 weeks after beginning treatment to confirm healing Offer high-dose PPI for 4-8 weeks then low-dose if symptoms recur Offer histamine antagonist if the response to treatment with a PPI is inadequate Interventional Endoscopy and Sclerotherapy/Coagulation
36
features of UC
Chronic diarrhoea Rectal bleeding Tenesmus Abdominal pain Weight loss Extra-GI Manifestations (uveitis, erythema nodosum)
37
Ix for UC
FBC: raised inflammatory markers Other Stool: faecal calprotectin Endoscopy (Flexible Sigmoidoscopy or Colonoscopy)
38
management for UC
Severity can be assessed using the Truelove and Witts severity index Mild-to-Moderate Disease Proctitis Induce Remission 1st Line: Topical Aminosalicylate 2nd Line: Add Oral Aminosalicylate 3rd Line: Add Topical OR Oral Steroid Maintain Remission Topical Aminosalicylate Oral Aminosalicylate with Topical Aminosalicylate Oral Aminosalicylate Alone Proctosigmoiditis and Left-Sided Ulcerative Colitis Induce Remission 1st Line: Topical Aminosalicylate 2nd Line: Add High-Dose Oral Aminosalicylate OR Switch to High-Dose Oral Aminosalicylate AND Topical Steroid 3rd Line: Stop Topical Treatment AND Start Oral Aminosalicylate AND Oral Steroid Maintain Remission Oral Aminosalicylate Extensive Disease Induce Remission 1st Line: Topical Aminosalicylate AND High-Dose Oral Aminosalicylate 2nd Line: Stop Topical Aminosalicylate AND Start High-Dose Oral Aminosalicylate AND Oral Steroid Maintain Remission Oral Aminosalicylate All Types of Disease Consider Oral Azathioprine or Oral Mercaptopurine to maintain remission: After 2 or more exacerbations requiring corticosteroids in 12 months If remission is not maintained by aminosalicylates alone Severe Disease (either first presentation or acute exacerbation) Step 1: IV Corticosteroids (e.g. Hydrocortisone 100 mg QDS) Alternative: IV Ciclosporin Step 2: Add IV Ciclosporin and Consider Surgery - if little/no improvement in 72hrs Alternative: Infliximab Features Increasing the Need for Surgery > 8 bowel motions per day Pyrexia Tachycardia Abdominal X-ray showing colonic dilatation (toxic megacolon) Low albumin, low haemoglobin, high platelet count, CRP above 45 mg/L
39
how to manage alc hep?
Alcohol Abstinence Alcohol Withdrawal: Chlordiazepoxide + Pabrinex Symptomatic Ascites: drain, diuretics, albumin Encephalopathy: lactulose, rifaximin Nutritional Supplementation Consider steroid treatment Sometimes used in severe alcoholic hepatitis with a Maddrey's Discriminant Function of 32 or more Consider liver transplantation
40
LFT pattern in alc hep?
gamma-GT is characteristically elevated the ratio of AST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis
41
different grades of HE?
Symptoms Grade 1: altered mood/behaviour, minimal change GCS Grade 2: asterixis, drowsy Grade 3: confused, incoherent Grade 4: comatose, unresponsive to pain GCS 3
42
mx for HE?
Management Treat underlying cause Lactulose (decreases intestinal production and absorption of ammonia) Rifaximin (modifies gut microbiome to reduce production of nitrogenous products that would then be absorbed and cause encephalopathy) Liver transplant
43
what does presence of E antigen mean in HBV serology?
active infection highly infective
44
PBC vs PSC
PSC - extra and intrahepatic bile ducts PBC - intrahepatic bile ducts
45
what is SAAG, explain and give examples ...
Serum ascites albumin gradient (SAAG) is a measure that is used to distinguish different causes of ascites. Equation SAAG = Serum Albumin Concentration - Ascites Albumin Concentration Interpretation 11 g/L or More Generally transudative causes Cirrhosis Heart Failure Renal Failure 11 g/L or Less Generally exudative causes (because inflammation leads to an increase in vascular permeability which, in turn, causes more protein leakage into the ascitic fluid) Peritonitis Malignancy Tuberculosis Nephrotic Syndrome This is an anomaly as it is NOT exudative. It causes a low SAAG because the patients lose albumin through their urine resulting in a low serum albumin concentration.
46
outline hereditary haemachromatosis
Definition Autosomal recessive disease of HFE gene resulting in increased intestinal absorption of iron which deposits in tissues causing organ damage Symptoms Asymptomatic until later stages of disease (50 years old) Pancreas → Diabetes mellitus Liver → Cirrhosis, liver failure, hepatomegaly Heart: Cardiac arrhythmias & myopathy Pituitary Gland and Sex Organs → Amenorrhoea, impotence, hypogonadism Skin → Tanned complexion Other → Arthropathy, fatigue Investigations Haematinics High Iron level Due to increased duodenal absorption of iron High Ferritin Ferritin is used by cells to take store iron IN (ferrous-IN) Increased ferritin to store iron in cells and out of the plasma Low Transferrin Transferrin carries iron in blood. When iron levels are low, transferrin increases to compensate. Thus if there are high iron levels then level of transferrin will be low Low TIBC TIBC measures the blood’s ability to bind iron to transferrin. As transferrin is low, it’s harder for iron to bind to it, meaning the TIBC is low Management Regular therapeutic phlebotomy (venesection) Personalised to individual in terms of frequency and volume of blood removed Iron-chelating medications eg. desferrioxamine
47
biochem features of refeeding syndrome ?
Biochemical Features: Hypophosphatemia others include: hypokalaemia, hypomagnesemia
48
outline wilsons disease
Definition Autosomal recessive disorder characterised by excessive accumulation of copper within body tissues. Aetiology and Risk Factors Occurs due to a mutation in copper transporting ATPase on chromosome 13 Reduced copper excretion leads to an accumulation within the circulation Deposition of copper within the liver and basal ganglia leads to cell death and dysfunction Symptoms Hepatic Features Jaundice Easy Bruising Encephalopathy Neuropsychiatric Features Personality Change Psychosis Movement Disorder Copper can deposit in the cornea (Kayser-Fleischer rings), heart (cardiomyopathy), kidneys (renal tubular dysfunction), bones (arthritis and osteoporosis) Investigations Bloods LFTs: Likely to be deranged Caeruloplasmin: Low Total Serum Copper: Low Though FREE serum copper (i.e. unbound to ceruloplasmin) will be raised 24 Hour Urinary Copper Excretion: High Other Liver Biopsy Genetic Analysis Management Medical Penicillamine (copper chelator) Zinc Therapy (blocks copper absorption in the intestines) Trientine Surgical Liver Transplantation
49
outline acoustic neuroma ?
Definition Schwann cell-derived tumour of cranial nerve VIII. Also known as a vestibular schwannoma. Aetiology and Risk Factors Arising from the vestibulocochlear nerve (cranial nerve VIII) Bilateral vestibular schwannomas are a common feature of Neurofibromatosis Type 2 Clinical Features Tinnitus Progressive sensorineural hearing loss Dizziness Facial numbness (advanced tumours) Investigations Bedside Otoscopy (rule out other causes of hearing loss) Tuning Fork Tests Imaging & Other Pure Tone Audiometry MRI Brain Management Active surveillance (if very small) Surgical excision Targeted radiotherapy
50
how does acoustic neuroma present ?
Clinical Features Tinnitus Progressive sensorineural hearing loss Dizziness Facial numbness (advanced tumours)
51
outline BPPV
Definition Vertiginous disorder characterised by sudden-onset dizziness triggered by certain head movements. Aetiology and Risk Factors Pathophysiology There are crystals (otoliths and otoconia) within an area of the inner ear called the utricle which are responsible for regulating orientation based on head movements. In BPPV, these crystal become displaced and migrate into the semicircular canals where it can cause abnormal endolymph displacement and the apparent sensation of movement. This gives rise to vertigo. Symptoms & Signs Sudden sensation of the room spinning that may resolve spontaneously Often triggered by a specific movement (e.g. turning head to the left) Investigations Bedside Dix-Hallpike Manoeuvre (diagnostic) Epley Manoeuvre (therapeutic) HINTS Examination (check for central cause of vertigo) Imaging & Other CT Head Posterior circulation stroke is an important differential in people presenting for the first time with vertiginous symptoms (especially if they have multiple risk factors and the vertigo is not resolving) Management Consider watchful waiting Offer Epley Manoeuvre Suggest Brandt-Daroff exercises that patients can perform at home Symptomatic treatment (e.g. prochlorperazine)
52
manoevres for BPPV
Dix-Hallpike Manoeuvre (diagnostic) Epley Manoeuvre (therapeutic)
53
sx of labrinthitis / vestibular neuronitis
Sudden vertigo Tinnitus Preceding symptoms of upper respiratory tract infection
54
menieres vs labrinthitis vs BPPV
Meniere's Disease: Presents with acute episodes of vertigo with sensory symptoms (ear fullness, tinnitus) Labyrinthitis and Vestibular Neuronitis: Usually presents with constant symptoms of subacute onset that worsens within 24-48 hours and resolves spontaneously after several days. May cause auditory symptoms. Thought to be related to a viral infection. Benign Paroxysmal Positional Vertigo: Presents with episodic vertigo that is fleeting (lasts seconds to minutes). Usually triggered by a certain movement.
55
ix and mx for menieres
Investigations Bedside Dix-Hallpike Manoeuvre (as BPPV is a differential) Tuning Fork Test Imaging & Other Pure Tone Audiometry Management Acute Treatment Short course of prochlorperazine or an antihistamine (e.g. cyclizine) If Severe: IM Prochlorperazine or Cyclizine If no improvement within 5-7 days, consider an alternative diagnosis Prevention Betahistine
56
how does menieres present ?
Symptoms Episodic Sudden vertigo Nausea and vomiting Tinnitus Hearing loss Ear fullness Signs Unilateral hearing loss Nystagmusou
57
outline otosclerosis
Definition Abnormal bone formation around the stapes impedes the normal movement of the ossicular chain, thereby resulting in conductive hearing loss. Aetiology and Risk Factors There is often a family history Typically presents in people aged 15-35 years Symptoms Hearing loss (particularly to low-frequency sounds) Signs Normal ear drum appearance on otoscopy Investigations Bedside Otoscopy Imaging & Other Pure Tone Audiometry High Resolution CT Management Conservative Management Auditory rehabilitation Assisted listening devices Medical Management Bisphosphonates can reduce adverse bone remodeling Hearing aids Surgical Management Stapedectomy (involves removal of the stapes and replacement with a prosthesis)
58
outline pinna haematoma
Definition Collection of blood within the pinna resulting from blunt trauma. Aetiology and Risk Factors Blunt trauma Clinical Features Swelling of the pinna soon after injury Investigations Primarily a clinical diagnosis Management Drain the haematoma before it solidifies (ideally within 24 hours of injury) Rule out other injuries
59
outline presbyacusis
Definition Progressive sensorineural hearing loss that occurs as patients grow older. Aetiology and Risk Factors Age is the main risk factor Symptoms Progressive bilateral hearing loss that initially primarily affects higher frequencies Investigations Bedside Otoscopy Tuning Fork Tests Imaging & Other Pure Tone Audiometry Management Hearing aids Cochlear implants Middle ear implants
60
acute rhinosinusitis classifications
Classification Viral Post-Viral Bacterial Common Organisms: S. pneumoniae, S. aureus, M. catarrhalis and H. influenzae
61
define acute rhinosinusitis
Inflammation of the mucosal lining of the nasal passages and surrounding sinuses that lasts less than 12 weeks
62
risk factors and complications of rhinosinusitis
Risk Factors Nasal polyps Septal deviation Cystic fibrosis Complications Periorbital and Orbital Cellulitis Periorbital: swelling of eye lid and pain around the eye Orbital: infection of the soft tissues of the eye socket behind the orbital septum Meningitis Brain Abscess Osteomyelitis
63
periorbital vs orbital cellultiis
Periorbital: swelling of eye lid and pain around the eye Orbital: infection of the soft tissues of the eye socket behind the orbital septum
64
clinical features of rhinosinusitis
Clinical Features Preceding coryzal symptoms Nasal discharge Facial pain Anosmia Headache
65
management of acute rhinosinusitis
Management Symptoms present for < 10 days Advise symptomatic management with paracetamol and ibuprofen NO need for antibiotics Symptoms present for > 10 days Consider high-dose nasal corticosteroid for 14 days (e.g. mometasone 200 µg BD) Consider back-up antibiotic prescription (to be used if symptoms worsen rapidly or fail to improve within 7 days) Usually phenoxymethylpenicillin 500 mg QDS for 5 days Consider Referral to Secondary Care if: Frequent recurrent episodes (more than 3 episodes requiring antibiotics in a year) Treamtent failure after extended courses of antibiotics Unusual or resistant bacteria Anatomical defects causing obstruction Immunocompromise Suspected allergic or immunological cause Comorbidities complicating management (e.g. nasal polyps)
66
define chronic rhinosinusitis
Generally defined as symptoms of sinusitis lasting more than 1 hour every day for over 2 weeks.
67
chronic rhinosinusitus causes?
Infection Allergic (season or perennial) Systemic diseases (e.g. cystic fibrosis) Drug-induced (can be caused by excessive use of decongestants)
68
features of chronic rhinosinusitis
Nasal congestion Rhinorrhoea Dry cough due to post-nasal drip Headache
69
mx for chronic rhinosinusitis
Management Avoid allergens Medical Management Intranasal Steroids Antihistamines Nasal Decongestants Surgical Management Functional Endoscopic Sinus Surgery Turbinate Reduction
70
where is the nose are old people more likely to experience epistaxis - why is this ? why old people ?
Posterior Nasal Septum Posterior bleeds are more common in elderly patients and tend to be more serious Sclerotic vessels fail to constrict sufficiently, leading to prolonged bleeding and clot formation. This clot can become dislodged and cause fatal airway obstruction. Commonly arise from the Woodruff plexus
71
key questions in a nosebleed hx
Key Questions: duration, interventions attempted, trauma, comorbidities and medications
72
ix for epistaxis
Bedside Examine oropharynx for evidence of a posterior bleed Examine nasopharynx using thudicum Bloods FBC, Clotting, G&S
73
epistaxis management
Management In Severe Cases --> A to E Assessment and Resuscitation IV Fluids Blood Products Reversal of Anticoagulation Conservative Measures Sit leaning forward and pinch soft cartilage of lower nose for 10-20 minutes Ice pack on nose or sucking ice cube 1. Anterior Bleed Nasal Cauterisation Adrenaline-soaked gauze Cauterisation with silver nitrate stick If Bleeding Persists and No Visible Bleeding Point Anterior Packing with Rapid Rhino 2. if Bleeding Persists with Evidence of Posterior Bleed Posterior Packing with Foley Catheter If Nasal Packing Fails Consider Surgical Intervention Usually involves ligation of the sphenopalatine artery, anterior ethmoidal artery or external carotid artery
74
what happens if you don't sort out a septal haematoma ?
Blunt trauma to the nose leads to separation of the nasal septal cartilage from the overlying perichondrium resulting in damage to blood vessels. Blood collects under the mucosal lining of the septum resulting in the formation of a septal haematoma. If untreated, it can result in avascular necrosis of the septal cartilage that leads to a saddle nose deformity
75
management of nasal polyps
Management Medical Management Symptoms of Rhinosinusitis --> Antihistamines Small Polyps --> Topical Steroids Large Polyps --> Oral Steroids Steroid Maintenance --> Steroid Nasal Spray Surgical Management Nasal Polypectomy
76
features of branchial cyst
Clinical Features Palpable, fluctuant neck lump (anterior to the sternocleidomastoid) Can become infected causing pain and a rapid increase in size Large cysts can affect swallowing, speaking and breathing Does NOT usually transilluminate (unlike cystic hygromas)
77
clinical features of thyroglossal cyst
Clinical Features Painless midline neck mass Can become infected resulting in pain and an acute increase in size Mass moves up upon tongue protrusion
78
how to manage a quinsy
Aspiration or Incision & Drainage Analgesia IV Fluids IV Antibiotics IV Steroids (usually dexamethasone to reduce the swelling) Complications Retropharyngeal Abscess Airway Obstruction Aspiration Pneumonitis Sepsis Post-Streptococcal Glomerulonephritis
79
how does quinsy present in terms of signs & sx
Symptoms Fever Sore Throat Voice Change (may be described as hot potato voice) Odynophagia Trismus Drooling Signs Unilateral tonsillar swelling Uvula deviation Lymphadenopathy
80
define epiglottitis and what is the usual bug?
Epiglottitis is inflammation and swelling of the epiglottis caused by infection, typically with haemophilus influenza type B
81
how does epiglottitis present ?
Presentation Suggesting Possible Epiglottitis Patient presenting with a sore throat and stridor Drooling Tripod position, sat forward with a hand on each knee High fever Difficulty or painful swallowing Muffled voice Scared and quiet child Septic and unwell appearance
82
ix for epiglottisi
If the patient is acutely unwell and epiglottitis is suspected then investigations should not be performed. Performing a lateral xray of the neck shows a characteristic “thumb sign” or “thumbprint sign”. This is a soft tissue shadow that looks like a thumb pressed into the trachea. This is caused by the oedematous and swollen epiglottis. Neck xrays are also useful for excluding a foreign body.
83
adolescent with a sore throat, who develops an itchy rash after taking amoxicillin
infectious Mononucleosis causes an intensely itchy maculopapular rash in response to amoxicillin or cefalosporins.
84
features of infectious mononnucleosis
Fever Sore throat Fatigue Lymphadenopathy (swollen lymph nodes) Tonsillar enlargement Splenomegaly and in rare cases splenic rupture
85
monospot test
EBV (infectious mononucleosis) Monospot test: this introduces the patient’s blood to red blood cells from horses. Heterophile antibodies (if present) will react to the horse red blood cells and give a positive result.
86
management of INfectious mononucleosis
Infectious mononucleosis is usually self limiting. The acute illness lasts around 2 – 3 weeks, however it can leave the patient with fatigue for several months once the infection is cleared. Patients are advised to avoid alcohol, as EBV impacts the ability of the liver to process the alcohol. Patients are advised to avoid contact sports due to the risk of splenic rupture. Emergency surgery is usually required if splenic rupture occurs.
87
features of OSA
Features Episodes of apnoea during sleep (reported by their partner) Snoring Morning headache Waking up unrefreshed from sleep Daytime sleepiness Concentration problems Reduced oxygen saturation during sleep
88
how to more objectively classify OSA ? What tool can you use ?
Epworth Sleepiness Scale The Epworth Sleepiness Scale is used to assess symptoms of sleepiness associated with obstructive sleep apnoea. TOM TIP: If interviewing someone you suspect has obstructive sleep apnoea, ask about daytime sleepiness and occupation. Daytime sleepiness is a crucial feature that should make you suspect obstructive sleep apnoea. Patients that need to be fully alert for work, for example, heavy goods vehicle operators, require an urgent referral and may need amended work duties whilst awaiting assessment and treatment.
89
mx OSA
Management Patients with obstructive sleep apnoea require referral to an ENT specialist or a specialist sleep clinic to perform sleep studies. This involves the patient sleeping in a laboratory whilst staff monitor their oxygen saturation, heart rate, respiratory rate and breathing to establish any episodes of apnoea and the extent of their snoring. The first step in management is to correct reversible risk factors by advising them to stop drinking alcohol, stop smoking and lose weight. The next step is to use a continuous positive airway pressure (CPAP) machine that provides continuous pressure to maintain the patency of the airway. Surgery is another option. This involves quite significant surgical reconstruction of the soft palate and jaw. The most common procedure is called uvulopalatopharyngoplasty (UPPP).
90
causes of otitis externa
The inflammation in otitis externa may be caused by: Bacterial infection Fungal infection (e.g., aspergillus or candida) Eczema Seborrhoeic dermatitis Contact dermatitis
91
swimmers ear is...
otitis externa
92
The two most common bacterial causes of otitis externa are:
Pseudomonas aeruginosa Staphylococcus aureus
93
where does pseudomonas aerginosa like to grow ?
warm moist oxygen rich environments... e.g. otitis externa colonise the lungs in CF Pseudomonas aeruginosa. It is a gram-negative aerobic rod-shaped bacteria. It likes to grow in moist, oxygenated environments. Other than causing otitis externa, an important exam-related point to remember is that it can colonise the lungs in patients with cystic fibrosis, significantly increasing their morbidity and mortality. It is naturally resistant to many antibiotics, making it very difficult to treat in children with cystic fibrosis. It can be treated with aminoglycosides (e.g., gentamicin) or quinolones (e.g., ciprofloxacin).
94
how does OE present ?
Presentation The typical symptoms of otitis externa are: Ear pain Discharge Itchiness Conductive hearing loss (if the ear becomes blocked) Examination can show: Erythema and swelling in the ear canal Tenderness of the ear canal Pus or discharge in the ear canal Lymphadenopathy (swollen lymph nodes) in the neck or around the ear The tympanic membrane may be obstructed by wax or discharge. It may be red if the otitis externa extends to the tympanic membrane. If it is ruptured, the discharge in the ear canal might be from otitis media rather than otitis externa.
95
mx OE
Mild otitis externa may be treated with acetic acid 2% (available over the counter as EarCalm). Acetic acid has an antifungal and antibacterial effect Moderate otitis externa is usually treated with a topical antibiotic and steroid, for example: Neomycin, dexamethasone and acetic acid (e.g., Otomize spray) severe or systemic symptoms may need oral antibiotics (e.g., flucloxacillin or clarithromycin) or discussion with ENT for admission and IV antibiotics. An ear wick may be used if the canal is very swollen, and treatment with ear drops or sprays will be difficult
96
what is a really bad thing to happen with otititis externa ?
Malignant otitis externa is a severe and potentially life-threatening form of otitis externa. The infection spreads to the bones surrounding the ear canal and skull. It progresses to osteomyelitis of the temporal bone of the skull. Malignant otitis externa is usually related to underlying risk factors for severe infection, such as: Diabetes Immunosuppressant medications (e.g., chemotherapy) HIV
97
mx for malignant otitis externa
Malignant otitis externa requires emergency management, with: Admission to hospital under the ENT team IV antibiotics Imaging (e.g., CT or MRI head) to assess the extent of the infection It can lead to complications of: Facial nerve damage and palsy Other cranial nerve involvement (e.g., glossopharyngeal, vagus or accessory nerves) Meningitis Intracranial thrombosis Death
98
outline anatomy and how it occurs for otittis media
Otitis media is the name given to an infection in the middle ear. The middle ear is the space that sits between the tympanic membrane (eardrum) and the inner ear. This is where the cochlea, vestibular apparatus and nerves are found. Bacteria enter from the back of the throat through the eustachian tube. A viral upper respiratory tract infection often precedes bacterial infection of the middle ear.
99
which bacteria for otitis media ?
Bacteria The most common bacterial cause of otitis media is streptococcus pneumoniae. This also commonly causes other ENT infections such as rhino-sinusitis and tonsillitis. Other common causes include: Haemophilus influenzae Moraxella catarrhalis Staphylococcus aureus
100
presentation and exam findings for otitis media
Presentation Ear pain is the primary presenting feature of otitis media in adults. It may also present with: Reduced hearing in the affected ear Feeling generally unwell, for example with fever Symptoms of an upper airway infection such as cough, coryzal symptoms and sore throat When the infection affects the vestibular system, it can cause balance issues and vertigo. When the tympanic membrane has perforated, there may be discharge from the ear. Examination An otoscope is used to visualise the tympanic membrane whilst gently pulling the pinna up and backwards. It may be challenging to visualise the tympanic membrane if there is significant discharge or wax in the ear canal. A normal tympanic membrane is “pearly-grey”, translucent and slightly shiny. You should be able to visualise the malleus through the membrane. Look for a cone of light reflecting the light of the otoscope. Otitis media will give a bulging, red, inflamed looking membrane. When there is a perforation, you may see discharge in the ear canal and a hole in the tympanic membrane.
101
mx for otitis media
Most otitis media cases will resolve without antibiotics within around three days, sometimes up to a week. Antibiotics make little difference to symptoms or complications. Complications (mainly mastoiditis) are rare. Simple analgesia (e.g., paracetamol or ibuprofen) can be used for pain and fever. There are three options for prescribing antibiotics: Immediate antibiotics Delayed prescription No antibiotics Consider immediate antibiotics at the initial presentation in patients who have significant co-morbidities, are systemically unwell or are immunocompromised. Consider a delayed prescription that can be collected and used after three days if symptoms have not improved or have worsened at any time. This can be a helpful strategy in patients pressing for antibiotics or where you suspect the symptoms might worsen. The NICE clinical knowledge summaries (updated January 2021) suggest: Amoxicillin for 5-7 days first-line Clarithromycin (in pencillin allergy) Erythromycin (in pregnant women allergic to penicillin)
102
what complication do you worry about in otitis media ?
mastoiditis
103
abx for bacterial tonsilitis
penicillin V (phenoxymethylpenicillin)
104
most common cause of tonislitis ?
viral
105
most commmon bacterial cause of tonsilitis
group A streptococcus (Streptococcus pyogenes)
106
tools for tonsilitis
Centor Criteria The Centor criteria can be used to estimate the probability that tonsillitis is due to bacterial infection and will benefit from antibiotics. A score of 3 or more gives a 40 – 60 % probability of bacterial tonsillitis, and it is appropriate to offer antibiotics. A point is given if each of the following features are present: Fever over 38ºC Tonsillar exudates Absence of cough Tender anterior cervical lymph nodes (lymphadenopathy) FeverPAIN Score The FeverPAIN score is an alternative to the Centor criteria. A score of 2 – 3 gives a 34 – 40% probability, and 4 – 5 gives a 62 – 65% probability of bacterial tonsillitis: Fever during previous 24 hours P – Purulence (pus on tonsils) A – Attended within 3 days of the onset of symptoms I – Inflamed tonsils (severely inflamed) N – No cough or coryza Consider prescribing antibiotics if the Centor score is ≥ 3, or the FeverPAIN score is ≥ 4
107
pre renal AKI causes
Dehydration Shock (e.g., sepsis or acute blood loss) Heart failure
108
renal AKI causes ?
Renal causes are due to intrinsic disease in the kidney. This may be due to: Acute tubular necrosis Glomerulonephritis Acute interstitial nephritis Haemolytic uraemic syndrome Rhabdomyolysis
109
post renal AKI causes
Post-renal causes involve obstruction to the outflow of urine away from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy. Obstruction may be caused by: Kidney stones Tumours (e.g., retroperitoneal, bladder or prostate) Strictures of the ureters or urethra Benign prostatic hyperplasia (benign enlarged prostate) Neurogenic bladder
110
acute tubular necrosis vs acute interstitial nephritis
ATN = damage and death (necrosis) of epithelial cells of renal tubules. you get muddy brown casts on urinaalysis e.g. due to ischaemia/ nephrotoxins AIN = inflammation of interstitium (space) between vessels and tubules caused by immune reaction. e.g. drugs, infection, autoimmune
111
sx of prostate pathology
good way to remmeber is FUN WISE (frequency, urgency, nocturia, weak stream, intermittency, straining, emptying incompletely) Hesitancy – difficult starting and maintaining the flow of urine Weak flow Urgency – a sudden pressing urge to pass urine Frequency – needing to pass urine often, usually with small amounts Intermittency – flow that starts, stops and varies in rate Straining to pass urine Terminal dribbling – dribbling after finishing urination Incomplete emptying – not being able to fully empty the bladder, with chronic retention Nocturia – having to wake to pass urine multiple times at night
112
ix for BPH
Digital rectal examination (prostate exam) to assess the size, shape and characteristics of the prostate Abdominal examination to assess for a palpable bladder and other abnormalities Urinary frequency volume chart, recording 3 days of fluid intake and output Urine dipstick to assess for infection, haematuria (e.g., due to bladder cancer) and other pathology Prostate-specific antigen (PSA) for prostate cancer, depending on the patient preference
113
management for BPH
Patients with mild and manageable symptoms may not require interventions. The medical options are: Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with rapid improvement in symptoms 5-alpha reductase inhibitors (e.g., finasteride) gradually reduce the size of the prostate The general idea is that alpha-blockers are used to treat immediate symptoms, and 5-alpha reductase inhibitors are used to treat enlargement of the prostate. They may be used together where patients have significant symptoms and enlargement of the prostate. 5-alpha reductase converts testosterone to dihydrotestosterone (DHT), which is a more potent androgen hormone. Inhibitors of 5-alpha reductase (i.e. finasteride) reduce DHT in the tissues, including the prostate, leading to a reduction in prostate size. It takes up to 6 months of treatment for the effects to result in an improvement in symptoms.
114
side effects of BPH meds ?
The notable side effect of alpha-blockers like tamsulosin is postural hypotension. If an older man presents with lightheadedness on standing or falls, check whether they are on tamsulosin and check their lying and standing blood pressure. The most common side effect of finasteride is sexual dysfunction (due to reduced testosterone).
115
surgical option for BPH ?
Transurethral resection of the prostate (TURP) is the most common surgical treatment of BPH. It involves removing part of the prostate from inside the urethra. A resectoscope is inserted into the urethra, and prostate tissue is removed using a diathermy loop. The aim is to create a more expansive space for urine to flow through, thereby improving symptoms.
116
bladder cancer notable risk factors
Aromatic amines are worth noting as a carcinogen that causes bladder cancer. Aromatic amines were used in dye and rubber industries but have been heavily regulated or banned for many years. They are also found in cigarette smoke and seem to be the reason smoking causes bladder cancer. Schistosomiasis causes squamous cell carcinoma of the bladder in countries with a high prevalence of the infection.
117
types of bladder cancer and how common?
Transitional cell carcinoma (90%) Squamous cell carcinoma (5% – higher in areas of schistosomiasis) Rarer causes are adenocarcinoma (2%), sarcoma and small-cell carcinoma
118
diagnosis of bladder cancer ? what ix?
Cystoscopy (a camera through the urethra into the bladder) can be used to visualise bladder cancers. The cystoscope can be rigid or flexible. Cystoscopy can be performed under local or general anaesthetic.
119
mx for bladder cancer
Transurethral resection of bladder tumour (TURBT) may be used for non-muscle-invasive bladder cancer. The involves removing the bladder tumour during a cystoscopy procedure. Intravesical chemotherapy (chemotherapy given into the bladder through a catheter) is often used after a TURBT procedure to reduce the risk of recurrence. Intravesical Bacillus Calmette-Guérin (BCG) may be used as a form of immunotherapy. Giving the BCG vaccine (the same one as for tuberculosis) into the bladder is thought to stimulate the immune system, which in turn attacks the bladder tumours. Radical cystectomy involves the removal of the entire bladder. Following removal of the bladder, there are several options for draining urine: Urostomy with an ileal conduit (most common) Continent urinary diversion Neobladder reconstruction Ureterosigmoidostomy Chemotherapy and radiotherapy may also be used.
120
if you have to remove the whole bladder what option do you have after this ?
urostomy
121
ckd staging
1 >90 2 60-89 3a 45-59 3b 30-44 4 15-29 5 < 15
122
types of diabetes inspipidus and causes of each
Nephrogenic diabetes insipidus is when the collecting ducts of the kidneys do not respond to ADH. It can be idiopathic, without a clear cause, or it can be caused by: Medications, particularly lithium (used in bipolar affective disorder) Genetic mutations in the ADH receptor gene (X-linked recessive inheritance) Hypercalcaemia (high calcium) Hypokalaemia (low potassium) Kidney diseases (e.g., polycystic kidney disease) Cranial diabetes insipidus is when the hypothalamus does not produce ADH for the pituitary gland to secrete. It can be idiopathic, without a clear cause, or it can be caused by: Brain tumours Brain injury Brain surgery Brain infections (e.g., meningitis or encephalitis) Genetic mutations in the ADH gene (autosomal dominant inheritance) Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)
123
what ix for diabetes insipidus
Low urine osmolality (lots of water diluting the urine) High/normal serum osmolality (water loss may be balanced by increased intake) More than 3 litres on a 24-hour urine collection
124
what test for diabetes inspipidus ?
The water deprivation test is also known as the desmopressin stimulation test test urine osmolality after water deprivation and then after giving them desmopressin. remains low in nephrogenic
125
causes of epididimo orhcitis
At the back of each testicle is the epididymis. Sperm are released from the testicle, into the head of the epididymis, connected at the top of the testicle. The sperm travel through the head, then body, then tail of the epididymis. Sperm mature and are stored in the epididymis. The epididymis drains into the vas deferens. Causes Escherichia coli (E. coli) Chlamydia trachomatis Neisseria gonorrhoea Mumps
126
Epididymo-orchitis how does it present ?
Epididymo-orchitis typically presents with a gradual onset, over minutes to hours, with unilateral: Testicular pain Dragging or heavy sensation Swelling of testicle and epididymis Tenderness on palpation, particularly over epididymis Urethral discharge (should make you think of chlamydia or gonorrhoea) Systemic symptoms such as fever and potentially sepsis
127
what is important when we are dealing with epididymo-orchitis
The key with epididymo-orchitis is to distinguish whether the cause is likely to be an enteric organism (e.g., E. coli) or a sexually transmitted organism (e.g., chlamydia or gonorrhoea). The features that make a sexually transmitted organism more likely are (as per NICE CKS 2020): Age under 35 Increased number of sexual partners in the last 12 months Discharge from the urethra Investigations to help establish the diagnosis are: Urine microscopy, culture and sensitivity (MC&S) Chlamydia and gonorrhoea NAAT testing on a first-pass urine Charcoal swab of purulent urethral discharge for gonorrhoea culture and sensitivities Saliva swab for PCR testing for mumps, if suspected Serum antibodies for mumps, if suspected (IgM – acute infection, IgG – previous infection or vaccination) Ultrasound may be used to assess for torsion or tumours
128
mx for epididomo-orchitis
Patients at risk of sexually transmitted infection should be referred urgently to genitourinary medicine (GUM) for assessment and treatment. Local guidelines guide the choice of antibiotic. The NICE clinical knowledge summaries (updated January 2022) suggest the following options where it is most likely caused by an enteric organism (e.g., E. coli): Ofloxacin for 14 days Levofloxacin for 10 days Co-amoxiclav for 10 days (where quinolones are contraindicated) The antibiotic choice in patients with a potential sexually transmitted infection will depend on the suspected or confirmed organism and antibiotic sensitivities. Empirical treatment typically involves some combination of: Intramuscular ceftriaxone (single dose) Doxycycline Ofloxacin
129
buzzwords in ix for Multiple myeloma
Serum protein electrophoresis (to detect paraproteinaemia) Serum-free light-chain assay (to detect abnormally abundant light chains) Urine protein electrophoresis (to detect the Bence-Jones protein) Bone marrow biopsy is required to confirm the diagnosis and perform cytogenetic testing.
130
nephritic vs nephrotic sx
nephrotic - proteinuria, hypoalbuminaemia, oedema e.g.- Minimal change disease. - Focal segmental glomerulosclerosis (FSGS). - Membranous nephropathy. - Diabetic nephropathy. nephritic - haematuria, hypertension, proteinuria, oliguria, e.g. Post-streptococcal glomerulonephritis (PSGN). - IgA nephropathy. - Lupus nephritis. - ANCA-associated vasculitis.
131
prostate cancer gold standard diagnostic
Multiparametric MRI of the prostate is now the usual first-line investigation for suspected localised prostate cancer. The results are reported on a Likert scale, scored as: 1 – very low suspicion 2 – low suspicion 3 – equivocal 4 – probable cancer 5 – definite cancer
132
tool for prostate cancer
Gleason Grading System The Gleason grading system is based on the histology from the prostate biopsies. It is specific to prostate cancer and helps to determine what treatment is most appropriate. The greater the Gleason score, the more poorly differentiated the tumour is (the cells have mutated further from normal prostate tissue) and the worse the prognosis is. The tissue samples are graded 1 (closest to normal) to 5 (most abnormal). The Gleason score will be made up of two numbers added together for the total score (for example, 3 + 4 = 7): The first number is the grade of the most prevalent pattern in the biopsy The second number is the grade of the second most prevalent pattern in the biopsy A Gleason score of: 6 is considered low risk 7 is intermediate risk (3 + 4 is lower risk than 4 + 3) 8 or above is deemed to be high risk
133
mx for prostate cancer
1. watchful wainting 2. external beam radiotherapy 3. brachytherapy - radiactive seeds in prostate 4. hormone therapy - e.g. Androgen-receptor blockers such as bicalutamide GnRH agonists such as goserelin (Zoladex) or leuprorelin (Prostap)
134
how does testicular cancer present ? differentiate from other differntials
The typical presentation is a painless lump on the testicle. Occasionally it can present with testicular pain. The lump will be: Non-tender (or even reduced sensation) Arising from testicle Hard Irregular Not fluctuant No transillumination
135
ix for testicular cancer ?
Scrotal ultrasound is the usual initial investigation to confirm the diagnosis.
136
mx for testicular cancer
Surgery to remove the affected testicle (radical orchidectomy) – a prosthesis can be inserted Chemotherapy Radiotherapy Sperm banking to save sperm for future use, as treatment may cause infertility
137
how to remember the nephrotic and nephritic syndrome exmaples
muther fucker marvin RIP nephrotic - minimal change - focal segmental glomerulosclerosis - membranous glomerulosclerosis nephritic, - rapdily progressiing glomerulonephritis - IgA nephropathy - post - strep glomerulonephritis
138
what is urodynamic testing ?
Urodynamic tests are a way of objectively assessing the presence and severity of urinary symptoms. Patients need to stop taking any anticholinergic and bladder related medications around five days before the tests. A thin catheter is inserted into the bladder, and another into the rectum. These two catheters can measure the pressures in the bladder and rectum for comparison. The bladder is filled with liquid, and various outcome measures are taken: Cystometry measures the detrusor muscle contraction and pressure Uroflowmetry measures the flow rate Leak point pressure is the point at which the bladder pressure results in leakage of urine. The patient is asked to cough, move or jump when the bladder is filled to various capacities. This assesses for stress incontinence. Post-void residual bladder volume tests for incomplete emptying of the bladder Video urodynamic testing involves filling the bladder with contrast and taking xray images as the bladder is emptied. Theses are only performed where necessary and not a routine part of urodynamic testing.
139
mx stress vs urge incontinuence
stress - pelvic floor exercises - duloxetine - surgical options Tension-free vaginal tape (TVT) procedures involve a mesh sling looped under the urethra and up behind the pubic symphysis to the abdominal wall. This supports the urethra, reducing stress incontinence. Autologous sling procedures work similarly to TVT procedures but a strip of fascia from the patient’s abdominal wall is used rather than tape Colposuspension involves stitches connecting the anterior vaginal wall and the pubic symphysis, around the urethra, pulling the vaginal wall forwards and adding support to the urethra Intramural urethral bulking involves injections around the urethra to reduce the diameter and add support urge incontience - bladder retraining - oxybutynin - mirabegron (alt to oxy) - invasive options Botulinum toxin type A injection into the bladder wall Percutaneous sacral nerve stimulation involves implanting a device in the back that stimulates the sacral nerves Augmentation cystoplasty involves using bowel tissue to enlarge the bladder Urinary diversion involves redirecting urinary flow to a urostomy on the abdomen
140
types of renal stones
Calcium oxalate (more common) Calcium phosphate Other types of kidney stones include: Uric acid – these are not visible on x-ray Struvite – produced by bacteria, therefore, associated with infection Cystine – associated with cystinuria, an autosomal recessive disease
141
ix for renal colic
- urine dip shows haematuria - blood tests for infection/kidney function - non contrast CT KUB
142
mx for renal colic
- NSAIDs - IM diclofenac - antiemtics (metoclopramide) - abx (infection) - watchful waiting - tamsulosin (alpha blocker can help passage of stone) - surgical interventions 1. Extracorporeal shock wave lithotripsy (ESWL): ESWL involves an external machine that generates shock waves and directs them at the stone under x-ray guidance. The shockwaves break the stone into smaller parts to make them easier to pass. 2. Ureteroscopy and laser lithotripsy: A camera is inserted via the urethra, bladder and ureter, and the stone is identified. It is then broken up using targeted lasers, making the smaller parts easier to pass. 3. Percutaneous nephrolithotomy (PCNL): PCNL is performed in theatres under a general anaesthetic. A nephroscope (small camera on a stick) is inserted via a small incision at the patient’s back. The scope is inserted through the kidney to assess the ureter. Stones can be broken into smaller pieces and removed. A nephrostomy tube may be left in place after the procedure to help drain the kidney. 4. Open surgery: Open surgery can be used to access the kidneys and remove the stones. This is rarely needed as other, less invasive, methods are usually effective.
143
duration of abx in UTI
The typical duration of antibiotics is: 3 days of antibiotics for simple lower urinary tract infections in women 5-10 days of antibiotics for immunosuppressed women, abnormal anatomy or impaired kidney function 7 days of antibiotics for men, pregnant women or catheter-related UTIs
144
how does acute close angle glaucoma present and what are the signs ?
Presentation A typical patient with acute angle-closure glaucoma presents appearing generally unwell, with a short history of: Severely painful red eye Blurred vision Halos around lights Associated headache, nausea and vomiting Signs on examination include: Red eye Hazy cornea Decreased visual acuity Mid-dilated pupil Fixed-size pupil Hard eyeball on gentle palpation
145
mx for acute angle closure glaucoma
initially by GP 1. lye patient on back with no pillow 2. pilocarpine eye drops (causes ciliary muscle contraction / pupil contriction) 3. acetazolamide (carbonic anhyddrase inhibitor - reduces production of aqueous humour) ' then secondary care from specialist 1. same as above + 2. mannitol (hyperosmotic agent) 3. timolol (reduces prodction of aqueous humour) defintiive treament = Laser iridotomy
146
what is blepharitis ?
Blepharitis refers to inflammation of the eyelid margins. manage with warm compresses
147
what is a Chalazion and how to manage ?
A chalazion occurs when a Meibomian gland becomes blocked and swells. It is often called a Meibomian cyst. It presents with a swelling in the eyelid that is typically not tender (however, it can be tender and red). Treatment is with warm compresses and gentle massage towards the eyelashes (to encourage drainage). Rarely, surgical drainage may be required.
148
outline Entropion in opthlal
Entropion refers to when the eyelid turns inwards with the lashes pressed against the eye. This causes pain and can result in corneal damage and ulceration. Initial management is by taping the eyelid down to prevent it from turning inwards. Definitive management is surgical. A same-day referral to ophthalmology is required if there is a risk to sight. When the eyelid is taped down, it is essential to prevent the eye from drying out by using regular lubricating eye drops.
149
outline ectropian in opthlal
Ectropion refers to when the eyelid turns outwards, exposing the inner aspect. It usually affects the bottom lid. This can result in exposure keratopathy, as the eyeball is exposed and not adequately lubricated and protected. Mild cases may not require treatment. Regular lubricating eye drops are used to protect the surface of the eye. More significant cases may require surgery to correct the defect. A same-day referral to ophthalmology is required if there is a risk to sight.
150
outline peri-orbital vs orbital cellulitis. how does it present and how to distinguish
Periorbital cellulitis (also known as preseptal cellulitis) is an eyelid and skin infection in front of the orbital septum (in front of the eye). It presents with swollen, red, hot skin around the eyelid and eye. It must be differentiated from orbital cellulitis, a sight and life-threatening emergency. Patients are referred urgently to ophthalmology for assessment. A CT scan can help distinguish them. Treatment is with systemic antibiotics (oral or IV). Preorbital cellulitis can develop into orbital cellulitis, so vulnerable patients (e.g., children) or severe cases may require admission for monitoring. Orbital cellulitis is an infection around the eyeball involving the tissues behind the orbital septum. Symptoms include pain with eye movement, reduced eye movements, vision changes, abnormal pupil reactions, and proptosis (bulging forward of the eyeball). Orbital cellulitis requires emergency admission under ophthalmology and intravenous antibiotics. Surgical drainage may be needed if an abscess forms.
151
presentation/signs/ mx for cataracts ?
Slow reduction in visual acuity Progressive blurring of the vision Colours becoming more faded, brown or yellow Starbursts can appear around lights, particularly at night Loss of the red reflex is a key examination finding. The lens can appear grey or white using an ophthalmoscope, even from a distance. This is also seen on photographs taken with a flash. mx= cataract surgery- remove lens and replace with artifical one
152
causes of Central retinal arterial occlusion
atherosclerosis also GCA
153
curtain coming down over vision?
retinal detachment
154
how does Central retinal arterial occlusion present ?
Blockage of the central retinal artery causes sudden painless loss of vision. It may be described as like a “curtain coming down” over the vision. There will be a relative afferent pupillary defect, where the pupil in the affected eye constricts more when light is shone in the other eye than when it is shone in the affected eye. The input is not sensed by the ischaemic retina when testing the direct light reflex but is sensed during the consensual light reflex. Fundoscopy will show a pale retina with a cherry red spot. The retina is pale due to a lack of perfusion. The cherry red spot is the fovea, which has a thinner surface and shows the red-coloured choroid below.
155
The key differentials for a sudden painless vision loss are....
retinal detachment, central retinal artery occlusion, central retinal vein occlusion vitreous haemorrhage (due to diabetic retinopathy). Amaurosis fugax describes a temporary loss of vision caused by a temporary interruption to the blood supply.
156
mx for central retinal artery occlusion
Management Central retinal artery occlusion is a vision-threatening emergency. Suspected cases should be referred immediately. Giant cell arteritis is a potentially reversible cause. Testing includes an ESR blood test and temporal artery biopsy. Treatment is with high-dose systemic steroids. Immediate management options attempt to dislodge/resolve the blockage. There is no consensus, guidelines or solid evidence base for these options: Ocular massage (massaging the eye) Anterior chamber paracentesis (removing fluid from the anterior chamber to reduce the intraocular pressure) Inhaled carbogen (5% carbon dioxide and 95% oxygen) (to dilate the artery) Sublingual isosorbide dinitrate (to dilate the artery) Oral pentoxifylline (to dilate the artery) Intravenous acetazolamide (to reduce the intraocular pressure) Intravenous mannitol (to reduce the intraocular pressure) Topical timolol (to reduce the intraocular pressure) Long-term management involves treating reversible risk factors and secondary prevention of cardiovascular disease.
157
Causes of an acute painless red eye include:
Conjunctivitis Episcleritis Subconjunctival haemorrhage
158
Causes of an acute painful red eye include:
Acute angle-closure glaucoma Anterior uveitis Scleritis Corneal abrasions or ulceration Keratitis Foreign body Traumatic or chemical injury
159
diabetic retiopathy examination findings with different stages
Diabetic retinopathy is graded based on the findings on fundus examination: Background – microaneurysms, retinal haemorrhages, hard exudates and cotton wool spots Pre-proliferative – venous beading, multiple blot haemorrhages and intraretinal microvascular abnormality (IMRA) Proliferative – neovascularisation and vitreous haemorrhage
160
what is diabetic maculopathy ?
Diabetic maculopathy also exists separately and involves: Exudates within the macula Macular oedema
161
mx for diabetic retinopathy
Non-proliferative diabetic retinopathy requires close monitoring and careful diabetic control. Treatment options for proliferative diabetic retinopathy are: Pan-retinal photocoagulation (PRP) – extensive laser treatment across the retina to suppress new vessels Anti-VEGF medications by intravitreal injection Surgery (e.g., vitrectomy) may be required in severe disease
162
define keratitis
Keratitis refers to inflammation of the cornea
163
how does keratitis present ?
Bacterial keratitis commonly causes unilateral symptoms. Typical symptoms may include: Ocular pain: this may be moderate or severe and include symptoms of irritation and foreign body sensation Red eye Reduced visual acuity: this may be near normal to markedly reduced Photophobia: intolerance to sunlight or normal room lighting Purulent discharge A history of contact lens wear is essential: Type of contact lenses used: daily disposable, monthly or extended-wear Duration of wear per day If they have ever slept, showered, or swam with their lenses in For more information, see the Geeky Medics guide to ophthalmic history taking.
164
mx for keratitis
Contact lens use should be discontinued immediately. Antibiotic therapy should be commenced: Topical antibiotics: initially with broad spectrum cover (e.g. fluoroquinolone monotherapy or cefuroxime and gentamicin duo therapy) until culture results return. Instillation may be up to hourly for the first 24-48 hours depending on severity, this can then be tapered off given response to treatment Oral antibiotics: may be required in severe cases Surgery (e.g. corneal transplantation) is rarely required, it is considered only in complicated (e.g. perforation) or medically refractory cases.
165
iritis vs uveitis
Uveitis: Definition: A general term for inflammation of the uveal tract of the eye. The uveal tract includes three parts: Iris (front part) Ciliary body (middle part) Choroid (back part) A specific form of anterior uveitis where the inflammation is confined primarily to the iris.
166
age related macular degneration differences 2 types. and how to manage each
Wet (also called neovascular), accounting for 10% of cases Dry (also called non-neovascular), accounting for 90% of cases (wet you can use anti-VEGF to manage - e.g. ranibizumab, aflibercept and bevacizumab)
167
how does age related macular degeneration present ? what are examination findings ?
Visual changes associated with AMD tend to be unilateral, with: Gradual loss of central vision Reduced visual acuity Crooked or wavy appearance to straight lines (metamorphopsia) WET progresses much faster Examination Key findings on examination are: Reduced visual acuity using a Snellen chart Scotoma (an enlarged central area of vision loss) Amsler grid test can be used to assess for the distortion of straight lines seen in AMD Drusen may be seen during fundoscopy Slit lamp examination gives a detailed view of the retina and macula. Optical coherence tomography gives a cross-sectional view of the layers of the retina and is used for diagnosing and monitoring AMD. Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to assess the blood supply, showing oedema and neovascularisation in wet AMD.
168
Central scotoma what is it ?
enlarged central blind spot - optic neuritis - age related macular degneration - central retinal vein occlusiomn
169
how does optic neuritis present ?
Central scotoma (an enlarged central blind spot) Pain with eye movement Impaired colour vision Relative afferent pupillary defect
170
explain RAPD and which conditions you find it in
A flashlight is moved back and forth between the eyes. In RAPD, the affected eye shows a paradoxical dilation (or less constriction) when exposed to light compared to the unaffected eye. conditions: - optic neuritis - central retinal artery occlusion - retinal detachement - central retinal vein occlusion -
171
how does retinal detachment present ?
Retinal detachment is a painless condition that can present with: Peripheral vision loss (often sudden and described as a shadow coming across the vision) Blurred or distorted vision Flashes and floaters
172
painless flashes and floaters
Patients presenting with painless flashes and floaters should have a detailed assessment to detect retinal tears and retinal detachment. Any suspicion of retinal detachment requires immediate ophthalmology referral.
173
how to mx retinal detachement / tears
Management of retinal tears aims to create adhesions between the retina and the choroid. The options are: Laser therapy Cryotherapy Management of retinal detachment aims to reattach the retina and reduce any traction or pressure that may cause it to detach again. The options for reattaching the retina are vitrectomy, scleral buckle or pneumatic retinopexy. Vitrectomy involves keyhole surgery on the eye, removing the vitreous fluid, fixing the tear, and then inserting gas or oil into the eye to hold the retina in place. Scleral buckling involves using a silicone “buckle” to put pressure on the sclera from outside the eye, squashing the eye inwards to reconnect the layers of the retina. It acts like a corset, squeezing the eye contents together. Pneumatic retinopexy involves injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble presses the separated layer back into place.
174
what conditions is scleritis associated with ?
Rheumatoid arthritis Vasculitis, particularly granulomatosis with polyangiitis)
175
features of scleritis
Scleritis usually presents with a more gradual onset. It can be unilateral or bilateral. Features include: Red, inflamed sclera (localised or diffuse) Congested vessels Severe pain (typically a boring pain) Pain with eye movement Photophobia Epiphora (excessive tear production) Reduced visual acuity Tenderness to palpation of the eye
176
how to manage scleritis
Patients should be referred for urgent assessment and management by an ophthalmologist. Patients should be assessed for an underlying systemic condition (e.g., rheumatoid arthritis or vasculitis). Management in secondary care may involve: NSAIDs (oral) Steroids (topical or systemic) Immunosuppression appropriate to the underlying systemic condition (e.g., methotrexate in rheumatoid arthritis) abx for infective scleritis
177
mx for thyroid eye disease
Management: Correct thyroid hormone levels to achieve euthyroidism in hyperthyroid patients. Smoking cessation advice. Artificial tears and tapes for corneal exposure symptoms. Steroids (IV methylprednisolone) for severe cases, especially compressive optic neuropathy. Surgery (orbital decompression, lid surgery) for significant corneal exposure or progressing proptosis.
178
what is anterior uveitiis associated with ?
Anterior uveitis may be associated with underlying an autoimmune condition, particularly: Seronegative spondyloarthropathies (e.g., ankylosing spondylitis, psoriatic arthritis and reactive arthritis) Inflammatory bowel disease Sarcoidosis Behçet’s disease
179
presentation and examination findings for anterior uveitiis
Anterior uveitis may present with symptoms of: Painful red eye (typically a dull, aching pain) Reduced visual acuity Photophobia (due to ciliary muscle spasm) Excessive lacrimation (tear production) Examination findings include: Ciliary flush (a ring of red spreading from the cornea outwards) Miosis (a constricted pupil due to sphincter muscle contraction) Abnormally shaped pupil due to posterior synechiae (adhesions) pulling the iris into abnormal shapes Hypopyon (inflammatory cells collected as a white fluid in the anterior chamber)
180
MX anterior uveitis
Steroids (eye drops, oral or intravenous) Cycloplegics (e.g., cyclopentolate or atropine eye drops)
181
most common complication of meales ?
otitis media
182
bilateral grittiness in eyes think ....
blepharitis
183
name of the hot blade they use to cut tissues in theatre ?
Diathermy Diathermy is the use of heat from an electrical current to cut tissue or seal blood vessels. Depending on the temperature reached, different outcomes will occur: 60 degrees -> cell death occurs -> fulguration (destruction of small growths or areas of tissue) 60 to 99 degrees -> dehydration occurs -> coagulation 100 degrees -> vaporisation of tissues occurs -> cutting There are TWO FORMS of diathermy: Monopolar and Bipolar Monopolar: current flows between the active electrode on the pen and a return electrode placed on the patient’s skin. This is most commonly used due to its versatility and effectiveness. Bipolar: both electrodes are found on the instrument itself. This requires less energy as lower voltages are used, and there’s more control over the area being targeted which reduces unwanted damage. However, it isn’t as good at cutting and coagulating large bleeding areas, so it’s typically used when the relevant tissue can be grabbed.
184
biliary colic presentation
Right upper quadrant pain Associated with eating fatty meals May subside without treatment Associated with nausea and vomiting
185
ix for biliary colic
Bloods LFTS USS - dilation of CBD / thickened gallbladder wall MRCP ERCP - has therapeutic potential
186
mx for biliary colic
Immediate Management NBM IV Fluids Regular Analgesia (usually IV morphine) Surgical All patients diagnosed with symptomatic gallstones should be offered a laparoscopic cholecystectomy
187
ix for acute cholangitis
Bloods FBC, CRP Raised WCC and CRP LFTs Raised ALP, raised GGT, raised bilirubin U+Es Amylase Blood cultures Imaging USS biliary tract Visualise gallstones Visualise biliary duct dilatation The common bile duct is usually < 6 mm in size CT If USS inconclusive To rule out other diagnoses Evaluate possible malignancy MRCP (Magnetic Resonance Cholangiopancreatography) To obtain detailed imaging of the biliary system prior to scoping ERCP (Endoscopic Retrograde Cholangiopancreatography) The gold standard investigation for cholangitis, as it is both diagnostic and therapeutic.
188
mx acute cholangitis
A-E think sepsis ? defintiive management 1. endoscopic biliary decompression 2. ERCP - retrieve stone elective cholecystecomy if gallstones underlying cause
189
types of abdominal wall hernias?
Umbilical Hernias Protrusions through the umbilical ring Congenital Acquired Obesity, ascites, pregnancy, chronic peritoneal dialysis Epigastric Hernias Protrusions through the linea alba Spigelian Hernias Protrusions through defects in the transversus abdominis Lateral to the rectus sheath Below the level of the umbilicus Along the semilunar line Incisional Hernias Protrusions through an incision from previous abdominal surgery Parastomal Hernia Hernia adjacent to a stoma site
190
what can happen to a hernia - and what symptoms does this give you ?
Abdominal or Groin lump If Incarcerated Irreducible (unable to return the contents of the hernia to their original cavity) If Obstructed Abdominal pain, distension, vomiting and absent bowel sounds If Strangulated Intense pain coming from an irreducible, tender and tense lump Requires urgent surgical intervention
191
types of groin hernias ?
Groin Hernias Inguinal Hernias Superior to the inguinal ligament Indirect: traverse the internal inguinal ring into the inguinal canal Direct: extend directly through a defect in the posterior wall of the inguinal canal (Hesselbach's triangle) Femoral Hernias Inferior to the inguinal ligament Protrude into the femoral canal
192
mx for hernias
Elective Repair (Open or Laparoscopic Mesh Repair) Incarcerated or Strangulated Hernia --> Urgent Surgical Repair asymptomatic inguinals hernias in men can be managed conservatively
193
signs and sx of acute mesenteric ischaemia
Symptoms Abdominal pain Poorly localised Nausea, Vomiting Fever Bloody diarrhoea Signs Often relatively normal abdominal examination Pain out of proportion with the clinical exam Pyrexia Tachycardia May have irregularly irregular pulse (suggestive of atrial fibrillation) Haemodynamic instability Peritonism (sign of advances ischaemia/necrosis)
194
tool for predicting liklihood of appendicitis ?
alvarado score
195
how does acoustic neuroma present?
The typical patient is aged 40-60 years presenting with a gradual onset of: Unilateral sensorineural hearing loss (often the first symptom) Unilateral tinnitus Dizziness or imbalance A sensation of fullness in the ear They can also be associated with a facial nerve palsy if the tumour grows large enough to compress the facial nerve.
196
mx acoustic neuroma
audiometry brain imaging (CT / MRI)
197
in ramsey hunt what to look out for
facial nerve palsy vesicular rash around their ear
198
define cerebral palsy and give causes
Cerebral palsy (CP) is the name given to the permanent neurological problems resulting from damage to the brain around the time of birth. It is not a progressive condition, however the nature of the symptoms and problems may change over time during growth and development. There is huge variation in the severity and type of symptoms, ranging from completely wheelchair bound and dependent on others for all activities of daily living, to para-olympic athletes with only subtle problems with coordination or mobility. Causes of Cerebral Palsy Antenatal: Maternal infections Trauma during pregnancy Perinatal: Birth asphyxia Pre-term birth Postnatal: Meningitis Severe neonatal jaundice Head injury
199
types of cerebral palsy
Spastic: hypertonia (increased tone) and reduced function resulting from damage to upper motor neurones Dyskinetic: problems controlling muscle tone, with hypertonia and hypotonia, causing athetoid movements and oro-motor problems. This is the result of damage to the basal ganglia. Ataxic: problems with coordinated movement resulting from damage to the cerebellum Mixed: a mix of spastic, dyskinetic and/or ataxic features Spastic CP is also known as pyramidal CP. Dyskinetic CP is also known as athetoid CP and extrapyramidal CP. Patters of Spastic Cerebral Palsy Monoplegia: one limb affected Hemiplegia: one side of the body affected Diplegia: four limbs are affects, but mostly the legs Quadriplegia: four limbs are affected more severely, often with seizures, speech disturbance and other impairments
200
what is Hypoxic ischemic encephalopathy (HIE)
Hypoxic ischemic encephalopathy (HIE) is a brain injury that occurs when a baby's brain doesn't receive enough oxygen or blood flow before, during, or shortly after birth. HIE can cause a range of issues, from mild to severe disabilities or even death.
201
signs & sx & examination for cerebral palsy
Signs and symptoms of cerebral palsy will become more evident during development: Failure to meet milestones Increased or decreased tone, generally or in specific limbs Hand preference below 18 months is a key sign to remember for exams Problems with coordination, speech or walking Feeding or swallowing problems Learning difficulties Neurological Examination You can gain a lot of information about a child from their gait: Hemiplegic / diplegic gait: indicates an upper motor neurone lesion Broad based gait / ataxic gait: indicates a cerebellar lesion High stepping gait: indicates foot drop or a lower motor neurone lesion Waddling gait: indicates pelvic muscle weakness due to myopathy Antalgic gait (limp): indicates localised pain
202
tool for cognitive impairment
Addenbrooke’s Cognitive Examination-III (ACE-III)
203
different presentations for diabetic neuropathy
altered sensation such as numbness, tingling or burning pain changes to normal body functions, like constipation or diarrhoea, bladder leaking or difficulty getting an erection weakness loss of reflexes. sensory loss in glove and stocking distribution. lower legs affected first due to length of neurons
204
mx for diabetic neuropathy
Diabetic neuropathy is now managed in the same way as other forms of neuropathic pain: first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin
205
outline encephalitis - features, pathophysiology, ix & mx
Features fever, headache, psychiatric symptoms, seizures, vomiting focal features e.g. aphasia peripheral lesions (e.g. cold sores) have no relation to the presence of HSV encephalitis Pathophysiology HSV-1 is responsible for 95% of cases in adults typically affects temporal and inferior frontal lobes Investigation cerebrospinal fluid lymphocytosis elevated protein PCR for HSV, VZV and enteroviruses neuroimaging medial temporal and inferior frontal changes (e.g. petechial haemorrhages) normal in one-third of patients MRI is better EEG lateralised periodic discharges at 2 Hz Management intravenous aciclovir should be started in all cases of suspected encephalitis
206
outline the different types of seizures
1. Generalised tonic clonic - tonic (muscle clenching) and clonic (muscle jerking) with complete LOC. often tonic before clonic. can have aura preceding and often have post ictal phase 2. partial seizure - often temporal lobe. can affect hearing, speech, memory etc... patient awake during simple partial seizuers but lose awareness during complex partial seizures 3. tonic seizures - go stiff and fall backawards 4. atonic seizures - go llimp and collapse 5. myoclonic - brief muscle contractions
207
seizures differentials
Vasovagal syncope (fainting) Pseudoseizures (non-epileptic attacks) Cardiac syncope (e.g., arrhythmias or structural heart disease) Hypoglycaemia Hemiplegic migraine Transient ischaemic attack
208
ix for seizure
EEG MRI brain is used to diagnose structural pathology (e.g., tumours). Additional investigations can be considered to exclude associated pathology: ECG Serum electrolytes, including sodium, potassium, calcium and magnesium Blood glucose for hypoglycaemia and diabetes Blood cultures, urine cultures and lumbar puncture where sepsis, encephalitis or meningitis is suspected
209
Generalised tonic clonic seizure mx
men / non-child bearing women = sodium valproate child bearing women = lamotrigine
210
partial/focal seizures
all = lamotrigine
211
myoclonic
men / non child bearing women = sodium valproate child bearing women = leviiricatem
212
tonic and atonic siezures mx
men / non child bear women = sodium valproate child bearing women = lamotrigine
213
absense seizure mx
all = ethosuximide
214
what teratogenic effects of sodium valproate ?
Sodium valproate in pregnancy can cause neural tube defects and developmental delay
215
how to manage status epilepticus
status iks defined after 5 mins 1. ABC (airway adjunct/o2/check BM) 2. benzodiazepine pre-hospital = PR diazepam/buccal midazolam hospital = IV lorazepam 3. if ongoing repeat after 5-10 mins 4. IV phenytoin 5. general anesatheisa / intubate / phenobarbital
216
features of essential tremor & how to manage
Fine tremor (6-12 Hz) Symmetrical More prominent with voluntary movement Worse when tired, stressed or after caffeine Improved by alcohol Absent during sleep Medications that may improve symptoms are: Propranolol (a non-selective beta blocker) Primidone (a barbiturate anti-epileptic medication)`
217
stroke with Contralateral hemiparesis and sensory loss, lower extremity > upper site of lesion?
anterior cerebral artery
218
stroke with Contralateral hemiparesis and sensory loss, upper extremity > lower Contralateral homonymous hemianopia Aphasia site of lesion?
middle cerebral artery
219
stroke with Contralateral homonymous hemianopia with macular sparing Visual agnosia site of lesion ?
posterior cerebral artery
220
stroke Ipsilateral: facial pain and temperature loss Contralateral: limb/torso pain and temperature loss Ataxia, nystagmus where is lesion?
Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)
221
how to diagnose malaria ?
The diagnosis is made using a malaria blood film. This is sent in an EDTA bottle (the same bottle used for a full blood count). A malaria blood film will show the parasites, the concentration (as a percentage) and the type. Three negative samples taken over three consecutive days are required to exclude malaria due to the parasites being released from red blood cells into the blood every 48-72 hours. The sample may be negative when the parasites are not released but positive a day or two later when the red blood cells rupture and release the parasites.
222
how to manage menieres disease ?
Management involves: Managing symptoms during an acute attack Prophylactic medication to reduce the frequency of attacks For acute attacks, short-term options for managing symptoms include: Prochlorperazine Antihistamines (e.g., cyclizine, cinnarizine and promethazine) Prophylaxis is with: Betahistine
223
types of motor neurone disease
1. Amyotrophic lateral sclerosis (ALS) is the most common and well-known type of motor neurone disease. Stephen Hawking had amyotrophic lateral sclerosis. 2. Progressive bulbar palsy is the second most common form of motor neurone disease. It primarily affects the muscles of talking and swallowing (the bulbar muscles). 3. Other types to be aware of are progressive muscular atrophy and primary lateral sclerosis.
224
how does Motor neurone disease present ?
The typical patient is a late middle-aged (e.g., 60) man, possibly with an affected relative. There is an insidious, progressive weakness of the muscles throughout the body, affecting the limbs, trunk, face and speech. The weakness is often first noticed in the upper limbs. There may be increased fatigue when exercising. They may complain of clumsiness, dropping things more often or tripping over. They can develop slurred speech (dysarthria). Signs of lower motor neurone disease: Muscle wasting Reduced tone Fasciculations (twitches in the muscles) Reduced reflexes Signs of upper motor neurone disease: Increased tone or spasticity Brisk reflexes Upgoing plantar reflex
225
what is musclar dystrophy ?
Muscular dystrophy is an umbrella term for genetic conditions that cause gradual weakening and wasting of muscles. The main muscular dystrophy to know about for the purpose of exams is Duchennes muscular dystrophy. It is worth being aware of the others.
226
how does duchennes musclar dystrophy present ?
Boys with Duchennes present around 3 – 5 years with weakness in the muscles around their pelvis. The weakness tends to be progressive and eventually all muscles will be affected. They are usually wheelchair bound by the time they become a teenager. They have a life expectance of around 25 – 35 years with good management of the cardiac and respiratory complications. Oral steroids have been shown to slow the progression of muscle weakness by as much as two years. Creatine supplementation can give a slight improvement in muscle strength. Genetic trials are ongoing. its X linked recessive
227
red flags for cauda equina
The key red flags to look out for are: Saddle anaesthesia (loss of sensation in the perineum – around the genitals and anus) Loss of sensation in the bladder and rectum (not knowing when they are full) Urinary retention or incontinence Faecal incontinence Bilateral sciatica Bilateral or severe motor weakness in the legs Reduced anal tone on PR examination
228
ix for infected bursitis ?
aspiration ---> microscopy & culture
229
mx for compartment syndrome
fasciotomy
230
how does compartment syndrome present ?
Bone fractures Crush injuries Acute compartment syndrome presents with the 5 P’s: P – Pain “disproportionate” to the underlying injury, worsened by passive stretching of the muscles P – Paresthesia P – Pale P – Pressure (high) P – Paralysis (a late and worrying feature)
231
how does fibromyalgia present ?
Pain at multiple sites. Low back pain with/without radiation to the buttocks and legs and pain in the neck and across the shoulders are common complaints.2 Patients may complain of "pain all over". Fatigue. Sleep disturbance (sleep may exacerbate symptoms and contribute to depression).8 Morning stiffness. Paraesthesiae. Feeling of swollen joints (with no objective swelling). Problems with cognition (eg, memory disturbance, difficulty with word finding). Headaches (may be migrainous). Light-headedness or dizziness. Fluctuations in weight. Anxiety and depression.
232
fibromyalgia mx
explanation aerobic exercise: has the strongest evidence base cognitive behavioural therapy medication: pregabalin, duloxetine, amitriptyline
233
X-ray of a joint affected by gout shows:
Maintained joint space (no loss of joint space) Lytic lesions in the bone Punched out erosions Erosions can have sclerotic borders with overhanding edges
234
Chondrocalcinosis on xray ?
pseudogout also similar changes to OA Other joint x-ray changes are similar to osteoarthritis, which can be remembered with the “LOSS” mnemonic: L – Loss of joint space O – Osteophytes (bone spurs) S – Subarticular sclerosis (increased density of the bone along the joint line) S – Subchondral cysts (fluid-filled holes in the bone)
235
mx psuedogout
Treatment of pseudogout is targeted at symptoms. There are no proven disease-modifying drugs, prophylactic treatments or dietary modifications. Asymptomatic changes on an x-ray do not require any treatment. Symptoms usually resolve spontaneously over several weeks. Symptomatic management options include: NSAIDs (e.g., naproxen) first-line (co-prescribed with a proton pump inhibitor for gastroprotection) Colchicine Intra-articular steroid injections (septic arthritis must be excluded first) Oral steroids
236
name of rash in lyme disease
erythema migrans
236
features of lyme disease
systemic features headache lethargy fever arthralgia Later features (after 30 days) cardiovascular heart block peri/myocarditis neurological facial nerve palsy radicular pain meningitis
237
4 key xray changes in OA?
The four key x-ray changes in osteoarthritis can be remembered with the “LOSS” mnemonic: L – Loss of joint space O – Osteophytes (bone spurs) S – Subarticular sclerosis (increased density of the bone along the joint line) S – Subchondral cysts (fluid-filled holes in the bone)
238
OA signs in the hands ?
Heberden’s nodes (in the DIP joints) Bouchard’s nodes (in the PIP joints) Squaring at the base of the thumb (CMC joint) Weak grip Reduced range of motion
239
mx osteomalacia
Treatment is with colecalciferol (vitamin D₃
240
most common cause of osteomyelitis
Staphylococcus aureus causes most cases of osteomyelitis.
241
ix for osteomyelitis
X-rays often do not show any changes, particularly in early disease. They cannot be used to exclude osteomyelitis. The potential signs of osteomyelitis on an x-ray are: Periosteal reaction (changes to the surface of the bone) Localised osteopenia (thinning of the bone) Destruction of areas of the bone MRI scans are the best imaging investigation for establishing a diagnosis. Blood tests will show raised inflammatory markers (e.g., WBC, CRP and ESR). Blood cultures may be positive for the causative organism. Bone cultures can be performed to establish the causative organism and the antibiotic sensitivities.
242
mx osteomyelitis
Management involves a combination of: Surgical debridement of the infected bone and tissues Antibiotic therapy Prolonged courses of antibiotics are required to treat osteomyelitis. The BNF page on osteomyelitis recommends for acute osteomyelitis: 6 weeks of flucloxacillin, possibly with rifampicin or fusidic acid added for the first 2 weeks
243
osteoporisis vs osteopenia ?
osteopenia = T score at hip between -1 to -2.5 osteoporisis = T score at the hip less than - 2.5
244
name of tools for estimated fracture risk in older person
QFracture tool (preferred by NICE) FRAX tool (NICE say this may underestimate the risk in some patients)
245
how to PMR present ?
The characteristic features of the pain and stiffness are: Worse in the morning Worse after rest or inactivity Interfere with sleep Take at least 45 minutes to ease in the morning Somewhat improve with activity Associated features include: Systemic symptoms (e.g., weight loss, fatigue and low-grade fever) Muscle tenderness Carpel tunnel syndrome Peripheral oedema
246
mx for PMR
steroids 15mg prednisolone reducing regime of prednisolone: 15mg until the symptoms are fully controlled, then 12.5mg for 3 weeks, then 10mg for 4-6 weeks, then Reducing by 1mg every 4-8 weeks
247
types of psoriasis
Plaque psoriasis features the thickened erythematous plaques with silver scales, commonly seen on the extensor surfaces and scalp. The plaques are 1cm – 10cm in diameter. This is the most common form of psoriasis in adults. Guttate psoriasis is the second most common form of psoriasis and commonly occurs in children. It presents with many small raised papules across the trunk and limbs. The papules are mildly erythematous and can be slightly scaly. Over time the papules in guttate psoriasis can turn into plaques. Guttate psoriasis is often triggered by a streptococcal throat infection, stress or medications. It often resolves spontaneously within 3 – 4 months. Pustular psoriasis is a rare severe form of psoriasis where pustules form under areas of erythematous skin. The pus in these areas is not infectious. Patients can be systemically unwell. It should be treated as a medical emergency and patients with pustular psoriasis initially require admission to hospital. Erythrodermic psoriasis is a rare severe form of psoriasis with extensive erythematous inflamed areas covering most of the surface area of the skin. The skin comes away in large patches (exfoliation) resulting in raw exposed areas. It should be treated as a medical emergency and patients require admission.
248
mx psoriasis
Topical steroids Topical vitamin D analogues (calcipotriol) Topical dithranol Topical calcineurin inhibitors (tacrolimus) are usually only used in adults Phototherapy with narrow band ultraviolet B light is particularly useful in extensive guttate psoriasis
249
signs in psoriatic arthritis
Plaques of psoriasis on the skin Nail pitting (tiny indents in the fingernails and toenails) Onycholysis (separation of the nail from the nail bed) Dactylitis (inflammation of the entire finger) Enthesitis (inflammation of the entheses, which are the points of insertion of tendons into bone)
250
xray changes in psoriatic arthritis ?M
Periostitis (inflammation of the periosteum, causing a thickened and irregular outline of the bone) Ankylosis (fixation or fusion of the bones at the joint) Osteolysis (destruction of bone) Dactylitis (inflammation of the whole digit, seen as soft tissue swelling) The classic x-ray finding in the digits is a “pencil-in-cup” appearance. There is erosion of the bones at the joint. There is central erosion on one side of the joint, giving a cup-like appearance. The other bone becomes pointed and looks like a pencil in the cup. This appearance is associated with arthritis mutilans.
251
psoriatic arthritis mx
Non-steroidal anti-inflammatory drugs (NSAIDs) Steroids DMARDs (e.g., methotrexate, leflunomide or sulfasalazine) Anti-TNF medications (etanercept, infliximab or adalimumab) Ustekinumab is a monoclonal antibody that targets interleukin 12 and 23
252
common triggers of reactive arthritis
The most common triggers of reactive arthritis are gastroenteritis or sexually transmitted infections. Chlamydia may cause reactive arthritis. Gonorrhoea typically causes septic arthritis rather than reactive arthritis.
253
reactive arthritis presentation
cant see, cant pee, cant climb a tree Bilateral conjunctivitis (non-infective) Anterior uveitis Urethritis (non-gonococcal) Circinate balanitis (dermatitis of the head of the penis)
254
mx reactive arthritis
Management of reactive arthritis (after septic arthritis is excluded) involves: Treatment of the triggering infection (e.g., chlamydia) NSAIDs Steroid injection into the affected joints Systemic steroids may be required, particularly where multiple joints are affected
255
most commonly affected joints in RA
Metacarpophalangeal (MCP) joints Proximal interphalangeal (PIP) joints Wrist Metatarsophalangeal (MTP) joints (in the foot)
256
hand signs in RA
Z-shaped deformity to the thumb Swan neck deformity (hyperextended PIP and flexed DIP) Boutonniere deformity (hyperextended DIP and flexed PIP) Ulnar deviation of the fingers at the MCP joints
257
RA ix
Rheumatoid factor Anti-CCP antibodies Inflammatory markers, such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) X-rays of the hands and feet for bone changes Ultrasound or MRI can be used to detect synovitis (useful when clinical findings are unclear)
258
XRAY CHANGES IN RA
Periarticular osteopenia Boney erosions Soft tissue swelling Joint destruction and deformity (in more advanced disease)
259
mx for RA
Short-term steroids (oral or intramuscular) may be used at initial presentation, when initiating a new treatment and during flares to settle the inflammation and control symptoms quickly. Treatment is with conventional disease-modifying anti-rheumatic drugs (cDMARDs) and biologic DMARDs: Monotherapy with methotrexate, leflunomide or sulfasalazine Combination treatment with multiple cDMARDs Biologic therapies (usually alongside methotrexate)
260
20-40 year old black female presenting with a dry cough and shortness of breath - what could this be ?
sarcoidosis They may have nodules on their shins, suggesting erythema nodosum.
261
rash on shin in sarcoidosis called ?
erythema nodosum
262
ix for suspected sarcoidosis
Blood Tests The blood test findings to remember are: Raised angiotensin-converting enzyme (ACE) (often used as a screening test) Raised calcium (hypercalcaemia) Imaging Various imaging investigations may be performed: Chest x-ray may show hilar lymphadenopathy High-resolution CT scanning may show hilar lymphadenopathy and pulmonary nodules MRI can show central nervous system involvement PET scan can show active inflammation in affected areas Histology Histology helps establish the diagnosis, often by bronchoscopy with an ultrasound-guided biopsy of mediastinal lymph nodes. Histology characteristically shows non-caseating granulomas with epithelioid cells. Other Tests Other tests may be used to determine which organs are affected: U&Es for kidney involvement Urine albumin-creatinine ratio to look for proteinuria LFTs for liver involvement Ophthalmology assessment for eye involvement ECG and echocardiogram for heart involvement Ultrasound for liver and kidney involvement
263
mx for sarcoidosis
Conservative management is considered in patients with no or mild symptoms. Oral steroids (for 6-24 months) are usually first-line where treatment is required. Bisphosphonates protect against osteoporosis whilst on long-term steroids. Methotrexate is a second-line option. Lung transplant is rarely required in severe pulmonary disease.
264
ix for lupus
autoantibodies (ANA / anti ds-DNA) Full blood count may show anaemia of chronic disease, low white cell count and low platelets CRP and ESR may be raised with active inflammation C3 and C4 levels may be decreased in active disease Urinalysis and urine protein:creatinine ratio shows proteinuria in lupus nephritis Renal biopsy may be used to investigate for lupus nephritis
265
lupus mx
Treatment aims to control symptoms and reduce complications with the least medications and side effects. Suncream and sun avoidance are essential measures in managing the photosensitive malar rash. First-line options include: Hydroxychloroquine NSAIDs Steroids (e.g., prednisolone)
266
causes of post renal AKI
lumininal - renal stone / cancer mural - stricture extra mural - prostate cancer
267
macules vs papules
Macules are flat marks on the skin Papules are small lumps on the skin
268
mx acne vulgaris
1. topical benzoyl peroxidase 2. topical abx (e.g clindamycin - prescribed alongside benzolyl peroxidase) 3. OCP for women .4. oral retinoids (isotretinoin)
269
tool for estimating individual risk of developing a pressure ulcer ?
waterlow score
270
compare arterial vs venous ulcers
location size depth appearance Typically, arterial ulcers: Occur distally, affecting the toes or dorsum of the foot Are associated with peripheral arterial disease, with absent pulses, pallor and intermittent claudication Are smaller than venous ulcers Are deeper than venous ulcers Have well defined borders Have a “punched-out” appearance Are pale colour due to poor blood supply Are less likely to bleed Are painful Have pain worse at night (when lying horizontally) Have pain is worse on elevating and improved by lowering the leg (gravity helps the circulation) Typically, venous ulcers: Occur in the gaiter area (between the top of the foot and bottom of the calf muscle) Are associated with chronic venous changes, such as hyperpigmentation, venous eczema and lipodermatosclerosis Occur after a minor injury to the leg Are larger than arterial ulcers Are more superficial than arterial ulcers Have irregular, gently sloping border Are more likely to bleed Are less painful than arterial ulcers Have pain relieved by elevation and worse on lowering the leg
271
mx arterial ulcer
The management of arterial ulcers is the same as peripheral arterial disease, with an urgent referral to vascular to consider surgical revascularisation. If the underlying arterial disease is effectively treated, the ulcer should heal rapidly. Debridement and compression are not used in arterial ulcers.
272
mx venous ulcer
Cleaning the wound Debridement (removing dead tissue) Dressing the wound Compression therapy is used to treat venous ulcers (after arterial disease is excluded with an ABPI).
273
heart failure signs on xray
A - alveolar oedema (bat wing opacities) B - Kerley B lines C - cardiomegaly D - dilated upper lobe vessels E - pleural effusion
274
how to manage acute HF on the ward ?
furosemide fluid restrict monitor weight check for low K+ fluid balance monitoring
275
why is SVT narrow QRS complez, but V tachy is broad complex
SVT starts above the ventricles, so once it reaches bundle of his / R/L bundle its smooth sailing and conduction is good However, with ventricular tachycardias. the electrical activity starts in the ventricle somewhere and it isn't a smooth path through ventricle cause its not on the classic highway
276
narrow vs broad complex on ECG - how many small squares / how long ?
< 120ms each small square is 0.04. which is 40ms. therefore < 3 small squares
277
different cardio scars I need to be aware of
midline sternotomy - CABG thoracotomy (anterolateral / posteriorlateral) - lobectomy/pneumectomy subclavicular incision - pacemaker
278
what does bradycardia in MI suggest ?
RCA since the RCA supplies the AV node. therefore we're thinking about heartblock
279
mx of acute STEMI
ABCDE antiplatelets - aspirin + clopidogrel anticoagulants - heparin anti-ischaemics - nitrates / ACE-i / BB high intensity statin deinfitive mx = PCI
280
UMN vs LMN lesions
UMN - hyperreflexia -hypertonia - clonus LMN - hypo reflexia - hypotonia - fascilations - wasting
281
pyramidal vs extrapyramidal tracts - explain
these are the descending fibres - ie motor fibres 1. pyramidal --> involved in voluntary movement. corticospinal and corticobulbar 2. extra pyramidal --> lots of different types. invovled in balance/tone etc
282
give some more sophistatced level to assessing tone
spasticity = velocity dependant. faster you go the more resistance you feel UMN pyramidal difference between flexion and extension rigidity = non velocity dependant (parkinsons). e,g, lead pipe. moving at the same speed the whole time extra pyramidal
283
how do you tell bells palsy vs stroke ?
bells palsy is LMN lesion and therefore no forehead sparing
284
outline features of charcot marie tooth disease
* High foot arches (pes cavus) * Distal muscle wasting causing “inverted champagne bottle legs” * Weakness in the lower legs, particularly loss of ankle dorsiflexion * Weakness in the hands * Reduced tendon reflexes * Reduced muscle tone * Peripheral sensory loss
285
peripheral neuropathy differentials
Causes of Peripheral Neuropathy A – Alcohol B – B12 deficiency C – Cancer and Chronic Kidney Disease D – Diabetes and Drugs (e.g. isoniazid, amiodarone and cisplatin) E – Every vasculitis
286
how many beats of foot flapping to be classified as true clonus ?
5 beats
287
what is this History: Tracey says she developed sudden severe left eye pain and complains of blurred vision. She says that the ceiling lights have strange halos around them. She vomited once during the consultation. Examination: Left eye is red and has a mid-dilated, fixed pupil. Some corneal oedema (haziness) is noted on slit lamp examination
acute angle closure glaucoma
288
sx and signs for acute angle closure galucoma
Severe ocular pain * Blurred vision * Nausea + vomiting * Halos around lights Signs: * Red eye * Mid-dilated fixed pupil * Corneal oedema (hazy cornea) * Hard eyeball on palpation
289
defintive mx for acute angle closure glaucoma
Laser peripheral iridotomy after acute attack has resolved
290
how do you get orbital cellutitis ?
* Bacterial infection spreading from the sinuses o Ethmoid sinusitis o Dental infection * Trauma that introduces bacteria directly into the orbit (e.g. injury, surgery) * Haematogenous spread (rare)
291
sx and signs for orbital cellutis
Symptoms: * Severe eye pain, with painful eye movements * Redness and swelling * Blurred vision * Fever, headache and malaise Signs: * Proptosis * Ophthalmoplegia * Chemosis * Eyelid erythema + oedema * Decreased visual acuity
292
ix and mx for orbital cellulitis ?
CT scan of orbits and sinuses - Microbiology swab + MC&S - Bloods + cultures Management - Emergency ophthalmology referral - Immediate IV antibiotics (e.g. cefotaxime or clindamycin) o IV vancomycin + cefotaxime + clindamycin if MRSA suspected
293
match these opthlal signs with their respective conditions A) Anterior chamber cells and flare B) Dilated pupil and corneal haze C) Retinal haemorrhage and macular oedema D) Corneal ulcer and hypopyon E) Conjunctival injection and foreign body
A) Anterior chamber cells and flare (Anterior uveitis) B) Dilated pupil and corneal haze (AACG) C) Retinal haemorrhage and macular oedema (Diabetic retinopathy) D) Corneal ulcer (Bacterial keratitis) E) Conjunctival injection and foreign body (Corneal abrasion or trauma)
294
sx and signs of anterior uveitis
Symptoms: * Deep, aching pain in eye * Redness around iris * Photophobia * Blurred vision * Increased tear production Signs: * Ciliary injection (red around cornea) * Small or irregular pupil * Hypopyon (severe cases) * Posterior synechiae * Anterior chamber cells and flare * Keratic precipitates
295
ix and mx for scleritis
Investigations: - Clinical diagnosis - Bloods --> FBC, U+E, CRP, ESR, RF, ANCA - Consider imaging (OCT, CT, MRI) Management - Emergency ophthalmology referral 1. Oral NSAIDs (e.g. ibuprofen) 2. High dose prednisolone +- immunosuppressive agent (e.g. methotrexate) for disease control - Investigation or further Rx for underlying disease
296
sx and signs of retinal detachment
Symptoms: * Gradual or sudden vision loss – veil/curtain descending * Flashes of light * Floaters – spots/cobwebs signs Reduced visual acuity * Loss of central vision * Loss of peripheral vision
297
outline central retinal vein occlusion
Pathophysiology: Embolus, thrombosis or ischaemia Symptoms: Sudden, painless vision loss Signs: Reduced visual acuity Fundoscopy: Retinal haemorrhages, cotton wool spots, tortuous retinal veins, macular oedema, "pizza pie" Investigations: Fluorescein angiogram to confirm Dx Management: - Uncomplicated: observation + control risk factors - Macular oedema: intravitreal VEGF inhibitors - Neovascularisation: pan-retinal photocoagulation
298
central retinal artery occlusion outline
Pathophysiology: Embolus, thrombosis or ischaemia Symptoms: Sudden, painless vision loss Signs: Reduced visual acuity Fundoscopy: Retinal pallor, cherry-red spot (fovea), retinal oedema, retinal haemorrhages Investigations: Fluorescein angiogram to confirm Dx Management: - Urgent evaluation for ?stroke - Firm ocular massage to dislodge obstruction - Lower IOP (acetazolamide) + dilate artery (hyperbaric O2) - Identify and address underlying causes
299
vitreous haemorrhage outline
Pathophysiology: Proliferative diabetic retinopathy, Posterior vitreous detachment, ocular trauma Symptoms: Sudden, painless vision loss, red hue to vision, new onset floaters/shadows/cobwebs Signs: Reduced visual acuity and/or visual field defects if haemorrhage large Investigations: Ultrasound orbit, fluorescein angiography Management: - Treat underlying cause if known - Vitrectomy if unable to treat cause
300
fundscopy findings for hypertensive retinopathy
Fundoscopy: Arteriolar narrowing and copper wiring, AV nicking, retinal haemorrhages, cotton wool spots, disc swelling
301
what is Small bowel bacterial overgrowth syndrome (SBBOS)
Risk factors * neonates with congenital gastrointestinal abnormalities * scleroderma * DM * Surgery- slow motility Dx (of exclusion) * hydrogen breath test * - Small bowel aspiration and culture: this is used less often as invasive, and results are often difficult to reproduce * ?antibiotics as a diagnostic trial Sx * chronic diarrhoea * bloating, flatulence * abdominal pain Mx * Diet, hydration * Correction of the underlying disorder * Abx (:rifaximin) or co-amoxiclav or metronidazole
302
classification of bowel obstruction
MECHANICAL OBSTRUCTION (bowel capable of contracting proximally) * Adhesions * Hernia * Colonic carcinoma * Volvulus * Diverticular disease FUNCTIONAL OBSTRUCTION (bowel unable to contract/not enough) * paralytic ileus * spinal cord injury (CES) * Toxic megacolon * pseudo-obstruction * Post-op ileus * Hirschsprung's disease
303
closed loop obstruction
A section of the bowel is blocked at two points, preventing the contents from moving forwards or backwards
304
Most common site of bowel perforation in closed loop obstruction?
caecum The law of Laplace states “in a long pliable tube, the site of largest diameter requires the least pressure to distend”. In a patient suffering a distal large bowel obstruction, in the setting of a competent ileocaecal valve, the caecum is the most common site of perforation.
305
upper limits of distention on XRAY for bowel obstruction
369 3 - small bowel 6 - colon 9 - caecum
306
stoma complciations ?
early: infection bleeding failure - no ouput ischaemia rettraction high output stoma late: stenosis prolapse parastomal hernia dermatitis fistulae
307
anal vs rectal cancers resections - explain
anal cancers are more agressive (sqcc) so you take out more * SqCC vs Adenocarninomas *Inguinal lymph nodes vs deeper pelvic nodes * Chemo radio anal>rectal * Preservation of normal bowel function * Lower anastomosis = higher complications anal cancer you do - Abdomino-perineal excision of rectum (APR) rectal cancer you can either do high/low anterior resection (w/ colo rectal anastamosis)
308
compare iliostomy and colostomy
iliostomy: RIF usually Watery contents Spout Perm: proctocolectomy Temp Anterior resection colostomy: LIF (usually) Formed faeces Flush Perm: AP resection Temp: Hartmann’s
309
difference between incarcerated vs strangulated
Incarcerated Contents of a hernia are trapped Strangulated Blood supply to the contents of the hernia is compromised
310
reducible vs irreducible hernias
Reducible Can be pushed back into the abdomen, Irreducible Cannot be pushed back into the abdomen
311
femoral vs inguinal hernia
Femoral hernia Below and Lateral to pubic tubercle- F>M, high risk of strangulation Inguinal hernia Above and Medial to pubic tubercle
312
indirect vs direct inguinal hernia
Indirect inguinal Pushes through inguinal canal Direct inguinal Pushes directly through weakness in abdominal wall - posterior wall of inguinal canal
313
How could the doctor ascertain the anatomy and subtype of this swelling for an inguinal hernia ?
allow reduction of hernia and then, Press on the deep inguinal ring and ask the patient to cough If a hernia reappears it is more likely to be a direct inguinal hernia whereas if it does not, it is more likely to be an indirect inguinal hernia
314
localising features of focal seizures
Frontal lobe (motor) Head/leg movements, posturing, post-ictal weakness, Jacksonian march Parietal lobe (sensory) Paraesthesia Occipital lobe (visual) Floaters/flashes Temporal lobe May occur with or without impairment of consciousness or awareness An aura occurs in most patients typically a rising epigastric sensation also psychic or experiential phenomena, such as dejà vu, jamais vu less commonly hallucinations (auditory/gustatory/olfactory) Seizures typically last around one minute automatisms (e.g. lip smacking/grabbing/plucking) are common
315
causes of splenomegaly
chronic liver disease (portal hypertension) haematology - chronic haemolytic anaemias / lympho/myeloproliferative disorders infection: TB inflammation: Sarcoid malignancy: Lymphoma
316
what drugs do you need after developing cardiovascular disease
A – Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor) A – Atorvastatin 80mg A – Atenolol (or an alternative beta blocker – commonly bisoprolol) titrated to the maximum tolerated dose A – ACE inhibitor (commonly ramipril) titrated to the maximum tolerated dose
317
which drugs after having an MI ?
Aspirin 75mg daily (continued indefinitely) Clopidogrel or ticagrelor (generally for 12 months before stopping)
318
which drug in peripheral arterial disease ?
clopidogrel
319
which drug following iscaemic stroke ?
clopidogrel
320
how to manage stable angina ?
symptomatic relief: GTN spray long term: beta blocker / calcium channel blokcer (maybe both in combination)
321
STEMI is diagnosed when the ECG shows either:
ST elevation New left bundle branch block
322
how to remember intial managment for patients presenting with ACS
CPAIN C – Call an ambulance P – Perform an ECG A – Aspirin 300mg I – Intravenous morphine for pain if required (with an antiemetic, e.g., metoclopramide) N – Nitrate (GTN)
323
definiitve management for STEMI
Patients with STEMI presenting within 12 hours of onset should be discussed urgently with the local cardiac centre for either: Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting) Thrombolysis (if PCI is not available within 2 hours)- e.g. alteplase
324
how to manage NSTEMI
The medical management of an NSTEMI can be remembered with the “BATMAN” mnemonic: B – Base the decision about angiography and PCI on the GRACE score A – Aspirin 300mg stat dose T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography) M – Morphine titrated to control pain A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography) N – Nitrate (GTN) Give oxygen only if their saturation drops (less than 95% in someone without COPD). Unstable patients are considered for immediate angiography, similar to with a STEMI. The GRACE score gives a 6-month probability of death after having an NSTEMI. 3% or less is considered low risk Above 3% is considered medium to high risk Patients at medium or high risk are considered for early angiography with PCI (within 72 hours).
325
secondary prevention following MI
6 As Aspirin 75mg once daily indefinitely Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months Atorvastatin 80mg once daily ACE inhibitors (e.g. ramipril) titrated as high as tolerated Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
326
complications of MI
DREAD D – Death R – Rupture of the heart septum or papillary muscles E – “oEdema” (heart failure) A – Arrhythmia and Aneurysm D – Dressler’s Syndrome
327
pericardial rub
pericarditits Pericardial friction rub on auscultation is a key examination finding
328
bloods and ECG for pericarditis
Blood tests show raised inflammatory markers (white blood cells, CRP and ESR). ECG changes include: Saddle-shaped ST-elevation PR depression
329
mx pericarditis q
Non-steroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment (e.g., aspirin or ibuprofen) Colchicine (taken longer-term, e.g., 3 months, to reduce the risk of recurrence)
330
ix for heart failure
Clinical assessment (history and examination, starting with an ABCDE approach in any acutely unwell patient) ECG to look for ischaemia and arrhythmias Bloods for anaemia, infection, kidney function, BNP, and consider troponin if suspecting myocardial infarction Arterial blood gas (ABG) Chest x-ray Echocardiogram
331
mx for acute left ventricular failure
this is normally due to decompensated heart failure SODIUM S – Sit up O – Oxygen D – Diuretics (furosemide) I – Intravenous fluids should be stopped U – Underlying causes need to be identified and treated (e.g., myocardial infarction) M – Monitor fluid balance
332
New York Heart Association Classification The New York Heart Association (NYHA) classification system is used to grade the severity of symptoms related to heart failure. Here is a simplified summary:
Class I: No limitation on activity Class II: Comfortable at rest but symptomatic with ordinary activities Class III: Comfortable at rest but symptomatic with any activity Class IV: Symptomatic at rest
333
first line medical treatments for chornic heart failure
The first-line medical treatment of chronic heart failure can be remembered with the “ABAL” mnemonic: A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone) L – Loop diuretics (e.g., furosemide or bumetanide)
334
number cut offs for diagnosis of hypertension
The NICE guidelines on hypertension (updated 2022) suggest a diagnosis of hypertension with a blood pressure above 140/90 in the clinical setting, confirmed with ambulatory or home readings above 135/85.
335
secondary causes of hypertension
Secondary causes of hypertension can be remembered with the “ROPED” mnemonic: R – Renal disease O – Obesity P – Pregnancy-induced hypertension or pre-eclampsia E – Endocrine D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)
336
different stages of hypertension based on numbers
stage 1 = Above 140/90 Above 135/85 (ambu) stage 2 = Above 160/100 Above 150/95 (ambu) stage 3 = Above 180/120
337
consequences of regurgigation and stenosis of valves for the chambers
aortic stenosis --> left ventricular hypertrophy aortic regurg --> left ventricular dilatation
338
consequences of mitral stenosis
malar flush atrial fibrilaltion (due to left atrial strain )
339
collapsing pulse cause ?
aortic regurg (also PDA)
340
sx and exam findings of infective endocarditis
Fever Fatigue Night sweats Muscle aches Anorexia (loss of appetite) The key examination findings are: New or “changing” heart murmur Splinter haemorrhages (thin red-brown lines along the fingernails) Petechiae (small non-blanching red/brown spots) on the trunk, limbs, oral mucosa or conjunctiva Janeway lesions (painless red flat macules on the palms of the hands and soles of the feet) Osler’s nodes (tender red/purple nodules on the pads of the fingers and toes) Roth spots (haemorrhages on the retina seen during fundoscopy) Splenomegaly (in longstanding disease) Finger clubbing (in longstanding disease)
341
ix for IE
Blood cultures are essential before starting antibiotics. Three blood culture samples are recommended, usually separated by at least 6 hours and taken from different sites. The gap between repeated sets may have to be shorter if antibiotics are required more urgently (e.g., sepsis). Echocardiography is the usual imaging investigation. Transoesophageal echocardiography (TOE) is more sensitive and specific than transthoracic echocardiography. Vegetations (an abnormal mass or collection) may be seen on the valves.
342
criteria for Infective endocardtitis
Modified Duke Criteria The Modified Duke criteria can be used to diagnose infective endocarditis. A diagnosis requires either: One major plus three minor criteria Five minor criteria Major criteria are: Persistently positive blood cultures (typical bacteria on multiple cultures) Specific imaging findings (e.g., a vegetation seen on the echocardiogram) Minor criteria are: Predisposition (e.g., IV drug use or heart valve pathology) Fever above 38°C Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions) Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis) Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)
343
reversal agent for apixaban
Andexanet alfa
344
reversal agent for rivaroxaban
Andexanet alfa
345
reversal agent for dabigatran
Idarucizumab
346
how to manage AF
1. rhythm and rate control 2. anticoagulation rate control for all patients except: - reversible cause - new onset < 48 hours - heart failure - sx despite rate control rate control = beta blocker/calcium channel blocker / digoxin rhythm control (cardioversion): Immediate cardioversion (either with pharmocolgical cardioversion - Flecainide Amiodarone or electrical cardioversion): - Present for less than 48 hours - Causing life-threatening haemodynamic instability Delayed cardioversion: - present for more than 48 hours and they are stable. Electrical cardioversion. this is because clot might have developed and you want to anticoagulate them for 3 weeks before doing this. another option is: Long-term rhythm control is with: Beta blockers first-line Dronedarone second-line for maintaining normal rhythm where patients have had successful cardioversion Amiodarone is useful in patients with heart failure or left ventricular dysfunction
347
steps in managing SVT
Step 1: Vagal manoeuvres Step 2: Adenosine (6,12,18) Step 3: Verapamil or a beta blocker Step 4: Synchronised DC cardioversion
348
what are the 4 cardiac arrrest rhythms (shockable ??)
Shockable rhythms: Ventricular tachycardia Ventricular fibrillation Non-shockable rhythms: Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse) Asystole (no significant electrical activity)
349
Management of unstable patients with bradycardia
Management of unstable patients and those at risk of asystole involves: Intravenous atropine (first line) Inotropes (e.g., isoprenaline or adrenaline) Temporary cardiac pacing Permanent implantable pacemaker, when available
350
indications for pacemaker
Symptomatic bradycardias (e.g., due to sick sinus syndrome) Mobitz type 2 heart block Third-degree heart block Atrioventricular node ablation for atrial fibrillation Severe heart failure (biventricular pacemakers)
351
pacemaker vs ICD
pacemaker = device implanted and has leads either going into RA/RV/LA or all three to coordinate contraction ICD (implantable cardiverter device) = monitor heart and give a defibrillator shock if VF/VT detected
352
medical mx postural hypotension
Fludrocortisone Fludrocortisone is a synthetic mineralocorticoid that expands plasma volume. It has demonstrated good efficacy for patients whose plasma volume fails to adequately increase with salt and bolus fluids
353
venturi vs non rebreather mask
A venturi mask is used when a fixed concentration of oxygen is needed. The non-rebreather mask is used mainly in emergency situations for acute respiratory conditions. use a venturi mask when you want to deliver a fixed amount of O2 for example for a patient with COPD.
354
retinal vein occlusion vs retinal artery occulsion
both sudden onset unilateral vision loss can differentiate on fundoscopy vein occlusion = widespread hyperaemia severe retinal haemorrhages - 'stormy sunset' artery occlusion = cherry red spotho
355
how to manage an aggressive patient
1. verbal de-escalation 2. haloperidol Whilst anti-psychotics are first-line to manage delirium where medication required, they are contra-indicated in Parkinson’s disease. (NICE CG103 Delirium: prevention, diagnosis and management). ==> Therefore you prescribe lorazepam for these patients instead of haloperidol
356
violent patient with parkinsons what do you do ?
after verbal de-escalation. you cannot give them haloperidol as anti-psychotics contrindicated therefore give lorazepam
357
how does prolapsed lumbar disc present ?
A prolapsed lumbar disc usually produces clear dermatomal leg pain associated with neurological deficits. Features leg pain usually worse than back pain often worse when sitting sensory changes as well. this differs depending at what level the compression is
358
features of osteomalacia
Features bone pain bone/muscle tenderness fractures: especially femoral neck proximal myopathy: may lead to a waddling gait
359
what is normal JVP ?
4. Measure the JVP by assessing the vertical distance between the sternal angle and the top of the pulsation point of the IJV (in healthy individuals, this should be no greater than 3cm)
360
what level of hyperkalaemia do you give calcium gluconate
All patients with severe hyperkalaemia (≥ 6.5 mmol/L) or with ECG changes should have emergency treatment IV calcium gluconate: to stabilise the myocardium insulin/dextrose infusion: short-term shift in potassium from ECF to ICF
361
what is contrast nephropathy and how do you prevent it ?
The patient is due to receive IV contrast and has existing CKD. He is an increased risk of contrast nephropathy. Volume expansion with 0.9% sodium chloride infusion (1 mL/kg) is recommended and shown to reduce the incidence of contrast nephropathy
362
important guidance when looking at creatine kinase in rhabdomylsis
the CK is significantly elevated, at least 5 times the upper limit of normal elevations of CK that are 'only' 2-4 times that of normal are not supportive of a diagnosis and suggest another underlying pathophysiology therefore CK > 10,000
363
ERCP VS MRCP
Endoscopic retrograde cholangiopancreatography - invasive scope goes down GI tract. can visualise biliary tree. remove stones. MR cholangiopancreatography - non-invasive imaging technique that gives a picture of biliary tree. this is preferred in PSC & PBC
364
nuclear enlargement, hyperchromasia and pleomorphism features of what ?
carcinoma
365
COPD mx
1. SABA/SAMA 2. determine if steroid responsiveness - hx of atopy/asthma - eosinophil raised - diurinal variation - variation of FEV1 > 400mls a. if steroid responsive features - add LABA + ICS b. if no steroid responsive features - add LABA + LAMA
366
mx acute exacerbation COPD
1. Regular inhalers or nebulisers (e.g., salbutamol and ipratropium) 2. Steroids (e.g., prednisolone 30 mg once daily for 5 days) 3. Antibiotics if there is evidence of infection more severe: 4. IV aminophylline 5. Non-invasive ventilation (NIV) 6. Intubation and ventilation with admission to intensive care
367
problems with prescribing oxybutinin for eldery frail person
anti-cholinergic side effects can increase risk of falls Consider non-anticholinergic medications for overactive bladder, such as mirabegron (a beta-3 adrenergic agonist), which has a lower risk of cognitive and systemic side effects.
368
mx for ileus
Supportive care involves: Nil by mouth or limited sips of water NG tube if vomiting IV fluids to prevent dehydration and correct the electrolyte imbalances Mobilisation to helps stimulate peristalsis Total parenteral nutrition (TPN) may be required whilst waiting for the bowel to regain function you can try and figuer out reversible causes - if not then may have to go back to surgery
369
which gastric ulcer is worse at night ?
Duodenal ulcers tend to be made worse with stress and the pain is often worse at night radiating into the back - it is relieved by eating and patients tend to put weight on - in contrast to a gastric ulcer which is made worse with eating and people often lose weight.
370
how to manage acute flare of gout in patient with CKD
NSAIDs (e.g., naproxen) first-line (co-prescribed with a proton pump inhibitor for gastroprotection) Colchicine second-line Oral steroids (e.g., prednisolone) third-line
371
in palliative patient who is dying what do you prescribe for restlessnes ?
Midazolam
372
In which part of the brain are changes most likely to be found in early Alzheimer’s disease?
temporal lobe
373
overdose of amitriptyline hydrochloride and ECG changes. also what are the ECG changes
IV Sodium bicarbonate ECG: prolonged QRS
374
COPD having surgery what do you need to bear in mind with their analgesia ?
major abdominal surgery in respiratory disease, opioid, by whatever route, should be avoided. Epidural is best because it can be topped up and titrated; spinal anaesthesia cannot.
375
outline different systems affected in haemachromatosis
Pancreas → Diabetes mellitus Liver → Cirrhosis, liver failure, hepatomegaly Heart: Cardiac arrhythmias & myopathy Pituitary Gland and Sex Organs → Amenorrhoea, impotence, hypogonadism Skin → Tanned complexion Other → Arthropathy, fatigue
376
important side effect of ciprofloxacin
quinolones (e.g. ciprofloxacin) are associated with an increased risk of Achilles tendinitis
377
ix for ankle fracture - what tool is used ?
Ottawa Ankle Rules Plain X-Ray of the ankle is indicated if any of the following are present: Bone tenderness within 6 cm of the posterior edge of the tip of the lateral malleolus Bone tenderness within 6 cm of the posterior edge of the tip of the medial malleolus Bone tenderness over the base of the 5th metatarsal Bone tenderness over the navicular Inability to weight bear immediately after the injury and in the Emergency Department CT may be considered in some cases where the fractures are complex
378
types of #NOF and what intervention
intracapsular 1. Garden 1/2 - cannulated hip screw - DHS 2. Garden 3/4 - hemi-arthoplasty - total hip reaplacement Extracapsular 1. Dynamic hip screw
379
how to describe a #NOF
Description of Fracture Location Subcapital (Intracapsular) Transcervical (Intracapsular) Basicervical (Intracapsular) Intertrochanteric (Extracapsular) Subtrochanteric (Extracapsular) Degree of Displacement: Garden Classification Garden I: incomplete and undisplaced fracture Garden II: Complete but undisplaced fracture Garden III: Complete fracture with partial displacement Garden IV: Complete fracture with 100% displacement
380
XRAY features in OA
Loss of joint space Osteophytes Subchondral cysts Subchondral sclerosis
381
mx for hip OA
Conservative Measures Physiotherapy Weight Loss Analgesia 1st Line: Paracetamol and/or Topical NSAIDs 2nd Line: Oral NSAID (e.g. ibuprofen) or highly-selective COX-2 inhibitor (e.g. celecoxib) Along with a PPI (e.g. omeprazole) Adjunct: Intra-articular Steroid Injection 3rd Line: Consider referral for joint replacement Surgical Management Total Hip Replacement Approaches Posterior (MOST COMMON) Anterolateral Anterior Approach
382
class hx for ACL tear
Sudden pain and rapid joint swelling Usually occurs after a sudden twisting movement of the knee (e.g. when changing directions during sports) Sensation of the leg 'giving way'
383
special tests for ACL tear
Lachman Test Place the knee at 30 degrees flexion, stabilise the femur with one hand and pull the knee forward to assess the degree of anterior displacement of the tibia relate to the femur Anterior Drawer Test Place the knee at 90 degrees flexion, place both hands on either side of the proximal tibia and pull the tibia forward to assess the degree of anterior displacement of the tibia relative to the femur.
384
gold standard ix for ACL tear
MRI
385
special tests for IT band syndrome
Nobles Test Lie the patient flat and place a finger no the lateral femoral condyle. Slowly extend the knee. Interpretation: Positive if pain at 30 degrees flexion Renne Test Whilst the patient is standing, put pressure on the lateral epicondyle of the affected knee and ask the patient to squat. Interpretation: Positive if pain at 30 degrees flexion
386
features of MCL tear and special test ?
Symptoms Knee pain Swelling Difficulty weight bearing Tenderness along medial margin of the knee A Grade II and III tear can be distinguished clinically on medial stress testing; Grade II is lax in 30 degrees of knee flexion but solid in full extension, whereas Grade III is lax in both these positions. Special Tests: Valgus Stress Test (excessive laxity noted)
387
valgus vs varus forces on knee ?
Valgum makes the knees stick together Valgus - knees going inwards. testing MCL Varus - knees going outward. testing LCL
388
Locking of the knee - what does this indicate ?
Meniscal tear Clinical Features Sudden-onset pain in the knee Swelling Locking of the knee (can occur due to fragments of loose tissue getting stuck within the joint)
389
special tests for meniscal tear
McMurray's Test Whilst supine, hold the knee with one hand and the foot with another. From a position of maximal hip and knee flexion, extend the knee whilst internally rotating the tibia and applying a varus stress. Reverse the movement and return the leg to maximal flexion with external rotation of the tibia and a valgus stress. Pain is suggestive of a meniscal tear
390
special tests for PCL injury
Posterior Sag Test Lie the patient flat and ask them to bend their knees to 90 degrees. Support the patient's foot and check whether the tibia sags posteriorly relative to the femur at the knee joint.
391
adhesive capsulitis featuers
Shoulder pain and severely restricted movement due to joint stiffness Tenderness on palpation May be described as having Three Stages Stage 1 (Freezing): Gradual onset of pain that leads to worsening range of motion. Stage 2 (Frozen): Gradual improvement in pain but stiffness remains. Stage 3 (Thawing): Range of motion gradually returns to normal over several months.
392
outline de quervain's tenosynovitis
Definition Inflammation of the tendons of extensor pollicis brevis and abductor pollicis longus resulting in wrist pain. Aetiology and Risk Factors Risk Factors Repetitive wrist movements (e.g. typing or writing) Female Pregnancy Symptoms Pain at the base of the thumb There may be associated swelling Finkelstein Test Apply longitudinal traction and ulnar deviation to the thumb on the affected hand This will elicit pain over the radial styloid in patients with De Quervain's tenosynovitis Investigations Clinical diagnosis Management Lifestyle advice (avoid repetitive actions) Wrist splint Steroid injections Surgical decompression of extensor compartment
393
3 types of fracture involving distal radius
Fracture involving the distal end of the radius. Three Types Colles' Fracture: distal radius fracture with dorsal displacement of the distal fracture component Smith Fracture: distal radius fracture with volar displacement of the distal fracture component Barton Fracture: intra-articular fracture of the distal radius associated with dislocation of the distal radioulnar joint Occurs following a fall onto an outstretched hand Symptoms History of a fall onto an outstretched hand Wrist pain Deformity Assess Neurovascular Status
394
Colles vs Smiths fracture
Colles' Fracture: distal radius fracture with dorsal displacement of the distal fracture component - palm hits ground Smith Fracture: distal radius fracture with volar displacement of the distal fracture component - dorsum of hand hits ground
395
test for duputrens contracture
Unable to lay hand flat on the table (Hueston Test)
396
Medial & Lateral Epicondylitis what is it
Chronic inflammation of the medial or lateral epicondyle. Medial: Golfer's Elbow Lateral: Tennis Elbow
397
role of 4 rotator cuff muscles
There are FOUR rotator cuff muscles that are responsbile for the following movements Supraspinatus: abduction (first 30 degrees) Infraspinatus: external rotation Teres Minor: external rotation Subscapularis: internal rotation
398
Tenderness over the anatomical snuffbox
scaphoid fracture
399
in acute A to E scenario what is a good acronym to remmeber for hx
Includes the following information: AMPLE Allergies Medications Past medical history Last meal Event leading to presentation
400
acute abdomen work up and mx
Work-Up Bedside: urinalysis, bladder scan Bloods: FBC, U&E, LFT, Amylase/Lipase, Clotting, G&S, CRP Imaging: Erect CXR, CT, Ultrasound Management Keep nil-by-mouth (as may require surgical intervention) Consider need for variable rate insulin infusion in patients with diabetes mellitus IV Fluids IV Antibiotics (if infectious process such as cholecystitis or appendicitis is suspected) IV Analgesia (often requires strong opioid analgesia) Urgent Discussion with Surgical Team (definitive management depends on cause of acute abdomen – e.g. cholecystectomy for cholecystitis)
401
which blood bottle for FBC (any haematolgy stuff)
purple / lavender Purple blood bottles contain EDTA (ethylenediaminetetraacetic acid), which acts as a potent anticoagulant by binding to calcium in the blood
402
explain the anitcipation of blood transfusion tests ?
Group and save (G&S): this simply means the patient’s blood is typed and tested for antibodies, then saved in the lab in case it is required; it DOES NOT get you blood products for transfusion. If you need blood products you have to request a crossmatch Crossmatch (XM): this means that the patient’s blood is typed and tested as above, then matched to specific units of blood, platelets or other products for transfusion. You need to specify on the form how many units you need, why you need them and when they are required. A full crossmatch takes about 45-60 minutes in the lab – if you have an unstable bleeding patient and think you’ll need blood products sooner than this, you still need to send a crossmatch sample, but you can ask the lab for units of type-specific blood (which take 10-20 minutes), or in a genuine emergency you can use their stocks of O negative blood from the fridge.
403
which bottle for GS/cross match ?
pink
404
which bottle for clotting stuff ?
blue
405
blue blood bottle for ?
clotting
406
gold blood bottle for ?
loads of stuff (U&Es, CRP, LFTs etcc)
407
grey blood bottle for ?
Glucose: this can be fasting or non-fasting, or part of a glucose tolerance test (GTT) Lactate
408
acute asthma exacerbation A-E findings
AIRWAY: Tongue swelling, cough, cyanosis, unable to complete sentences BREATHING: Wheeze, reduce chest expansion, tachypnoea, increased respiratory effort, silent chest CIRCULATION: Tachycardia DISABILITY: Drowsiness (CO2 retention) EXPOSURE: Rashes (anaphylaxis is a differential)
409
work up in patient with acute asthma exacerbation
Bedside: PEFR, ECG, ABG, SaO2 Bloods: FBC, U&E Imaging: CXR
410
mx for acute asthma exacerbation
Management WARN ICU if severe or life-threatening asthma attack Bronchodilation: nebulised salbutamol 5 mg with high flow oxygen Steroids: IV hydrocortisone 100 mg or PO prednisolone 40-50 mg Oxygen: 15 L/min oxygen through a non-rebreathe mask if saturations < 92% If Life-Threatening - Add nebulised ipratropium bromide 500 µg 6-hourly - Administer IV magnesium sulphate 1.2-2 g over 20 mins If Responding to Treatment - 4-hourly salbutamol nebulisers - Prednisolone 40-50 mg OD for 5-7 days - Monitor PEFR and SaO2 If NOT Responding to Treatment Refer to ICU for intensified therapy (e.g. intubation, IV aminophylline)
411
A to E in COPD exacerbation
AIRWAY: Cough (productive?) BREATHING: Wheeze, crepitations (infection?), bronchial breathing, increased respiratory effort CIRCULATION: Tachycardia, raised JVP (right heart strain) DISABILITY: EXPOSURE: Fever
412
acute exacerbation of COPD work up
Work-Up Bedside: ECG, ABG Bloods: FBC, U&E, CRP, sputum culture Imaging: CXR
413
mx for acute asthma exacerbation
Bronchodilator: nebulised salbutamol 5 mg/4hr + nebulised ipratropium bromide 500 µg/6hr Oxygen: if hypoxic, start the patient on high-flow oxygen via a non-rebreather mask. Once an ABG has been performed and the patient’s carbon dioxide retainer status is established, this can be titrated aiming for target saturations of 88-92% if they are a retainer. Steroids: IV hydrocortisone 200 mg (or oral prednisolone) Antibiotics: following trust guidelines (e.g. amoxicillin, doxycycline) If NO Response to Treatment à Refer to ICU Consider IV aminophylline Consider NIV Consider intubation and ventilation Consider respiratory stimulant (e.g. doxapram)
414
what to do with oxygen therapy for someone coming in with acute exacerbation of COPD ?
if hypoxic, start the patient on high-flow oxygen via a non-rebreather mask. Once an ABG has been performed and the patient’s carbon dioxide retainer status is established, this can be titrated aiming for target saturations of 88-92% if they are a retainer (then you would use a venturi mask when you can control the specific amount )
415
work up for ACS
A to E Findings AIRWAY: BREATHING: Shortness of breath CIRCULATION: Tachycardia, arrhythmia, cardiogenic shock DISABILITY: EXPOSURE: Sweating, anxiety Work-Up Bedside: 12-lead ECG, capillary glucose Bloods: troponin, FBC, U&E, blood glucose, cholesterol Imaging: CXR
416
ACS management
Management Immediate IV Morphine 5-10 mg (repeat after 5 mins if necessary) IV Metoclopramide 10 mg 15 L/min oxygen via non-rebreathe mask if hypoxic PO Aspirin 300 mg AND PO Clopidogrel 300 mg OR PO Ticagrelor 180 mg STEMI Percutaneous coronary intervention if able to reach PCI centre within 120 mins of first medical contact Fibrinolysis (alteplase) within 30 mins of admission if PCI unavailable NSTEMI SC Fondaparinux 2.5 mg OD Assess risk and need for angiography (e.g. GRACE score) Drugs to Take Away on Discharge Dual antiplatelet therapy (aspirin 75 mg OD for life AND clopidogrel 75 mg OD for 1 year OR ticagrelor 90 mg BD for 1 year) ACE inhibitors (e.g. ramipril 1.25-2.5 mg OD – increasing up to 10 mg) Statin (e.g. atorvastatin 80 mg OD) Beta-Blocker (e.g. bisoprolol 2.5 mg OD – increasing up to 10 mg)
417
A to E findings in acute heart failure
AIRWAY: Cough, pink frothy sputum BREATHING: Cardiac wheeze, tachypnoea, bibasal crepitations CIRCULATION: Tachycardia, raised JVP, S3 gallop rhythm, displaced apex DISABILITY: Anxious, sweaty EXPOSURE: Pale, sitting up, ankle swelling
418
work up for acute heart failure
Work-Up Bedside: ECG, ABG Bloods: troponin, U&E, BNP Imaging: CXR, echocardiogram
419
mx for acute heart failure
Sit upright 15 L/min oxygen via non-rebreather mask Gain IV access Diamorphine 1.25-5 mg IV (caution in liver failure and COPD) Furosemide 40-80 mg IV STAT GTN Spray 2 Puffs Sublingual If NO response to treatment Repeat furosemide dose Consider CPAP Consider nitrate infusion Consider ITU admission If stable following response to treatment Monitor daily weight Repeat CXR Switch to oral diuretics (furosemide or bumetanide) To take away on discharge ACE inhibitor Beta-blocker Consider spironolactone
420
A to E findings in AKI
AIRWAY: Vomiting BREATHING: Tachypnoea, cough (pulmonary oedema), bibasal crackles CIRCULATION: Tachycardia, fluid overload DISABILITY: Confusion (uraemia), oliguria EXPOSURE: Abdominal pain (retention)
421
work up in AKI
Bedside: ECG (hyperkalaemia), urinalysis, urine sample (MC&S, ACR), ABG (acidosis), bladder scan Bloods: U&E, calcium, phosphate, FBC, CRP/ESR, LFTs, CK, renal screen Imaging: USS, CXR
422
mx for AKI
Treat HYPERKALAEMIA: 10-30 mL 10% Calcium Gluconate IV over 2-10 mins (can repeat every 15 mins up to 5 doses until K+ corrected) N.B. IV calcium gluconate must be administered by a doctor (i.e. not a nurse) due to risk of arrhythmia 10 U Actrapid with 100 mL 20% glucose IV over 10 mins Consider 5 mg Salbutamol nebuliser Monitor ECG and ensure quick access to defibrillator Repeat U&E ABG to check for acidosis Treat the CAUSE: - Hypovolaemia --> IV fluids - Retention --> catheterise - Pulmonary oedema --> cautious use of furosemide Indications for Urgent - -Dialysis - Refractory hyperkalaemia - Refractory pulmonary oedema - Uraemic complications (e.g. pericarditis, encephalopathy) - Severe metabolic acidosis (pH < 7.2)
423
A to E findings and work up for anayphylaxis
A to E Findings AIRWAY: Stridor, angioedema BREATHING: Cyanosis, wheeze, reduced breath sounds due to airway obstruction CIRCULATION: Hypotension DISABILITY: Low GCS EXPOSURE: Rash (urticaria), allergy bracelet Work-Up Go straight to management if anaphylaxis suspected
424
anaphylaxis mx
Management If airway compromised: secure airway and give high flow oxygen Administer 0.5 mg adrenaline IM (i.e. 0.5 mL of 1:1000) Repeat every 5 mins if needed Secure IV access Refractory Anaphylaxis (if no improvement after 2 doses of IM adrenaline) - Low-Dose IV Adrenaline Infusion (starting at 0.5-1.0 mL/kg/hour and titrating according to clinical response) The administration of chlorphenamine and steroids are no longer part of the acute management of anaphylaxis Administer IV fluid bolus if in shock Ongoing Management Allergy clinic to identify allergen (skin prick testing + specific IgE) Discharge with two adrenaline auto-ejectors Teach to self-inject adrenaline
425
work up for patient with decompensated chronic liver disease
Bedside: Urinalysis, BM Bloods: VBG, U&E, LFT, Clotting, G&S, CRP, Blood Cultures Imaging: CXR, US Abdomen, Ascitic Tap
426
which abx for supspected SBP
Tazocin
427
A to E for DKA
A to E Findings AIRWAY: Vomit, ketotic breath BREATHING: Laboured breathing (Kussmaul) CIRCULATION: Tachycardia, dehydrated DISABILITY: Drowsy, confused EXPOSURE: Insulin injection sites, insulin pump
428
work up for DKA
Work-Up Bedside: capillary glucose and ketones, urine dipstick, ECG Bloods: lab glucose and ketones, U&E, VBG, FBC, blood culture, amylase Imaging: CXR (as pneumonia can be a precipitant)
429
mx DKA
Management Insulin Add 50 U Actrapid to 50 mL 0.9% NaCl Infuse continuously at 0.1 U/kg/hour Aim for fall in ketones of 0.5 mmol/L/hour OR rise in venous bicarbonate of 3 mmol/L/hour with a fall in glucose of 3 mmol/L/hour If not achieving these targets, increase insulin infusion by 1 U/hour until targets are achieved Check VBG at 1 hour, 2 hours and 2 hourly thereafter Focus on pH, bicarbonate, glucose and potassium Consider low molecular weight heparin Once glucose < 14 mmol/L, start the patient on 10% glucose at 125 mL/hour alongside saline Continue fixed-rate insulin until ketones < 0.3 mmol/L, venous pH > 7.3 and venous bicarbonate > 18 mmol/L Treat any precipitants of DKA (e.g. infection) Fluid Replacement Use 0.9% NaCl Usual fluid deficit: 100 mL/kg Replace fluid deficit over 48 hours Potassium Replacement Usual deficit: 3-5 mmol/kg Do NOT add K+ to the first bag Monitor urine output and only add K+ once urine output > 30 mL/hour Check U&E hourly and replace as necessary If serum K+ is 3.5-5.5 mmol/L à add 40 mmol of K+ to 1 L of fluid
430
work up for head injury
Work-Up Bedside: Neurological examination, BM Bloods: FBC, U&E, blood alcohol, toxicology screen, VBG, clotting, G&S Imaging: CT Head
431
head injury mx
Oxygen if saturations < 92% (if concerned about raised intracranial pressure (ICP), patient may require intubation and hyperventilation) If concerned about C-spine, immobilise until imaging performed Stop blood loss and support circulation with fluids and blood products Treat seizures (e.g. with benzodiazepines) Check for CSF leak (e.g. rhinorrhoea) and features of basal skull fracture (e.g. Battle sign) Involve neurosurgeons early if concerned about raised ICP
432
major haemorrhage protocol
Indication: Clinical concern that the patient is bleeding and requires multiple blood products Launch: 2222 Adult Major Haemorrhage and state the ward and the bay Nominate: Ask one person to liaise with blood bank (request blood products + fibrinogen) Who Comes: Med Reg, Surgical Reg, Porter Blood Products Immediate: O- from the fridge 15 mins: Typed blood 40 mins: X-matched How to Administer Blood Check the blood products and the patient’s name and details (ask them to confirm) If needing rapid administration – use the Belmont rapid transfuser Patent needs to be monitored for features of anaphylaxis, TACO and TRALI
433
work up for patient with pneumothorax
Bedside: ECG Bloods: FBC, Clotting, G&S Imaging: CXR
434
PE mx
Management 15 L/min oxygen via non-rebreathe mask if hypoxic Morphine 5-10 mg IV (with metoclopramide 10 mg IV) treatment-dose anticoagulation (LMWH, UFH or DOAC) If CRITICALLY ILL with massive PE à immediate thrombolysis Ongoing Management Compression stockings Continue LMWH alongside warfarin until INR > 2 for 24 hours Duration of Warfarin Treatment If obvious cause for VTE à 3 months If NO obvious cause for VTE à 3-6 months
435
work up for patient with PE
Work-Up Bedside: ECG, ABG Bloods: FBC, U&E, clotting, D-Dimer, troponin, BNP Imaging: CXR, CTPA
436
work up for patient with seizure
Bedside: ECG, BM Bloods: FBC, U&E, Bone Profile, Magnesium, VBG (Lactate), Anticonvulsant Levels Imaging: CT Head
437
full mx for someone having a seizure
During Seizure Ensure that space surrounding the patient is clear of anything that could cause damage Start timing Gain IV access and blood (including VBG) If Status Epilepticus If IV Access IV Lorazepam 4 mg After 5-10 mins... IV Lorazepam 4 mg After 5-10 mins... Levetiracetam or Phenytoin or Sodium Valproate If no response... Try alternative second line agent If no response... Phenobarbital or General Anaesthesia (requiring intubation and ventilation) If IV access is proving to be difficult, intraosseous access should be considered. If NO IV Access Buccal midazolam or rectal diazepam After Seizure Reassess the patient using an A to E approach Correct any potential precipitants (e.g. hypoglycaemia, electrolyte imbalance)
438
work up for patient with suspected stroke
Bedside: ECG, capillary glucose Bloods: FBC, U&E, lipids, clotting, cardiac enzymes, G&S Imaging: CT head, carotid doppler
439
mx of stroke
Oxygen if SaO2 < 94% Nil by mouth Treat arrhythmia and low glucose if present Request urgent CT head scan Once haemorrhagic stroke has been RULED OUT: Aspirin 300 mg PO STAT (administer PR if concerns about swallow) Consider thrombolysis with tPA if: Age < 80 yrs and < 4.5 hours from start of symptoms Age > 80 yrs and < 3 hours from start of symptoms N.B. If it is a haemorrhagic stroke, the case should be urgently discussed with the on-call neurosurgeons. Will need physiotherapy and SALT input To Take Away: - After 2 weeks, switch from 300 mg Aspirin to 75 mg Clopidogrel OD PO - Statin (e.g. atorvastatin 80 mg) - Blood pressure medication - Anticoagulants (e.g. apixaban or warfarin) if co-existing AF
440
upper GI bleed work up
Bedside: BP Bloods: group and save, X-match 6-10 units of blood, clotting screen, LFT, FBC, U&E Imaging: endoscopy Scoring System: Rockall
441
mx for upper GI bleed
Protect airway and keep NBM Insert two large-bore cannulas Rapid IV crystalloid infusion up to 1 L Use O- blood until X-match is complete if grade 3-4 shock Correct clotting abnormalities (e.g. vitamin K, FFP, PCC) Consider referral to ICU for central venous line Insert catheter to monitor urine output Urgent endoscopy If MASSIVE BLEED: may require tamponade with Sengstaken-Blakemore tube Medical Management Major Ulcer Bleeding à Consider high-dose PPI after an endoscopy has been performed Variceal Bleeding à Terlipressin 2 mg SC/IV QDS
442
most important surg mx for PBH
TURP transurethral rescetion of the prostate
443
important medical mx for BPH
tamsulosin (decrease smooth muscle tone of the prostate and bladder) finasteride (block the conversion of testosterone to dihydrotestosterone (DHT), which is known to induce BPH)
444
mx of DVT in patient with CKD
This patient has a deep vein thrombosis (DVT) on a background of reduced renal function. NICE recommend specific drugs based on the patients eGFR. In patients with an eGFR of 15-50ml/min, a direct oral anticoagulant (DOAC) is recommended. In patients with an eGFR of <15ml/min, unfractionated heparin (UFH) or dose-adjusted low molecular weight heparin (LMWH) is recommended.
445
features of large vs small bowel obstruction on XRAY
small bowel - valvulae conitantes large bowel - haustra (do not traverse bowel)
446
how to investigate thyroid nodule?
Ultrasonography is the first-line imaging of choice, which may help determine if the nodule has features suspicious of malignancy.
447
ix for chlamydia
Nucleic acid amplification tests (NAATs) are the investigation of choice for Chlamydia
448
reverible causes of cardiac arrest
4 Hs: Hypoxia, hypovolemia, hypo/hyperthermia, and hyper/hypokalemia 4 Ts: Cardiac tamponade, tension pneumothorax, thrombosis, and toxins
449
BIPAP vs CPAP for COPD patient with acute exacerbation?
BIPAP Both CPAP and BiPAP provide positive airway pressure throughout the respiratory cycle, but BiPAP provides higher pressure during inspiration and lower pressure during expiration, which is why it is more beneficial for some COPD patients. This helps expel the excess CO2 and have enough O2 to transfer to tissues.
450
patient with metastic lung cancer. breathless with no revisble cause found (normal o2 sats) - which is best to prescribe ?
ANSWER = LORAZEPAM manage anxiety component of bretahlessnesss non-pharm - Talking therapy - CBT Pharm - benzodiazpine (short acting one like lorazepam ) (diazepam and chlorodiazapoxide - these very long acting and not appropriate - this is because you dont want it hanging around and making them drowsy )
451
indications for external fixation of a fracture
soft tissue injury / increased risk of infection
452
fracture complications
general: - fat embolus dvt infection uti chest infection Specific: - neurovascular injury - muscle tendon injry - non-union / mal union - degnerative change - reflex sympathetic dsystrophy
453
work up for patient with septic arthritis
Investigations joint aspiration: for culture. Will show a raised WBC raised inflammatory markers blood cultures
454
2 types of knee reapclemnt
total unicompartmental
455
Colle's vs smith fracture
colles = dorsally displaced distal fragment smiths= volar angulation
456
pneumonic for describing a fracture
OLD ACID Open vs closed Location Degree (complete vs incomplete) Articular involvement Comminution and pattern Intrinsic bone quality Displacement, angulation, rotation
457
hand findings in OA
heberdens nodes (DIP) bouchards nodes (PIP)
458
hand findings in RA
Boutoneieres of thumb swann neck ulnar deviation of MCP joints
459
compare morning stiffness of RA and OA
in RA morning stiffness > 30 mins in OA morning stiffness < 30 mins
460
mx carpal tunnnel
Conservative: Wrist splinting, more frequent breaks, avoidance of tasks which worsen symptoms. * Medical: NSAIDs, corticosteroids * Surgical: Carpal tunnel release
461
diagnostic criteria for SLE
SOAP BRAIN MD * Serositis (pleurisy, pleuritis, pleural effusion, pericarditis) * Oral or nasal ulcers * Arthritis (in 2 or more peripheral joints) * Photosensitivity * Bloods (pancytopaenia, haemolytic anaemia, leukopaenia, thrombocytopaenia) * Renal disease (urine casts, proteinuria, nephrotic syndrome) * ANA (not specific as raised in many conditions) * Immunological disorder (anti-dsDNA (60%), antismith antibody, anti-phospholipid) * Neurological disease (depression, psychosis, seizures) * Malar rash (butterly rash) * Discoid rash
462
haemoptysis, sinusitis, epistaxis, oral ulcers and rash ?
Granulomatous with polyangiitis
463
severe headache 24 hrs after spinal anasthetic - what is the dx
low pressure headache
464
important ix with temporal arteritis
Investigations raised inflammatory markers ESR > 50 mm/hr (note ESR < 30 in 10% of patients) CRP may also be elevated temporal artery biopsy skip lesions may be present note creatine kinase and EMG normal
465
PMR features, ix and mx
Features typically patient > 60 years old usually rapid onset (e.g. < 1 month) aching, morning stiffness in proximal limb muscles weakness is not considered a symptom of polymyalgia rheumatica also mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats Investigations raised inflammatory markers e.g. ESR > 40 mm/hr note creatine kinase and EMG normal Treatment prednisolone e.g. 15mg/od patients typically respond dramatically to steroids, failure to do so should prompt consideration of an alternative diagnosis
466
hydrocele vs epidydimal cyst
Epididymal cyst A fluid-filled lump that develops in the epididymis, the coiled tube that carries sperm from the testicle. Epididymal cysts are located above or behind the testicle, and they push the testicle forward and down. hx = well-defined, non tender, spherical mass 1cm right side of scrotum superior to testis/transluminates Hydrocele A fluid-filled swelling that occurs in the scrotum or around the testicle. Hydroceles are located in front of the testicle, and they push the testicle to the back of the scrotum.
467
cyclical mastalgia ?
think fibrocystic disease
468
thrombophlebitis what is it mx
Superficial thrombophlebitis, as the name suggests describes the inflammation associated with thrombosis of one of the superficial veins, usually the long saphenous vein of the leg. This process is usually non-infective in nature but secondary bacterial infection may rarely occur resulting in septic thrombophlebitis. mx = NSAIDS (naproxen)
469
screening outcome cut offs for AAA
< 3cm = normal - reassure and discharge 3 - 4.4 cm = Small aneurysm - Rescan every 12 months 4.5 - 5.4 cm - Medium aneurysm - Rescan every 3 months ≥ 5.5cm Large aneurysm= Refer within 2 weeks to vascular surgery for probable intervention Only found in 1 per 1,000 screened patients
470
older person with unilateral hearing loss / maybe tinnitis as well - what are you thinking and what ix would you want to do ?
acoustic neuroma ix = MR imaging of internal acoustic meatus
471
features of Infectious mononucleosuss
The classic triad of sore throat, pyrexia and lymphadenopathy is seen in around 98% of patients: sore throat lymphadenopathy: may be present in the anterior and posterior triangles of the neck, in contrast to tonsillitis which typically only results in the upper anterior cervical chain being enlarged pyrexia Other features include: malaise, anorexia, headache palatal petechiae splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture hepatitis, transient rise in ALT lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes haemolytic anaemia secondary to cold agglutins (IgM) a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
472
ix for infectious mononucleosus
epstein - barr virus serology
473
474
TB drugs side effects
Rifampicin mechanism of action: inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA potent liver enzyme inducer hepatitis, orange secretions flu-like symptoms Isoniazid mechanism of action: inhibits mycolic acid synthesis peripheral neuropathy: prevent with pyridoxine (Vitamin B6) hepatitis, agranulocytosis liver enzyme inhibitor Pyrazinamide mechanism of action: converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase (FAS) I hyperuricaemia causing gout arthralgia, myalgia hepatitis Ethambutol mechanism of action: inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan optic neuritis: check visual acuity before and during treatment dose needs adjusting in patients with renal impairment
475
patient with alc hep and distended abdomen what ix and why
Ascitic tap (paracentesis is essential to diagnose underlying cause of ascites; it will tell you whether there is spontaneous bacterial peritonitis or malignancy or portal hypertension. Untreated SBP has a very high mortality rate)
476
colloquial name for haemochromatosis
Hemochromatosis has been called “bronze diabetes” due to the discoloration of the skin and associated disease of the pancreas
477
causes of foot drop
Foot drop is caused by weakness of the muscles of ankle dorsiflexion (tibialis anterior) supplied by the common peroneal nerve (L4, L5 and S1 nerve root). Foot drop may therefore be caused by: Isolated common peroneal nerve palsy (e.g. secondary to trauma or compression) L5 radiculopathy (e.g. disc prolapse) Generalized polyneuropathy involving multiple nerves (e.g. diabetic neuropathy, motor neurone disease, Charcot-Marie Tooth disease)
478
outline types of laxatives with examples
1. softening agents (lubricate the stool - surface softeners) - e..g docusate sodium/ liquid parafin 2. bulking agents (increase faceal mass, stimulating peristalsis) - do not use in palliative care due to poor oral intake/ poor bowel motility e.g. bran/fybogel 3. stimulant agent (increase intestinal motility) - may cause cramps (griping) - avoid in intestinal obstruction / colostomy e.g. senna / docusate sodium 4. osmotic agents (pull liquid into stool) e.g. lactulose, macrogols
479
outline common causes of N&V in palliative patient
1. delayed gastric emptying - gastric paresis - obstruction - constipation 2. damage to bowel - surgery / infectioon 3. CNS causes - raised ICP / SOL - infection - injury 4. chemical disturbances - hypercalcaemia/ renal failure / lliver failure - necrosis / iscaemia - drugs 5. labrinth - motion sickness 6. pscyhological factors - stress - anticipation
480
anti emetic for chemical cause of vomiting (ie hypercalcaemia)? in palliative care. and what route ?
best drug = haloperidoll also can use cyclizine/ metochlopramide best route = continuous subcutaneous infusion (CSCI)
481
4 different anti-emetics and give indications + side effects
1. cyclizine - cental vomtiing / CNS lesions/ labrinthititis side effects= irritant SC, severe heart failure no good 2. ondansetron - restricted to 1. chemo 2. abdominal surgery 3. abdominal radiotherapy side effects = very constipating / QT prolongation 3. haloperidol - chemical causes, renal failure, drug induced side effects = avoid in parkinsons disease 4. metochlopramide / domperidone - delayed GIT transit / bowel obstruction without colic side effects = BO with colic don't use, not for parkinsons, not for cardiac conduction disorders
482
WHO analgesic ladder steps
step 1 = non opioid - paracetemol - NSAID step 2 = weak opioid - codeine - dihydrocodeine - tramadol step 3 = strong opioid morphine sulphate oxycodone fentanyl
483
patient with cardiac chest pain at rest / exertion already on treatment
CT coronary angio
484
conversion oral morphine to codeine/tramadol
morphine x10 more powerful
485
SC morphine conversion to oral morphine sulphate
SC morphine is x2 more potent
486
how to calculate PRN morphine for breakthrough pain?
1/6 total 24 hour opioid dose
487
opioid prescribing in renal impariment
safe - fentanyl - alfetnyaln - buprernoprhine accumulate in renal impairment/unsafe - morphine - codeine - diamorphine - tramadal
488
common sx in the last hours to days of life
1. pain 2. agitiation 3. respiratory tract secretions 4. breathlessness 5. nausea/vomiting
489
what are the anticipaotry medications for people in their last days of life?
1. pain (morphine sulphate SC) 2. secretions (glycopyrronium / hyoscine hydro bromide SC) 3. agitation (midazolam SC) 4. breathlessness (midazolam / morphine SC) 5. nausea and vomiting (haloperidol / cyclizine SC)
490
which anti-emetic for reduced gastric motility cause of N&V in palliative patient
metoclopramide and domperidone However, NICE indicate that metoclopramide should not be used when pro-kinesis may negatively affect the gastrointestinal tract, particularly in complete bowel obstruction, gastrointestinal perforation, or immediately following gastric surgery
491
drug therapy for VT
Drug therapy amiodarone: ideally administered through a central line lidocaine: use with caution in severe left ventricular impairment procainamide
492
Raised intra-cranial pressure cause of N&V - what anti emtics ?
Raised intra-cranial pressure Cyclizineis recommended first-line for nausea and vomiting due to intracranial disease
493
Vestibular cause of N&V - what anti emtics ?
Vestibular BMJ best practice recommends use of cyclizine as a first-line treatment in disorders due to the vestibular system
494
laxatives to prescribe when giving a patient opioids
A stimulant laxative (such as bisacodyl or senna) is recommended, with the dose adjusted according to response. If there is a lack of response at the highest dose of a stimulant laxative and/or there has been no bowel movement within 3–4 days, an osmotic laxative (such as macrogol 3350 or lactulose) should be added to the regimen with further titration as needed
495
what mx for compete heart block (ie symptoamtic bradyarrthmia)M
dual chamber pacemaker
496
oxycodone vs morphine - pros and cons
Oxycodone generally causes less sedation, vomiting and pruritis than morphine but more constipation.
497
palliative care hiccups what to prescribe ?
In patients with hiccup due to gastric distension with or without gastro-oesophageal reflux, a prokinetic (such as metoclopramide), an antiflatulent (such as peppermint oil or simeticone), or a proton pump inhibitor (such as lansoprazole or omeprazole) can be given.
498
salter harris fracture types
I Fracture through the physis only (x-ray often normal) II Fracture through the physis and metaphysis III Fracture through the physis and epiphysis to include the joint IV Fracture involving the physis, metaphysis and epiphysis V Crush injury involving the physis (x-ray may resemble type I, and appear normal)
499
what are the different types of incontinence ?
A) Urge incontinence - urgency/frequency/wake up at night B)overflow incontinence - poor stream/incomplete emptying C) stress incontinence - leak when cough D) functional incontinence - physical disability prevent from urinate (eg.wheelchair/bedridden) E) mixed incontinence - (UI + SI) ———- PS: mixed incontinence did not include overflow incontinence
500
explain findings of rinee and webers test
Weber's normal = equal sensorineural = lateralises to good ear conductive = lateralises to bad ear Rinees normal = AC > BC (think about the function of the ear as an amplifier) conductive = BC > AC sensorineural = AC > BC (both are worse, so both go down, but this still means that air conduction is better than bone conduction - just both are wortse)
501
stable angina main ix
CT coronary angiogram
502
good blood test to find out severity of PE ?
troponinn can give a measure of R heart strain
503
what do you measure for someone with suspected CO poisoning ?
carboxyhaemoglobin levels pulse oximetry may be falsely high due to similarities between oxyhaemoglobin and carboxyhaemoglobin
503
64 y/o vomiting / severe chest pain after eating large meal + haemodynamic instability + subcut empysema on left side of his neck ?
Boerhaave's syndrome is a spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting. The rupture is usually distally sited and on the left side. Subcutaneous emphysema may be observed on the chest wall. Diagnosis is CT contrast swallow.
504
dx + mx for prolactinoma
Diagnosis MRI Management in the majority of cases, symptomatic patients are treated medically with dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland surgery is performed for patients who cannot tolerate or fail to respond to medical therapy. A trans-sphenoidal approach is generally preferred unless there is a significant extra-pituitary extension
505
The anaesthetist advises using an airway device to protect the lungs from regurgitated stomach contents - what is this device?
only the tracheal tube can seal the trachea off and protect against aspiration
506
best ariway device to use for cardiac arrest ?
i-gel (supraglottic airway)
507
anti-CCP vs Rheumatoid factor ?
(Anti CCP) antibody. This is the test that has the highest specificity for rheumatoid arthritis, which is what the question is asking. CCP antibodies are found in 80% of people with rheumatoid arthritis, but fewer than 0.5% of healthy individuals. Rheumatoid factor is present in up to 10% of the healthy population, and whilst of similar sensitivity to CCP, is much less specific. CRP is a non-specific marker of inflammation, and can often be normal in early rheumatoid. ANA testing is high sensitivity (but low specificity) test for connective tissue disorders such as SLE and Sjorgren’s.
508
which resp test is used to measure respiratory function in myasthenia gravis ?
Myasthenic crisis is an acute respiratory failure characterised by forced vital capacity (FVC) below 1 L, negative inspiratory force (NIF) of 20 cm H2O or less, and the need for ventilatory support.
509
mx for sinus bradycardia
need to treat if haemodynamic compromise Atropine (500mcg IV) is the first line treatment in this situation. If there is an unsatisfactory response the following interventions may be used: atropine, up to a maximum of 3mg transcutaneous pacing isoprenaline/adrenaline infusion titrated to response features of haemodynamic compromise:shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness syncope myocardial ischaemia heart failureshock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness syncope myocardial ischaemia heart failure
510
most common pathogen in leg cellulitis (including in patients with diabetes)
Streptococcus pyogenes
511
what regional lymph nodes is ovarian tumour most likely to spread initially?
The main lymphatic drainage of the ovary is to the para-aortic nodes
512
patient with advanced lung cancer + CT scan of chest shows mediastinal lymphadenopathy compressing the superior vena cava
The patient has superior vena cava obstruction. The standard initial treatment is dexamethasone to reduce tumour swelling. There is no evidence of thrombus to justify systemic anticoagulation and systemic thrombolysis has no place
513
surgical option for large AAA
NICE = open unless contraindictaed elective endovascular repair (EVAR) or open repair if unsuitable
514
4 intervetion indications for AAA
1. > 5.5 cm 2. > 4cm and > 1cm yearly growth 3. Symptomatic 4. rupture
515
work up for someone with AAA
blood gas fbc u&E lactate clotting G&S + XM Point of care ultrasound scan (POCUS) CT angio = gold standard mx = 30 min rule permissive hypotension - systolic aimed for 80-100 intervention = surgery
516
aortic dissection workup
BP ECG D-dimer troponin amylase G&S + XM VBG (lactate) imaging: TOE CT aortagram CXR (widened mediastinum)
517
mx acute limb iscaemia
medical: high flow o2 heparin infusion surgical - embolectomy thrombloysdsi s angiopasty
518
explain how diabetic foot syndrome comes about ...
3 things Poor perfusion (peripheral arterial disease) * Hyperglycaemia, oxidative stress, atherosclerosis * Reduces tissue healing Sensorimotor neuropathy * Foot deformity * Loss of protective sensation Precipitant * Macrotrauma: standing on nail * Microtrauma: pressure damage due to deformity/abnormal load
519
ix for diabetic foot syndrome
high risk of sepsis/ osteomuletiis necoriss and gangrene YOu need to XRAY / MRI mx = 24hr DFU MDT referral Mechanical offloading Debridement Amputation
520
2 types of gangrene and when you get each of them ?
Dry * Arterial occlusion: ischaemia causes drying of tissue * Good demarcation from normal tissue * Bacteria can't survive Wet * Area of poor healing or venous occlusion with cell death * Poor demarcation * Bacteria infect dead tissue high risk of sepsis
520
ix and mx for arterial vs venous ulcers
arterial ABPI Angio Lifestyle DAPT, statin Revascularisation Amputation venous USS duplex Compression therapy Varicose vein Mx
521
outline what is lymphoedema
* Primary: congenital lymphatic malformation * Secondary: radiotherapy, resection * Poor pitting When they remove lymph due to breast cancer this can cause lymphoedema NICE management: * Lymphovenous anastamosis during axillary node clearance * Liposuction may have utility
522
angina vs heart failure first line drugs ?
angina: NICE recommend using either a beta-blocker or a calcium channel blocker first-line based on 'comorbidities, contraindications and the person's preference' Heart failure: ACE-i / beta blocker - usually will start one before the other and then can switch to using both
523
why do we use the benzo we use in alcohol withdrawal ?
Both chlordiazepoxide and diazepam are licenced for the use of alcohol-related withdrawal symptoms in the UK. This is because long-acting benzodiazepines with active metabolites (such as chlordiazepoxide and diazepam) have a lower chance of recurrent withdrawal or seizures due to missed doses than shorting acting benzodiazepines. A notable exception is in patients with severe liver impairment, where a shorter acting benzodiazepine such a lorazepam may be preferred – this should only be prescribed by a specialist team.
524
sore throat scoring systems - go through the things in them
The Centor criteria are: score 1 point for each (maximum score of 4) presence of tonsillar exudate tender anterior cervical lymphadenopathy or lymphadenitis history of fever absence of cough FeverPAIN criteria are: score 1 point for each (maximum score of 5) Fever over 38°C. Purulence (pharyngeal/tonsillar exudate). Attend rapidly (3 days or less) Severely Inflamed tonsils No cough or coryza
525
HIV patient with pneumonia ? thoughts? and how to manage it ?
This is a typical presentation of a patient with HIV and Pneumocystis pneumonia (PCP). Co-trimoxazole is the drug of choice for treatment of PCP and both IV and Oral preparations are recommended by the BNF
526
when giving someone high dose steroids for a prolonged period what do you need to think about also prescribing? `
This patient is receiving a high-dose of corticosteroid and is likely to continue doing so for a prolonged period (at least 3 months). She is therefore at high-risk of developing osteoporosis and prophylaxis should be prescribed alongside her prednisolone. Alendronate (alendronic acid) is first line in this case
527
what is atropine used for ?
bradycardia algorithm
528
what is amiodorone used for ?
VT
529
V Fib Mx
Unlike in VT, amiodarone should not be given for definite TdP. Magnesium sulfate IV 2g over 10 minutes is the best option
530
anterior vs posterior circulation stroke
anterior: hemiparesis aphraxia neglect (face arm legs) posterior: diploplo dysarthria dizziness dysphagia (crossed findings)
531
long term antithrombotic for stroke ?
clopidogrel
532
patient with dysarthria / gaze evoked nystagmus, R dysdiadochokinesai and intention tremor - where is lesion?
R cerebellum cerebellum problems are ipislateral
533
go over this mixed signs stuff again /.... .
weakness contralateral mixed signs th left side of body - think about where it corrses over
534
mx medical for alzeihmers disease
Acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) are recommended as options for the management of mild to moderate AD. Memantine monotherapy is recommended only for those who are intolerant to acetylcholinesterase inhibitors or who have severe AD
535
how to manage refeeeding syndrome
He now has biochemical evidence of refeeding syndrome (hypokalaemia, hypomagnesaemia, hypophosphatemia, hypocalcaemia, hyponatraemia and fluid overload). The most important abnormality to correct in this case is the phosphate. This is best done via an IV infusion. Phosphate polyfusor, 50 mmol, IV, over 12 hours
536
what are the stroke windows ?
Within 4.5 hours: Thrombolysis with Alteplase, followed 24 hours later by aspirin 300mg After 4.5 hours: No thrombolysis; just give Aspirin 300mg
537
bowens disease vs actinic keratosis
actinic keratosis Small, rough, scaly patches or plaques on sun-exposed areas. Often skin-colored, red, or brown; feels "sandpaper-like." bowens disease Persistent, well-demarcated red or pink plaques with a scaly or crusted surface. May resemble eczema or psoriasis.
538
list causes of obstructive and restrictive lung disease
obstructive: - Asthma - Chronic obstructive pulmonary disease (COPD): Chronic bronchitis, emphysema - Bronchiectasis - Cystic fibrosis restrictive: - Interstitial lung disease (e.g., pulmonary fibrosis) - Sarcoidosis - Obesity hypoventilation syndrome - Neuromuscular disorders (e.g., ALS, muscular dystrophy) - Pleural diseases (e.g., pleural effusion, pneumothorax)
539
homonymous quadrantanopias - how to tell the difference between ?
PITS Parietal-Inferior Temporal-Superior
540
which drug to treat oedema caused by brain tumour ?
Dexamethasone is a potent steroid with predominantly glucocorticoid effects. It is used to treat vasogenic oedema that occurs due to the break down of the blood-brain barrier. A common use within neurosurgery is to treat oedema caused by brain tumours. Where there is life threatening rising ICP such as in extradural haematoma and whilst theatre is prepared or transfer arranged use of IV mannitol/ frusemide may be required.
541
common drug causes of hyponataemia
PPI SSRIs Syndrome of Inappropriate ADH Secretion (SIADH) - Antidepressants: SSRIs (e.g., sertraline), tricyclics (e.g., amitriptyline). - Antipsychotics: Haloperidol, risperidone. - Antiepileptics: Carbamazepine, oxcarbazepine, valproate. - Cancer drugs: Vincristine, cyclophosphamide. - Others: NSAIDs, opioids. Diuretics - Thiazide diuretics: Hydrochlorothiazide, chlorthalidone. - Loop diuretics (less common): Furosemide, bumetanide. Osmotic effects or solute depletion - Glucose-lowering drugs: Sulfonylureas (e.g., chlorpropamide). - Others: Mannitol. Renal salt wasting - Aminoglycosides: Gentamicin. - Antifungals: Amphotericin B. Altered water balance - Desmopressin (ADH analogue). - Oxytocin. Miscellaneous - Proton Pump Inhibitors (PPIs): Omeprazole. - ACE inhibitors/ARBs: Enalapril, losartan. - Ecstasy (MDMA).
542
mx anal fissure
Management of an acute anal fissure (< 1 week) soften stool dietary advice: high-fibre diet with high fluid intake bulk-forming laxatives are first-line - if not tolerated then lactulose should be tried lubricants such as petroleum jelly may be tried before defecation topical anaesthetics analgesia Management of a chronic anal fissure the above techniques should be continued topical glyceryl trinitrate (GTN) is first-line treatment for a chronic anal fissure if topical GTN is not effective after 8 weeks then secondary care referral should be considered for surgery (sphincterotomy) or botulinum toxin
543
upper rectal cancer. The malignancy is localised and the team decides to perform an anterior resection to excise it. The surgeon thinks that to obtain an optimal result in the long term it is necessary to temporarily defunction the colon to protect the colorectal anastomosis. what type of stoma ?
A loop ileostomy can be used to defunction the colon to protect an anastomosis
544
how to manage a critically hypoxic patient who has COPD ?
non-rebreather mask The correct answer is reservoir mask at 15 litres/min. The British Thoracic Society guidelines clearly indicate that any critically ill patient (including CO2 retainers) should initially be treated with high flow oxygen because hypoxia can kill the patient very rapidly. Once an acceptable saturation has been reached, you should try and tailor the saturation levels to the patient.
545
ix for guillaine barre syndrome
lumbar puncture rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%
546
what additional drug do you want to use in subarachnoid haemorrhage
Nimodipine is used to prevent vasospasm in aneurysmal subarachnoid haemorrhages
547
upper GI bleed score for dtermining medical intervention
Glasgow-Blatchford score
548
score used after endoscopy in upper GI bleed and provides a percentage risk of rebleeding and mortality
rockall score
549
patient with CKD and ACR > 30 - what do you do?
prescribe ramiprilAll patients with a urinary ACR of >30 mg/mmol and associated hypertension (regardless of age or ethnicity) should be prescribed an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) over other anti-hypertensives, as this is particularly beneficial in reducing the progression of kidney damage
550
how to decide whether a COPD patient needs to go on long term oxygen therapy ?
COPD - LTOT if pO2 of 7.3 - 8 kPa AND one of the following: secondary polycythaemia peripheral oedema pulmonary hypertension
551
most common cause of peritonitis secondary to peritoneal dialysis ? what organism ?
Coagulase-negative Staphylococcus is the most common cause of peritonitis secondary to peritoneal dialysis staphylococcus epidermis
552
following ACS all patients should be offered ?
Following an ACS, all patients should be offered: dual antiplatelet therapy (aspirin plus a second antiplatelet agent) - aspirin + prasugrel ACE inhibitor beta-blocker statin
553
when to use unsyncronised DC cardioversion?
Unsynchronised DC This is known as defibrillation and delivers a shock at any point in the cardiac cycle, and is used in shockable rhythms such as ventricular tachycardia (VT) or ventricular fibrillation (VF) where the patient has no pulse (pulseless). VT would show a broad-complex (QRS >0.12 s) tachycardia on the ECG and VF would demonstrate random and chaotic deflections with no identifiable P waves, QRS complexes, or T waves. The ECG does not demonstrate these features and shows a regular, narrow-complex tachycardia, making the likely diagnosis SVT.
554
what drug to give in symptomatic bradycardia ?
Atropine which is the first-line temporising measure. This works as an anti-cholinergic to block the parasympathetic nervous system and thus increases heart rate. It only lasts a short time so there are more definitive measures that can be used to treat bradycardia such as isoprenaline infusions, temporary pacing or a permanent pacemaker.
555
mx rosacea
- simple measures recommend daily application of a high-factor sunscreen camouflage creams may help conceal redness - predominant erythema/flushing topical brimonidine gel may be considered for patients with predominant flushing but limited telangiectasia - mild-to-moderate papules and/or pustules topical ivermectin is first-line - moderate-to-severe papules and/or pustules combination of topical ivermectin + oral doxycycline
556
what is the criteria for discharging someone who has just had an acute asthma attack ?
His peak expiratory flow rate (PEFR) is correct. After managing an acute asthma exacerbation, there are criteria that the patient must meet before being safely discharged, due to the risk of symptoms recurring. They must be stable on their discharge medication for at least 12 hours, have a good inhaler technique, and have a PEFR of >75% of their best or predicted value. This patient's PEFR is 65% of their best value, therefore, they cannot safely be discharged at this point in time.
557
most accurate marker of assessing function of liver ?
prothrombin time is best Prothrombin has a shorter half-life than albumin, making it a better measure of acute liver failure
558
driving after seizure what are trhe conditions
6 months is the correct answer. Following a first unprovoked seizure, a patient should not drive for 6 months provided there are no structural abnormalities on imaging and there is no epileptiform activity on EEG. 12 months is the incorrect answer. Patients cannot drive for 12 months after a seizure if there is abnormal brain imaging or an abnormal EEG.
559
young person needing a replacement valve what do you give them ?
In general, younger patients should be provided with a mechanical heart valve since these have a significantly greater lifespan compared to bioprosthetic valves. The average lifespan of a bioprosthetic valve is estimated to be approximately 15 years
560
left bundle branch block and right bundle branch block ?
LBBB - WILIAM v1 - W v6 - M RBBB - MAROW v1 - M v6 - W
561
what type of hearing loss with otosclerosis ?
conductive
562
outline urethral stricture
Based on the symptoms described, the most likely diagnosis for the 24 year old man is urethral stricture. Urethral stricture is a condition that occurs when the urethra narrows, which can cause difficulty in passing urine and a slow urinary stream. This can lead to a feeling of incomplete emptying of the bladder and a need to strain to empty the bladder completely. Urethral stricture follows previous urethral inflammation due to infection
563
how to manage patient with aortic stenosis ?
if asymptomatic then observe the patient is a general rule if symptomatic then valve replacement if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
564
Management of myasthenic crisis
- plasmapheresis - intravenous immunoglobulins
565
mechanism of myasthenia gravis drug and give name
long-acting acetylcholinesterase inhibitors pyridostigmine is first-line
566
which dermatome is Big toe, dorsum of foot (except lateral aspect)
L5
567
which dermatome for Lateral foot, small toe ?
S1
568
INR 5.0-8.0 No bleeding wioth warfarin what do you do ?
Withhold 1 or 2 doses of warfarin Reduce subsequent maintenance dose
569
INR 5.0-8.0 Minor bleeding with warfarin what do you do ?
Stop warfarin Give intravenous vitamin K 1-3mg Restart when INR < 5.0
570
INR > 8.0 No bleeding with warfarin what do you do ?
Stop warfarin Give vitamin K 1-5mg by mouth, using the intravenous preparation orally Repeat dose of vitamin K if INR still too high after 24 hours Restart when INR < 5.0
571
INR > 8.0 Minor bleeding with warfarin what do you do ?
Stop warfarin Give intravenous vitamin K 1-3mg Repeat dose of vitamin K if INR still too high after 24 hours Restart warfarin when INR < 5.0
572
Major bleeding (e.g. variceal haemorrhage, intracranial haemorrhage) and taking warfarin ?
Stop warfarin Give intravenous vitamin K 5mg Prothrombin complex concentrate - if not available then FFP*
573
what do you need to make a diagnosis of acute pancreatitis ?
history + amylase (you don't need imaging)
574
damage to hypoglossal nerve - what happens ?
Pathology to CN XII is a relatively uncommon event. Damage to this structure may be caused by penetrating trauma to the nerve, malignancies or vascular lesions. Patients will present with tongue deviation toward the side of the lesion in the presence of fasciculations. Muscle wasting of the tongue is a relatively late occurrence, but can be a diagnostic clue.
575
common side effects of ACE inhibitors
* Cough * Hyperkalaemia
576
common side effects of Bendroflumethiazide
* Gout * Hypokalaemia * Hyponatraemia * Impaired glucose tolerance
577
common side effects of Calcium channel blockers
* Headache * Flushing * Ankle oedema
578
common side effects of Beta-blockers
* Bronchospasm (especially in asthmatics) * Fatigue * Cold peripheries
579
examples of antihistamines you can use ?
Examples of sedating antihistamines - chlorpheniramine Examples of non-sedating antihistamines - loratidine - cetirizine
580
how to manage actinic keratoses?
. 5-fluorouracil (Efudix ® ) cream
581
how to manage bowens disease ?
. 5-fluorouracil (Efudix ® ) cream
582
how to manage graves ?
first give propanolol for sx then.... carbimazole is started at 40mg and reduced gradually to maintain euthyroidism typically continued for 12-18 months the major complication of carbimazole therapy is agranulocytosis an alternative regime is termed 'block-and-replace' carbimazole is started at 40mg thyroxine is added when the patient is euthyroid treatment typically lasts for 6-9 months patients following an ATD titration regime have been shown to suffer fewer side-effects than those on a block-and-replace regime Radioiodine treatment often used in patients who relapse following ATD therapy or are resistant to primary ATD treatment contraindications include pregnancy (should be avoided for 4-6 months following treatment) and age < 16 years. Thyroid eye disease is a relative contraindication, as it may worsen the condition the proportion of patients who become hypothyroid depends on the dose given, but as a rule the majority of patient will require thyroxine supplementation after 5 years
583
equation for serum osmolality ?
Serum osmolality is 2 x(Na) + Urea + glucose
584
which antibiotic do you use for MRSA ?
The following antibiotics are commonly used in the treatment of MRSA infections: vancomycin alternatively you can use: teicoplanin linezolid
585
painful red eye what goes through your head ?
acute angle closure glaucoma anertior uveitis scleritis
586
what test is the best measure of liver synthetic function ?
PT
587
what do actinic keratoses look like ?
Actinic keratoses are pink and scaly or hyperkeratotic and do not ulcerate.
588
what is digoxin used for ?
Digoxin is a cardiac glycoside now mainly used for rate control in the management of atrial fibrillation. As it has positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure.
589
what are the different types of AF ?
AF may by classified as either first detected episode, paroxysmal, persistent or permanent. first detected episode (irrespective of whether it is symptomatic or self-terminating) recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF terminate spontaneously then the term paroxysmal AF is used. Such episodes last less than 7 days (typically < 24 hours). If the arrhythmia is not self-terminating then the term persistent AF is used. Such episodes usually last greater than 7 days in permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate. Treatment goals are therefore rated control and anticoagulation if appropriate
590
haematuria + loin pain + urinalysis blood +++ and masses palpable both flanks. what is it ? and what ix ?
USS renal tract polycystic kidney disease
591
history of sinusitis, oral ulceration and haemoptysis
Granulomatosis with polyangiitis
592
history of 1) oral ulcers 2) genital ulcers 3) anterior uveitis
Behcet's syndrome is a complex multisystem disorder associated with presumed autoimmune-mediated inflammation of the arteries and veins. The precise aetiology has yet to be elucidated however. The classic triad of symptoms are oral ulcers, genital ulcers and anterior uveitis
593
infectious mononucleosus- give the classic triad with the extended sx as well
The classic triad of sore throat, pyrexia and lymphadenopathy is seen in around 98% of patients: sore throat lymphadenopathy: may be present in the anterior and posterior triangles of the neck, in contrast to tonsillitis which typically only results in the upper anterior cervical chain being enlarged pyrexia Other features include: malaise, anorexia, headache palatal petechiae splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture hepatitis, transient rise in ALT lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes haemolytic anaemia secondary to cold agglutins (IgM) a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
594
TB drugs side effects
Rifampicin hepatitis, orange secretions flu-like symptoms Isoniazid peripheral neuropathy: prevent with pyridoxine (Vitamin B6) hepatitis, agranulocytosis liver enzyme inhibitor Pyrazinamide: hyperuricaemia causing gout arthralgia, myalgia hepatitis Ethambutol: optic neuritis: check visual acuity before and during treatment dose needs adjusting in patients with renal impairment
595
patient has problems with oral candidiasis from ICS inhaler - what can you do ?
This patient has developed oral candidiasis and this is most likely due to local deposition of the inhaled steroid (beclometasone dipropionate). The risk of this happening again can be reduced by using a large volume spacer as there will be less local deposition of the drug in her mouth
596
if plueral fluid is between 25-35 protein level so you can't really easily distinguish between transudate and exudate what do you do ?
Light's criteria was developed in 1972 to help distinguish between a transudate and an exudate. The BTS recommend using the criteria for borderline cases: exudates have a protein level of >30 g/L, transudates have a protein level of <30 g/L if the protein level is between 25-35 g/L, Light's criteria should be applied. An exudate is likely if at least one of the following criteria are met: pleural fluid protein divided by serum protein >0.5 pleural fluid LDH divided by serum LDH >0.6 pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
597
features of HIV presentation
Features sore throat lymphadenopathy malaise, myalgia, arthralgia diarrhoea maculopapular rash mouth ulcers rarely meningoencephalitis
598
lesions in herpes vs syphallis vs genital warts
The presence of multiple tender ulcers on the preputial skin following recent sexual intercourse is suggestive of herpes simplex virus infection. Genital warts usually present as painless, raised, andcauliflower-like growths on the genital skin. Ulcers in syphilis are typically painless
599
outline mesenteric adenitis
Mesenteric adenitis is inflamed lymph nodes within the mesentery. It can cause similar symptoms to appendicitis and can be difficult to distinguish between the two. It often follows a recent viral infection and needs no treatment including crampy abdominal pain, poor appetite, sore throat, fever, cervical lymphadenopathy, and tenderness in the right iliac fossa, suggest mesenteric adenitis, which is an inflammation of the lymph nodes in the mesentery that can be caused by viral or bacterial infections, such as streptococcal pharyngitis
600
ix for neuroleptic malignant syndrome
Serum creatine kinase (CK), which is a muscle enzyme that can be elevated in NMS
601
Spondylolisthesis vs herniated disc/prolapsed disc vs
Spondylolisthesis is where one of the bones in your spine, called a vertebra, slips forward Spondylosis is a condition in which there is abnormal wear on the cartilage and bones of the neck (cervical vertebrae). It is a common cause of chronic neck pain. Spondylosis is caused by chronic wear on the spine. prolapsed hisc / herniated disc - as is
602
woman with pelvic organ prolapse (following vaginal delivery)
if first or second degree: first line = pelvic floor exercises Referral to urogynaecology clinic is usually needed if there is a severe prolapse e.g. 3rd degree or severe urinary bowel incontinence or failed PFEs when management may include more invasive options such as surgical repair also it doesn't matter if the woman is young
603
Superior vena cava (SVC) obstruction - how does it present ? and give some causes as well ?
Superior vena cava (SVC) obstruction is an oncological emergency caused by compression of the SVC. It is most commonly associated with lung cancer. Features - dyspnoea is the most common symptom - swelling of the face, neck and arms - conjunctival and periorbital oedema may be seen - headache: often worse in the mornings - visual disturbance - pulseless jugular venous distension Causes common malignancies: small cell lung cancer, lymphoma other malignancies: metastatic seminoma, Kaposi's sarcoma, breast cancer aortic aneurysm mediastinal fibrosis goitre SVC thrombosis
604
outline induction of labour and what to do ?
low bishops score - vaginal prostaglandin - balloon catheter high bishops - amniotomy - IV oxytocin
605
patient b12 deficiency how should you manage ?
Initial treatment for vitamin B12 deficiency, especially in the presence of neurological symptoms such as blurred vision and poor concentration, is intramuscular hydroxocobalamin. The recommended regimen for patients with neurological involvement is 1 mg of hydroxocobalamin intramuscularly on alternate days until there is no further improvement, followed by maintenance dose every 2 months. This allows rapid replenishment of B12 stores to address the neurological symptoms effectively.
606
congenital heart disease mx?
to close PDA = ibuprofen, indomethacin or paracetamol however, if the baby is cyanotic then you need to keep PDA open --> you should give ... If the PDA is associated with another congenital heart defect amenable to surgery prostaglandin E1 is useful to keep the duct open until after surgical repair
607
mx post partum haemorrhage
most common cause is uterine atony therefore, give oxytocin
608
how does chlamydia present ?
women: cervicitis (discharge, bleeding), dysuria men: urethral discharge, dysuria
609
how does gonorrhea present ?
males: urethral discharge, dysuria females: cervicitis e.g. leading to vaginal discharge rectal and pharyngeal infection is usually asymptomatic
610
ix of choice for chlamydia ?
nuclear acid amplification tests (NAATs) are now the investigation of choice
611
normal range for menstrual cycle and what does it indicate if its not in this range ?
The woman’s menstrual cycle is longer than the normal range of 21-32 days, which suggest that she may not be ovulating regularly therefore she's going to have problems potentially with her fertility you can think about PCOS in this situation
612
which virus is associated with squamous cell carcinoma of the oropharynx, which includes the tonsils (typically palatine tonsils and lingual tonsils)
Human papilloma virus
613
which treatment can improve breathlessness in . The patient is experiencing severe dyspnea, which is a common symptom in end-stage heart failure.
Morphine is an opioid analgesic with respiratory depressant effects that can reduce the sensation of dyspnea
614
how does temporal arteritis (GCA) present ? And what investigations ?
features: - headache - jaw claudication - tender palpable temporal artery - vision loss/ disturbances Investigations - raised inflammatory markers ESR > 50 mm/hr (note ESR < 30 in 10% of patients) - CRP may also be elevated - temporal artery biopsy - skip lesions may be present - note creatine kinase and EMG normal
615
anti psychotic extra pyramidal side effects and what to give for each ?
acute dystonia - invol painful sustained muscle contractions (e.g. oculogyric) --> procylidine akathisia - restlessness --> propanolol // benzo parkinsonism - tremor, rigitidy, bradykinesia --> procyclidine tardive dyskinesia - rhythm movements (chewing, sucking, grimace, blinking) --> tetrabenazine
616
management for lymphoma ?
chemotherapy
617
what to do with your insulin therapy if you become sick ?
Do not stop insulin therapy if you're sick. this is to prevent DKA. this appplies to both type 1 and 2
618
type 2 diabetics - what to do about diabetic meds ?
do not stop insulin medication may be restarted once the person is feeling better and eating and drinking for 24-48 hours - metformin: stop treatment if there is a risk of dehydration, to reduce the risk of lactic acidosis. - sulfonylureas: may increase the risk of hypoglycaemia - SGLT-2 inhibitors: check for ketones and stop treatment if acutely unwell and/or at risk of dehydration, due to the risk of euglycaemic DKA - GLP-1 receptor agonists: stop treatment if there is a risk of dehydration, to reduce the risk of AKI
619
what to do with someone's insulin peri-operatively ?
take evening long acting insulin the night before: if morning list: omit morning insulin since they'll be fasting from midnight if afternoon list: take usual morning dose with breakfast, and omit lunchtime dose
620
which diabetic drugs should you omit peri-operatively ?
sulphonylurea (gliclazide) SGLT-2 inhibitors
621
how does scarlet fever present ?
high fever, sore throat, and a characteristic sandpaper-like rash that starts on the trunk and spreads to the extremities
622
how does measles present ?
fever and rash, but typically presents with a cough, runny nose, and red, watery eyes
623
excessive and persistent fear of social situations, including public speaking. It can cause significant distress and interfere with daily activities --> what is this ?
social phobia This is not panic disorder - panic disorder essentially goes hand in hand with GAD
624
weak grip, cough and shallow breathing - post operatively - what do you do ?
These suggest residual effects of neuromuscular blockade Neostigmine is a cholinesterase inhibitor and is the most appropriate agent to administer to reverse the effects of neuromuscular blockade. It reduces the breakdown of acetylcholine at the neuromuscular junction increasing its availability to bind to the acetylcholine receptor and therefore trigger muscular contraction and increased strength
625
cancer of the middle third of the oesophagus and hepatic metastases - how to manage dysphagia ?
Oesophageal stent
626
Which type of study would provide the highest quality evidence?
Meta-analysis of trials
627
CEA tumour marker ?
colorectal cancer
628
electrolytes in tumour lysis syndrome
main one = raised urate potassium phosphate calcium
629
sepsis / septic shock - blood pressure not responding to lots of fluid resus - what do you do ?
initiate vasopressor support, such as noradrenaline / norepinephrine infusion, to increase systemic vascular resistance and maintain blood pressure
630
A full term newborn boy is discharged home 48 hours after birth. The next day, his 2 year old sibling develops a florid chickenpox rash. His mother has detectable varicella antibodies. The newborn remains clinically well.
The most appropriate management decision is no action is necessary. The newborn remains clinically well, and the mother has detectable varicella antibodies, indicating potential passive immunity transfer to the newborn. The fact that the newborn is clinically well also supports a conservative approach with no specific treatment or observation required
631
indications for starting NIV in a patient with acute exacerbation of COPD ?
Patients with COPD are prone to develop type 2 respiratory failure. If this develops then non-invasive ventilation may be used typically used for COPD with respiratory acidosis pH 7.25-7.35 the BTS guidelines state that NIV can be used in patients who are more acidotic (i.e. pH < 7.25) but that a greater degree of monitoring is required (e.g. HDU) and a lower threshold for intubation and ventilation should be used bilevel positive airway pressure (BiPaP) is typically used
632
how do you manage pre-eclampsia ?
oral labetalol is now first-line following the 2010 NICE guidelines. Nifedipine (e.g. if asthmatic) and hydralazine may also be used Magnesium sulphate is used to both prevent seizures in patients with severe pre-eclampsia
633
how to manage paeds constipation ?
1. macrogol (polyethylene glycol + electrolytes- this is an osmotic laxative which draws water into the bowel ) 2. if no change after 2 weeks then can add a stimulant laxative like senna
634
how to manage consitpation due to opioid induced ?
In patients with opioid-induced constipation, an osmotic laxative e.g. macrogol (or docusate sodium to soften the stools) and a stimulant laxative (e.g. senna) is recommended. Bulk-forming laxatives should be avoided.
635
what counts as elderly in NICE ?
The term "elderly" is generally used to describe people who are 65 years of age or older. However, the definition is not strict because people age at different rates.
636
2 important drugs for asthmatics to avoid ?
beta blockers NSAIDS
637
patient already taking allopurinal has acute flare of gout - what do you do ?
continue allopurinol and prescribe NSAIDS/colchicine be careful with NSAIDs in patients with GORD or ulcers
638