Practice Paper 2 Flashcards
What are the most common causes of an elderly patients acute confusion?
Infection: UTI and upper respiratory infection
Which conditions are associated with HLA B27 ?
Crohn's Psoriasis UC Uveitis Ankylosing Spondylitis
What signs do you expect on examination of a HF patient?
Hepatomegaly Pitting oedema Pulsus alternans Raised JVP Ascites Tricuspid regurg Bilateral basal crackles s3 gallop
Whats the Glasgow score? What is it used for?
It’s used for the assessment of acute pancreatitis
+1 for each of the following:
Age >55 WCC Urea Glucose Arterial pO2 Albumin Calcium Lactate dehydrogenase
Whats the alternative name for Giant cell arteritis?
Temporal arteritis
Define Giant cell arteritis
Granulomatous inflammation of large arteries, particularly branches of the external carotid artery, most commonly the TEMPORAL ARTERY
Whats the aetiology and RF for temporal arteritis?
UNKOWN
Whats the epidemiology of temporal arteritis?
More common in FEMALES
Peak age of onset: 65M70 yrs
Recognise the presenting symptoms of giant cell arteritis
- Subacute onset (usually over a few weeks)
- Headache
- Scalp tenderness
- Jaw claudication
- Blurred vision
- Sudden blindness in one eye
- Systemic: malaise, low-grade fever, lethargy, weight loss, depression
- Symptoms of polymyalgia rheumatica - early morning pain and stiffness of muscles of the shoulder and pelvic girdle (present in 20% of presentation) §
o NOTE: 40-60% of GCA has polymyalgia rheumatica
How does a classic presentation of temporal arteritis present?
Acute visual loss Headache before that - severe Headache worst on talking and eating (jaw claudication) Lethargy the past few weeks Shoulder stifness No relevant PMH
Identify appropriate investigations for giant cell arteritis
BLOODS
o High ESR
o FBC - normocytic anaemia of chronic disease
TEMPORAL ARTERY BIOPSY *
o Must be performed within 48 hrs of starting corticosteroids
o Negative biopsy doesn’t necessarily rule out GCA
Define Chronic Myeloid Leukemia
Chronic myeloblastic leukaemia is a malignant clonal disease characterised by proliferation of granulocyte precursors in the bone marrow and blood, distinguished
from AML by its slower progression
Explain the aetiology/risk factors of chronic myeloid leukaemia
• Malignant proliferation of stem cells
• 95% of cases have a chromosomal translocation between chromosomes 9 and 22 to form the Philadelphia chromosome
• Variants of CML include:
o Ph-negative CML
o Chronic neutrophilic leukaemia
o Eosinophilic leukaemia
Whats the pathogenesis of CML? (regarding the philadelphia gene)
o The Philadelphia chromosome results in the formation of the BCR-ABL fusion gene
o The product of this gene enhances tyrosine kinase activity and drives cell replication
What are the 3 phases of CML?
• THREE phases of CML
o Relatively stable chronic phase (4-6 yr duration)
o Accelerated phase (3-9 months)
o Acute leukaemia phase - blast transformation
Summarise the epidemiology of chronic myeloid leukaemia
- Incidence increases with age
- Mean age of diagnosis: 40-60 yrs
- 4 x more common in MALES
Recognise the presenting symptoms of chronic myeloid leukaemia
• ASYMPTOMATIC in 40-50% of cases M diagnosed on routine blood count
HYPERMETABOLIC SYMPTOMS:
o Weight loss
o Malaise
o Sweating
BONE MARROW FAILURE SYMPTOMS: o Lethargy o Dyspnoea o Easy bruising o Epistaxis * o Abdominal discomfort and early satiety
o Rare symptoms:
• Gout
• Hyperviscosity symptoms (visual disturbance, headaches, priapism)
o May present during a blast crisis with symptoms of AML and ALL
Recognise the signs of chronic myeloid leukaemia on physical examination
• SPLENOMEGALY - most common physical finding (90% of cases) • Signs of bone marrow failure: o Pallor o Bleeding o Ecchymosis
Identify appropriate investigations for chronic myeloid leukaemia
BLOODS o FBC • High WCC • Low Hb • High basophils/neutrophils/eosinophils • High/normal/low platelets • High uric acid • High B12 and transcobalamin I
BLOOD FILM
o Immature granulocytes
BONE MARROW ASPIRATE OR BIOPSY
o Hypercellular with raised myeloid-erythroid ratio
CYTOGENETICS
o Show the Philadelphia chromosome
Define Osteoarthritis
Age - related degenerative joint disease when cartilage destruction exceeds repair, causing pain and disability
Whats the pathogenesis of osteoarthritis
o Synovial joint cartilage destruction
o Eventually, there is loss of joint volume due to altered chondrocyte activity
o Patchy chronic synovial inflammation
o Fibrotic thickening of joint capsules
Summarise the epidemiology of osteoarthritis
- COMMON
- 25% of those > 60 yrs
- More common in FEMALES, CAUCASIANS and ASIANS
Recognise the presenting symptoms of osteoarthritis
- Joint pain and discomfort - which is use related
- Stiffness or gelling after inactivity
- Difficulty with certain movements
- Feelings of instability
- Restriction walking, climbing stairs and doing manual tasks
- Systemic features are usually absent
Recognise the signs of osteoarthritis on physical examination
• Local joint tenderness
• Bony swellings along joint margins
o Heberden’s Nodes - DISTAL interphalangeal joint
o Bouchard’s Nodes - PROXIMAL interphalangeal joint
- Crepitus and pain during joint movement
- Joint effusion
- Restriction of range of joint movement
What are the four classic features of OA on Xray?
o Loss of joint space (narrowing)
o Osteophytes
o Subchondral cysts
o Subchondral sclerosis
Name 4 main AB types and their predominant cover
Co-amoxiclav --> broad spectrum gram+ and - Flucloxacillin --> gram + Vancomycin --> gram + Gentamicin --> gram - Metronidazole --> anaerobic cover
Define spinal cord compression
Injury to the spinal cord with neurological symptoms dependent on the site and extent of the injury
Explain the aetiology of spinal cord compression
• MOST CASES: trauma and tumours • Trauma can lead to compression by: o Direct cord contusion o Compression by bone fragments o Haematoma o Acute disk prolapse • Tumours are more frequently METASTASES (prostate - buzz) • Other causes: spinal abscess, TB (Pott's disease)
What are the Rf for spinal cord compression?
o Trauma
o Osteoporosis
o Metabolic bone disease
o Vertebral disc disease
Recognise the presenting symptoms of cord compression
- History of trauma or malignancy
- Pain
- Weakness
- Sensory loss
- Disturbance of bowel and bladder function
• A large central lumbar disc prolapse may cause:
o Bilateral sciatica
o Saddle anaesthesia (loss of sensation in the area of the buttocks that is covered by a bike seat)
o Urinary retention
Recognise the signs of cord compression on physical examination
- Diaphragmatic breathing
- Reduced anal tone **
- HYPOreflexia
- Priapism (persistent and painful erection)
- Spinal shock (low blood pressure without tachycardia) • Sensory Loss - at level of the lesion
• Motor
o Weakness or paralysis
o Downward plantars (in acute phase)
o UMN signs below the level of the lesion
o LMN signs at the level of the lesion
• Brown-Sequard Syndrome - seen with hemisection of the spinal cord
Identify appropriate investigations for cord compression
RADIOLOGY
o Lateral radiographs of spine to look for loss of alignment, fractures etc.
o MRI or CT
BLOODS - FBC, U&Es, calcium, ESR, immunoglobulin electrophoresis (multiple myeloma)
• Urine - look for Bence Jones proteins (multiple myeloma)
Define varicella zoster
• Primary infection is called varicella (chickenpox). Reactivation of the dormant virus (found in dorsal root ganglia), causes zoster (shingles).
o NOTE: varicella zoster is also known as herpes zoster
Summarise the epidemiology of varicella zoster
- Chicken pox peak incidence: 4M10 yrs
- Shingles peak incidence: > 50 yrs
- 90% of adults are VZV IgG positive
Recognise the presenting symptoms of varicella zoster
• Chickenpox
o Prodromal malaise
o Mild pyrexia
o Sudden appearance of intensely itchy spreading
rash mainly affecting face and trunk
o Vesicles weep and CRUST over
o New vesicles appear
o Contagious from 48 hrs before the rash until after
the vesicles have all crusted over (7-10 days)
Recognise the presenting symptoms of varicella zoster
• Shingles
o May occur after a period of stress
o Tingling/hyperaesthesia in a dermatomal distribution
• Dermatomal because the rash remains dormant in the dorsal root ganglia and
reactivation makes the virus travel down the sensory axon to produce a dermatomal shingles rash
o Painful skin lesions
o Recovery: 10-14 days
Recognise the signs of varicella zoster on physical examination • Chickenpox
o Maculopapular rash
o Areas of weeping and crusting
o Skin excoriation (from scratching)
o Mild pyrexia
Recognise the signs of varicella zoster on physical examination
• Shingles
o VESICULAR maculopapular rash
o Dermatomal distribution
o Skin excoriation
Identify appropriate investigations for varicella zoster
- Usually CLINICAL diagnoses
- Vesicle fluid may be sent for electron microscopy viral PCR (RARELY necessary)
- Chicken pox in an adult with previous history of varicella infection may require HIV testing
Generate a management plan for varicella zoster
• Chickenpox
o Children M treat symptoms
o Adults M consider aciclovir
Generate a management plan for varicella zoster
• Shingles
o Aciclovir, valaciclovir, famciclovir
• Prevention
o Varicella Zoster Ig (VZIG) M may be considered in immunosuppressed or pregnant
What is Ramsay Hunt syndrome?
• DEFINITION: reactivation of VZV in the geniculate ganglion causing zoster of the ear and facial nerve palsy. Vesicles may be seen behind the pinna of the ear or in the ear canal
Summarise the prognosis for patients with varicella zoster
Summarise the prognosis for patients with varicella zoster
• Depends on complications
• Worse in pregnancy, elderly and immunocompromised
Define asthma
Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation
Recognise the presenting symptoms of asthma
Episodic history
Wheeze
Breathlessness
Cough (worse in the morning and at night) ***
IMPORTANT: ask about previous hospitalisation due to acute attacks - this gives an indication of the severity of the asthma
Recognise the signs of asthma on physical examination
Tachypnoea Use of accessory muscles Prolonged expiratory phase Polyphonic wheeze Hyperinflated chest
Recognise the signs of asthma on physical examinatiob for a SEVERE attack
PEFR < 50% predicted
Pulse > 110/min
RR > 25/min
Inability to complete sentences
Recognise the signs of asthma on physical examination for a LIFE THREATENING ATTACK
PEFR < 33% predicted Silent chest * Cyanosis Bradycardia Hypotension Confusion Coma
Why is a normal PCO2 worrying in an asthma attack?
A normal PCO2 is a BAD SIGN in a patient having an asthma attack
This is because during an asthma attack they should be hyperventilating and blowing off their CO2, so PCO2 should be low
A normal PCO2 suggests that the patient is fatiguing and not blowing off as enough of pco2 as they should.
Chronic management steps of asthma
STEP 1
Inhaled SABA used as needed
If needed > 1/day then move onto step 2
STEP 2
Step 1 + regular inhaled low-dose steroids (400 mcg/day)
STEP 3
Step 2 + inhaled LABA
If inadequate control with LABA, increase steroid dose (800 mcg/day)
If no response to LABA, stop LABA and increase steroid dose (800 mcg/day)
STEP 4
Increase inhaled steroid dose (2000 mcg/day)
Add 4th drug (e.g. leukotriene antagonist, slow-release theophylline or beta-2 agonist tablet)
STEP 5
Add regular ORAL steroids Maintain high-dose oral steroids
Refer to specialist care
Management of acute asthma
ABCDE
Resuscitate
High-flow oxygen
Salbutamol nebulizer (5 mg, initially continuously, then 2-4 hourly)
Ipratropium bromide (0.5 mg QDS)
Steroid therapy –> 100-200 mg IV hydrocortisone
followed by, 40 mg oral prednisolone for 5-7 days
If no improvement MM> IV magnesium sulphate
Consider IV aminophylline infusion
Consider IV salbutamol
Invasive ventilation may be needed in severe attacks
Define adrenal insufficiency
Deficiency of adrenal cortical hormones (e.g. mineralocorticoids, glucocorticoids and androgens)
Aldosterone & Cortisol insufficiency
Explain the aetiology/risk factors of adrenal insufficiency
Primary Adrenal Insufficiency
o Addison’s disease (usually autoimmune!!)
Secondary Adrenal Insufficiency
o Pituitary or hypothalamic disease
Infections
o Tuberculosis
Infiltration Infarction Inherited Surgical Iatrogenic
How does a patient with chronic adrenal insufficiency present?
Non spefic and vague symptoms o Dizziness o Anorexia o Weight loss o Diarrhoea and Vomiting o Abdominal pain o Lethargy o Weakness o Depression
How does a patient with acute (addisonian crisis) present?
o Acute adrenal insufficiency
o Major haemodynamic collapse ** (without neuro symptoms)
o Precipitated by stress (e.g. infection, surgery)
Recognise the signs of adrenal insufficiency on physical examination
• Postural hypotension
• Increased pigmentation
o More noticeable on buccal mucosa, scars, skin creases, nails and pressure points
• Loss of body hair in women (due to androgen deficiency)
• Associated autoimmune condition (e.g. vitiligo)
Addisonian crisis signs OE
o Hypotensive shock o Tachycardia o Pale o Cold o Clammy o Oliguria
Identify appropriate investigations for adrenal insufficiency
To confirm the diagnosis:
9 am Serum Cortisol (< 100 nmol/L is diagnostic of adrenal insufficiency)
• > 550 nmol/L makes adrenal insufficiency unlikely
Short Synacthen Test
• IM 250 μg tetrocosactrin (synthetic ACTH)
• Serum cortisol < 550 nmol/L at 30 mins indicates adrenal failure
• Investigations in Addisonian crisis
o FBC (neutrophilia MM> infection) o U&Es • High urea • Low sodium • High potassium o CRP/ESR o Calcium (may be raised) o Glucose - low o Blood cultures o Urinalysis o Culture and sensitivity
Generate a management plan for ACUTE adrenal insufficiency
• Addisonian Crisis
o Rapid IV fluid rehydration
o 50 mL of 50% dextrose to correct hypoglycaemia
o IV 200 mg hydrocortisone bolus
o Followed by 100 mg 6 hourly hydrocortisone until BP is stable
o Treat precipitating cause (e.g. antibiotics for infection)
Generate a management plan for CHRONIC adrenal insufficiency
Replacement of:
• Glucocorticoids with hydrocortisone (3/day)
• Mineralocorticoids with fludrocortisone
o Hydrocortisone dosage needs to be increased during times of acute illness or stress
o NOTE: if the patient also has hypothyroidism, give hydrocortisone BEFORE thyroxine (to prevent precipitating an Addisonian crisis)
Advice
o Have a steroid warning card
o Wear a medicMalert bracelet
o Emergency hydrocortisone on hand
Identify the possible complications of adrenal insufficiency
- HYPERKALAEMIA
* Death during Addisonian crisis
Summarise the prognosis for patients with adrenal insufficiency
- Adrenal function rarely recovers
* Normal life expectancy if treated
How does spontaneous bacterial peritonitis presetn?
Severe generalised abdominal pain Ascites Vomiting Fever Rigors
Alcohol abuse history
How is SBP diagnosed?
Paracentesis of ascitic fluid and if the WCC is above 250 the pt requires IV AB
Define sarcoidosis
• Multisystem granulomatous inflammatory disorder
Explain the aetiology/risk factors of sarcoidosis
- UNKNOWN
* Transmissible agents (e.g. viruses), environmental triggers and genetic factors have all been suggested
Explain the pathogenesis of sarcoidosis
An UNKNOWN antigen is presented on MHC class 2 complexes on macrophages to CD4+ T-lymphocytes These accumulate and release cytokines This leads to the formation of non-caseating granulomas in organs
Summarise the epidemiology of sarcoidosis
- Most common in AFRICANS and SCANDINAVIANS
* Can occur at any age but tends to be in adults > 50 yrs
Recognise the presenting symptoms and the signs of sarcoidosis
GENERAL SYMPTOMS o Fever o Malaise o Weight loss o Bilateral parotid swelling o Lymphadenopathy o Hepatosplenomegaly
PULMONARY SYMPTOMS o Breathlessness o Dry cough * o Chest discomfort o Minimal clinical signs
MSK SYMPTOMS
o Bone cysts (e.g. dactylitis)
o Polyarthralgia
o Myopathy
EYE SYMPTOMS
o Keratoconjunctivitis sicca (inflammation of the conjunctivitis and surrounding tissues due to the eyes being dry)
o Uveitis
o Papilloedema
SKIN SYMPTOMS
o Lupus pernio (red-blue infiltrations of the nose, cheeks, ears and terminal phalanges)
o Erythema nodosum *** red patches on shin
o Maculopapular eruptions
NEUROLOGICAL SYMPTOMS o Lymphocytic meningitis o Space-occupying lesions o Pituitary infiltration o Cerebellar ataxia o Cranial nerve palsies o Peripheral
CARDIAC SYMPTOMS o Arrhythmia o Bundle branch block o Pericarditis o Cardiomyopathy o Congestive cardiac failure
Identify appropriate investigations for sarcoidosis
BLOODS
o High serum ACE
o High calcium
o High ESR
o FBC M WCC may be low due to lymphocyte sequestration in the lungs
o Immunoglobulins - polyclonal hyperglobulinaemia
o LFTs M high ALP + GGT
• 24 hr Urine Collection
o Hypercalciuria
• CXR
o Stage 0 - may be clear
o Stage 1 (right) -bilateral hilar lymphadenopathy
o Stage 2 - stage 1 with pulmonary infiltration and
paratracheal node enlargement
o Stage 3 - pulmonary infiltration and fibrosis
• High-Resolution CT Scan
o Check for diffuse lung involvement
• Gallium Scan - shows areas of inflammation
• Pulmonary Function Tests
o Low FEV1
o FVC shows restrictive picture
• Bronchoscopy and Bronchoalveolar Lavage
o High lymphocytes
o High CD4: CD8 ratio
• Transbronchial Lung Biopsy (or lymph node biopsy)
o Shows non-caseating granulomas consisting of:
• Epithelioid cells (activated macrophages)
• Multinucleate Langerhans cells
• Mononuclear cells (lymphocytes)
What are the diagnostic tests for sarcoidosis?
Biopsy and Histology
Shows non-ceseating granulomas
How is sarcoidosis staged? And what are the stages.
CXR:
o Stage 0 - may be clear
o Stage 1 (right) -bilateral hilar lymphadenopathy
o Stage 2 - stage 1 with pulmonary infiltration and
paratracheal node enlargement
o Stage 3 - pulmonary infiltration and fibrosis
What do you expect to find on LP results following a Multiple sclerotic clinical history?
Oligoclonal bands on electrophoresis
Define multiple sclerosis
• Inflammatory demyelinating disease of the CNS
What are the types of MS?
• Types
o Relapsing- Remitting MS –> COMMONEST form
• Clinical attacks of demyelination with complete recovery in between attacks
o Clinically Isolated Syndrome
• Single clinical attack of demyelination
• The attack in itself does NOT count as MS
• 10-50% progress to develop MS
o Primary Progressive MS
• Steady accumulation of disability with NO relapsing-remitting pattern
o Marburg Variant
• Severe fulminant variant of MS leading to advanced disability or death within weeks
What are the RF/aetiolofy of MS?
Aetiology:
UNKOWN
RF:
o EBV exposure
o Prenatal vitamin D levels
Summarise the epidemiology of multiple sclerosis
- UK prevalence: 1/1000
- 2 x as common in FEMALES
- Age of presentation: 20-40 yrs
Recognise the presenting symptoms of multiple sclerosis
Varies depending on the site of inflammation
• Optic Neuritis (COMMONEST) ***
o Unilateral deterioration of visual acuity and colour perception
o Pain on eye movement
o Common first symptoms of multiple sclerosis
• Sensory
o Pins and needles
o Numbness
o Burning
• Motor o Limb weakness o Spasms o Stiffness o Heaviness
• Autonomic o Urinary urgency o Hesitancy o Incontinence o Impotence
• Psychological
o Depression
o Psychosis
- Uhthoff’s Sign - worsening of neurological symptoms as the body gets overheated from hot weather, exercise, saunas, hot tubs etc.
- Lhermitte’s Sign - an electrical sensation that runs down the back and into the limbs when the neck is flexed
Recognise the signs of multiple sclerosis on physical examination
• Optic Neuritis
o Impaired visual acuity (MOST COMMON)
o Loss of coloured vision
• Visual Field Testing
o Central scotoma (if optic nerve is affected)
• Scotoma = a blind spot in the normal visual field
o Field defects (if optic radiations are affected)
• Relative Afferent Pupillary Defect (RAPD)
• Internuclear Ophthalmoplegia
o Lateral horizontal gaze causes failure of adduction of the contralateral eye
o Indicates lesion of the contralateral medial longitudinal fasciculus
• Sensory
o Paraesthesia
• Motor
o UMN signs
• Cerebellar
o Limb ataxia (intention tremor, past-pointing, dysmetria) o Dysdiadochokinesia
o Ataxic wide-based gait
o Scanning speech
What should happen for MS diagnosis?
Diagnosis is based on the finding of two or more CNS lesions with corresponding symptoms, separated in time and space M McDONALD CRITERIA
What investigations should you perform for MS?
• Lumbar Puncture
o Microscopy - exclude infection/inflammatory causes
o CSF electrophoresis shows UNMATCHED OLIGOCLONAL ANTIBODIES
• MRI Brain, Cervical and Thoracic Spine (with gadolinium)
o Plaques can be identified
o Gadolinium enhancement shows active lesions
• Evoked Potentials
o Visual, auditory and somatosensory evoked potentials may show delayed conduction velocity
What should you suspect with a pt presenting with: acute onset RUQ pain tender hepatomegaly ascites no jaundice history of polycythaemia vera
Budd Chiari syndrome
Sudden onset ascites with tender hepatomegaly in the absence of jaundice should hold a high degree suspicion of budd chiari syndrome
What is Budd Chiari syndrome?
This syndrome describes the effects of hepatic vein outflow obstruction
Commonly by thrombosis or malignant obstuction
RF: malignancy, thrombophilias, trauma, oral contraceptive pill.
Diagnosis: made by doppler scanning of the hepatic vein
Define TB
Granulomatous disease caused by Mycobacterium tuberculosis
What are the 3 stages of TB?
Primary TB: initial infection may be pulmonary or (more rarely) gastrointestinal
Miliary TB: results from haematogenous dissemination of TB
Post-Primary TB: caused by reinfection or reactivation
Summarise the epidemiology of tuberculosis
Annual mortality = 3 million (95% in developing countries) Annual UK incidence = 6000
ASIAN IMMIGRANTS** are the highest risk group in the UK
Recognise the symptoms and signs of tuberculosis
Primary TB: Mostly ASYMPTOMATIC Fever Malaise Cough Wheeze Erythema nodosum Phlyctenular conjunctivitis
Miliary TB Fever
Weight loss
Meningitis Yellow caseous tubercles spread to other organs
Post-Primary TB Fever/night sweats Malaise Weight loss Breathlessness Cough Sputum Haemoptysis Pleuritic chest pain Signs of pleural effusion Collapse Consolidation Fibrosis
Non-Pulmonary TB - occurs mainly in the immunocompromised
Lymph Nodes
Suppuration of cervical lymph nodes leading to abscesses or sinuses
CNS -
meningitis, tuberculoma
Skin - lupus vulgaris (jellylike reddishMbrown glistening plaques)
Heart -
pericardial effusion, constrictive pericarditis
GI - Subacute obstruction Change in bowel habit Weight loss Peritonitis Ascites
Genitourinary - UTI symptoms Renal failure Epididymitis Endometrial or tubal involvement Infertility Adrenal insufficiency
Bone/Joint -
osteomyelitis, arthritis, vertebral collapse (Pott’s disease), spinal cord compression from an abscess
Identify appropriate investigations for tuberculosis
Sputum/Pleural Fluid/Bronchial Washings - MC&S
NOTE: culturing TB takes a long time (around 6 weeks)
Tuberculin Tests
Positive if the patient has had previous exposure to M. tuberculosis or BCG
Mantoux Test
A purified protein derivative (PPD) is injected intradermally
Erythema occurs after 72 hours
Heaf Test Place a drop of PPD on the forearm Fire a spring-loaded needle gun Check again after 3-7 days Graded according to papule size and vesiculation
Interferon Gamma Tests Useful in latent TB
Exposure of host T cells to TB antigens leads to release of interferon
CXR
Primary Infection
Peripheral consolidation
Hilar lymphadenopathy
Miliary Infection
Fine shadowing
PostJPrimary Upper lobe shadowing Streaky fibrosis and cavitation Calcification Pleural effusion Hilar lymphadenopathy
HIV Testing
CT-
lymph nodes, pleural biopsy, sampling of other affected systems
What are the findings on CXR of TB?
PRIMARY INFECTION
Peripheral consolidation
Hilar lymphadenopathy
MILIARY INFECTION
Fine shadowing
POST PRIMARY INFECTION Upper lobe shadowing Streaky fibrosis and cavitation Calcification Pleural effusion Hilar lymphadenopathy
Which drug commonly causes thrombocytopenia?
Heparin
Define meningitis
Inflammation of the leptomeningeal (pia and arachnoid mater) coverings of the brain, most commonly due to infection
What’s the most common causing organisms of meningitis in adults and elderly?
o Adults
• Neisseria meningitidis
• Streptococcus pneumoniae
• Tuberculosis
o Elderly
• Streptococcus pneumoniae
• Listeria monocytogenes
What are the RF for meningitis?
o Close communities (e.g. college halls) o Basal skull fractures o Mastoiditis o Sinusitis o Inner ear infections o Alcoholism o Immunodeficiency o Splenectomy o Sickle cell anaemia o CSF shunts o Intracranial surgery
Summarise the epidemiology of meningitis
Summarise the epidemiology of meningitis
• UK: 2500 notifications/yr
Recognise the presenting symptoms of meningitis
- Acute onset Severe headache *
- Photophobia *
- Neck or backache NECK STIFNESS
- Irritability
- Drowsiness
- Vomiting
- High-pitched crying or fits (common in children)
- Reduced consciousness
- Fever
What are signs of meningism on examination?
• Signs of MENINGISM
o Photophobia
o Neck stiffness
o Kernig’s Sign = with the hips flexed, there is pain/resistance on passive knee extension
o Brudzinski’s Sign = flexion of the hips when the neck is flexed
• Signs of INFECTION o Fever o Tachycardia o Hypotension o Skin rash o Altered mental state
Identify appropriate investigations for meningitis
• Bloods
o Two sets of blood cultures
• Imaging
o CT scan - exclude mass lesion or raised ICP before LP
• Lumbar Puncture o MC&S o Bacterial meningitis: • Cloudy CSF • High neutrophils • High protein • Low glucose o Viral meningitis: • High lymphocytes • High protein • Normal glucose o TB meningitis: • Fibrinous CSF • High lymphocytes • High protein • Low glucose
Generate a management plan for meningitis
• IMMEDIATE IV Antibiotics (before LP)
o First choice: 3rd generation cephalosporin (e.g. cefotaxime or ceftriaxone)
o Benzylpenicillin may be used as an initial blind therapy
• Dexamethasone IV
o Given shortly before or with the first dose of antibiotics o Associated with a reduced risk of complications
• Resuscitation
o Manage in ITU
o Notify public health services
Identify possible complications of meningitis
- Septicaemia
- Shock
- DIC
- Renal failure
- Seizures
- Peripheral gangrene
- Cerebral oedema
- Cranial nerve lesions
- Cerebral venous thrombosis
- Hydrocephalus
- Waterhouse-Friderichsen Syndrome (bilateral adrenal haemorrhage caused by severe meningococcal infection)
What could an inverted T wave indicate on ECG?
LBBB Left ventricular hypertrophy Myocardial infarction Myocardial ischaemia Hypokalemia
How does hyperkalemia present on an ECG?
Tented T waves
How does hypokalemia present on an ECG?
U waves
How does overflow diarrhoea present?
Elderly immobile pt
Suffering from constipation
Then watery diarrhoea episodes
No indication of infection or anything else.
Constipation management
CONSERVATIVE High fibre diet Loads of water Encourage mobilisation Remove constipation drugs such as opiates MEDICAL osmotic laxatives like lactulose bulk forming laxatives like bran stimulant laxatives such as movicol
A pt presents with known HIV with a 3 week history of cough, increasing SOB, fever, weight loss and night sweats. What do you suspect? And what is the most appropriate investigation?
Pneumocystis pneumonia
Is the commonest AIDS-defining ilness
Caused by fungus: Pneumocystis jiroveci/carinii
Best investigation is bronchoalveolar lavage (very specific and sensitive)
Perihilar ground-glass might be seen on CXR as well.
A 65yo female pt presents with tiredness, increasing sob, loss of sensation in her feet. What do you suspect? What do you expect to find OE?
b12 deficiency
60yo + tiredeness + neurological symptoms = b12
OE: angular stomatitis* glossitis* peripheral neuropathy pale subacute combined degeneration of the spinal cord.
How is b12 absorbed in the body?
B12 is found in meat and animal protein Absorption occurs in the terminal ileum and requires intrinsic factor (produced by gastric parietal cells)
This means that vegans and IBD patients have a decreased b12 absorbtion (the former due to lack of ingesting it and the latter due to terminal ileum disease - crohns)
68yo male pt with acid reflux history presents with epigastric pain and weight loss. His reflux has been managed by his GP. What do you suspect? What is the most appropriate next step?
weight loss + >50yo = cancer
history of acid reflux = gastric cancer
Given that his reflux is managed and weight loss you suspect gastric cancer.
The next best step is endoscopy
Endoscopy to bx and do a histology diagnosis and then CT to stage and metastasis.
What is the most common type of gastric cancer?
Adenocarcinoma
Where is gastric cancer more prelevant in the world?
Japan
How does a typical gastric cancer pt present?
History of reflux
Epigastric pain
FLAWS
Usually they present at a quite late stage unfortunately.
What are the signs of gastric cancer OE?
- Epigastric mass
- Abdominal tenderness
- Ascites
- Signs of anaemia
- Virchow’s Node ** (aka Troisier’s sign)
- Sister Mary Joseph’s Nodule (metastatic node on the umbilicus)
- Krukenberg’s Tumour (ovarian metastases)
What are some NSAID contraindications
History of gi ulcers
Asthma
Aspirin use
Congestive heart failure
(can be used along steroids though)
Pt presents with acute, sharp central chest pain radiating to the left arm
Worst on inspiration and at night
Pt has upper respt infection and this pain is bothering them from coughing
What do you suspect?
Key here is recent history of chest infection
= ACUTE PERICARDITIS
Relieved by sitting forward & worst at night **
Doesn’t allow you to cough properly - pleuritic chest pain
What is acute pericarditis?
• Inflammation of the pericardium o It may be acute, subacute or chronic its uncommon Its idiopathic Can follow an infection
What do you expect to see on an ECG of pericarditis?
Widespread saddle shaped ST elevation
in sinus rhythm
What do you expect to find OE of pericarditis?
• Bi-basal crackles = Pleural effusion
• Fever
• Pericardial friction rub
o Heard best at lower left sternal edge, with patient leaning forward during expiration
Current hospitalised patient with catheter in has normal basic observations but severely decreased urine output. What’s the first thing you do
Flush catheter with 50ml warm saline and aspirate
This is to remove any clots or other stuff blocking the catheter.
Always have this in mind with oligouria with no other symptoms or other explanation.
Elderly alcoholic woman is admitted post fall due to hip pain. She starts geting impaired GCS and focal neurology. What do you expect?
Recent possible head trauma = cranial haemorrhage
Alcoholic = Subdural
SUBDURAL HAEMATOMA
How are subdural haematomas classified?
Classification
o ACUTE: < 72 hrs
o SUBACUTE: 3M 20 days
o CHRONIC: > 3 weeks
Typical presentation of subdural haematoma
Trauma in elderly
Preceding decreased consciousness
40yo Female pt presents with weight loss, irritability, blurred vision, lid lag
What are you thinking?
Grave’s disease
lid lag*
Grave’s is the commonest cause of hyperthyroidism - an autoimmune disease which igG stimulate the TSHR to release thyroxine into the circulation
The same antibodies also attack retro-orbital structures causing proptosis , ophthalmoplegia and peri-orbital oedema.
Anti-TPO antibodies (thyroid peroxidase) M found in 75% of Graves
