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GET AHEAD medicine > Practice Paper 2 > Flashcards

Practice Paper 2 Flashcards

1
Q

What are the most common causes of an elderly patients acute confusion?

A

Infection: UTI and upper respiratory infection

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2
Q

Which conditions are associated with HLA B27 ?

A 
Crohn's
Psoriasis
UC
Uveitis
Ankylosing Spondylitis
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3
Q

What signs do you expect on examination of a HF patient?

A 
Hepatomegaly
Pitting oedema
Pulsus alternans
Raised JVP
Ascites
Tricuspid regurg
Bilateral basal crackles
s3 gallop
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4
Q

Whats the Glasgow score? What is it used for?

A

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
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5
Q

Whats the alternative name for Giant cell arteritis?

A

Temporal arteritis

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6
Q

Define Giant cell arteritis

A

Granulomatous inflammation of large arteries, particularly branches of the external carotid artery, most commonly the TEMPORAL ARTERY

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7
Q

Whats the aetiology and RF for temporal arteritis?

A

UNKOWN

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8
Q

Whats the epidemiology of temporal arteritis?

A

More common in FEMALES

Peak age of onset: 65M70 yrs

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9
Q

Recognise the presenting symptoms of giant cell arteritis

A
  • 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

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10
Q

How does a classic presentation of temporal arteritis present?

A 
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
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11
Q

Identify appropriate investigations for giant cell arteritis

A

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

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12
Q

Define Chronic Myeloid Leukemia

A

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

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13
Q

Explain the aetiology/risk factors of chronic myeloid leukaemia

A

• 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

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14
Q

Whats the pathogenesis of CML? (regarding the philadelphia gene)

A

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

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15
Q

What are the 3 phases of CML?

A

• 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

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16
Q

Summarise the epidemiology of chronic myeloid leukaemia

A
  • Incidence increases with age
  • Mean age of diagnosis: 40-60 yrs
  • 4 x more common in MALES
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17
Q

Recognise the presenting symptoms of chronic myeloid leukaemia

A

• 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

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18
Q

Recognise the signs of chronic myeloid leukaemia on physical examination

A 
•  SPLENOMEGALY - most common physical finding (90% of cases) 
•  Signs of bone marrow failure: 
o  Pallor 
o  Bleeding  
o  Ecchymosis
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19
Q

Identify appropriate investigations for chronic myeloid leukaemia

A 
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

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20
Q

Define Osteoarthritis

A

Age - related degenerative joint disease when cartilage destruction exceeds repair, causing pain and disability

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21
Q

Whats the pathogenesis of osteoarthritis

A

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

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22
Q

Summarise the epidemiology of osteoarthritis

A
  • COMMON
  • 25% of those > 60 yrs
  • More common in FEMALES, CAUCASIANS and ASIANS
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23
Q

Recognise the presenting symptoms of osteoarthritis

A
  • 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
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24
Q

Recognise the signs of osteoarthritis on physical examination

A

• 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
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25
Q

What are the four classic features of OA on Xray?

A

o Loss of joint space (narrowing)
o Osteophytes
o Subchondral cysts
o Subchondral sclerosis

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26
Q

Name 4 main AB types and their predominant cover

A 
Co-amoxiclav --> broad spectrum gram+ and -
Flucloxacillin --> gram + 
Vancomycin --> gram + 
Gentamicin --> gram - 
Metronidazole --> anaerobic cover
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27
Q

Define spinal cord compression

A

Injury to the spinal cord with neurological symptoms dependent on the site and extent of the injury

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28
Q

Explain the aetiology of spinal cord compression

A 
•  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)
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29
Q

What are the Rf for spinal cord compression?

A

o Trauma
o Osteoporosis
o Metabolic bone disease
o Vertebral disc disease

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30
Q

Recognise the presenting symptoms of cord compression

A
  • 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

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31
Q

Recognise the signs of cord compression on physical examination

A
  • 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

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32
Q

Identify appropriate investigations for cord compression

A

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)

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33
Q

Define varicella zoster

A

• 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

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34
Q

Summarise the epidemiology of varicella zoster

A
  • Chicken pox peak incidence: 4M10 yrs
  • Shingles peak incidence: > 50 yrs
  • 90% of adults are VZV IgG positive
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35
Q

Recognise the presenting symptoms of varicella zoster

• Chickenpox

A

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)

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36
Q

Recognise the presenting symptoms of varicella zoster

• Shingles

A

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

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37
Q

Recognise the signs of varicella zoster on physical examination • Chickenpox

A

o Maculopapular rash
o Areas of weeping and crusting
o Skin excoriation (from scratching)
o Mild pyrexia

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38
Q

Recognise the signs of varicella zoster on physical examination
• Shingles

A

o VESICULAR maculopapular rash
o Dermatomal distribution
o Skin excoriation

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39
Q

Identify appropriate investigations for varicella zoster

A
  • 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
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40
Q

Generate a management plan for varicella zoster

• Chickenpox

A

o Children M treat symptoms

o Adults M consider aciclovir

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41
Q

Generate a management plan for varicella zoster

• Shingles

A

o Aciclovir, valaciclovir, famciclovir

• Prevention
o Varicella Zoster Ig (VZIG) M may be considered in immunosuppressed or pregnant

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42
Q

What is Ramsay Hunt syndrome?

A

• 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

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43
Q

Summarise the prognosis for patients with varicella zoster

A

Summarise the prognosis for patients with varicella zoster
• Depends on complications
• Worse in pregnancy, elderly and immunocompromised

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44
Q

Define asthma

A

Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation

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45
Q

Recognise the presenting symptoms of asthma

A

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

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46
Q

Recognise the signs of asthma on physical examination

A 
Tachypnoea  
Use of accessory muscles   
Prolonged expiratory phase   
Polyphonic wheeze   
Hyperinflated chest
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47
Q

Recognise the signs of asthma on physical examinatiob for a SEVERE attack

A

PEFR < 50% predicted
Pulse > 110/min
RR > 25/min
Inability to complete sentences

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48
Q

Recognise the signs of asthma on physical examination for a LIFE THREATENING ATTACK

A 
PEFR < 33% predicted   
Silent chest *
Cyanosis   
Bradycardia   
Hypotension   
Confusion  
Coma
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49
Q

Why is a normal PCO2 worrying in an asthma attack?

A

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.

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50
Q

Chronic management steps of asthma

A

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

51
Q

Management of acute asthma

A

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

52
Q

Define adrenal insufficiency

A

Deficiency of adrenal cortical hormones (e.g. mineralocorticoids, glucocorticoids and androgens)
Aldosterone & Cortisol insufficiency

53
Q

Explain the aetiology/risk factors of adrenal insufficiency

A

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
54
Q

How does a patient with chronic adrenal insufficiency present?

A 
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
55
Q

How does a patient with acute (addisonian crisis) present?

A

o Acute adrenal insufficiency
o Major haemodynamic collapse ** (without neuro symptoms)
o Precipitated by stress (e.g. infection, surgery)

56
Q

Recognise the signs of adrenal insufficiency on physical examination

A

• 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)

57
Q

Addisonian crisis signs OE

A 
o  Hypotensive shock  
o  Tachycardia 
o  Pale  
o  Cold  
o  Clammy  
o  Oliguria
58
Q

Identify appropriate investigations for adrenal insufficiency

A

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

59
Q

• Investigations in Addisonian crisis

A 
o  FBC (neutrophilia MM> infection)   
o  U&amp;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
60
Q

Generate a management plan for ACUTE adrenal insufficiency

• Addisonian Crisis

A

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)

61
Q

Generate a management plan for CHRONIC adrenal insufficiency

A

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

62
Q

Identify the possible complications of adrenal insufficiency

A
  • HYPERKALAEMIA

* Death during Addisonian crisis

63
Q

Summarise the prognosis for patients with adrenal insufficiency

A
  • Adrenal function rarely recovers

* Normal life expectancy if treated

64
Q

How does spontaneous bacterial peritonitis presetn?

A 
Severe generalised abdominal pain
Ascites
Vomiting
Fever
Rigors

Alcohol abuse history

65
Q

How is SBP diagnosed?

A

Paracentesis of ascitic fluid and if the WCC is above 250 the pt requires IV AB

66
Q

Define sarcoidosis

A

• Multisystem granulomatous inflammatory disorder

67
Q

Explain the aetiology/risk factors of sarcoidosis

A
  • UNKNOWN

* Transmissible agents (e.g. viruses), environmental triggers and genetic factors have all been suggested

68
Q

Explain the pathogenesis of sarcoidosis

A 
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
69
Q

Summarise the epidemiology of sarcoidosis

A
  • Most common in AFRICANS and SCANDINAVIANS

* Can occur at any age but tends to be in adults > 50 yrs

70
Q

Recognise the presenting symptoms and the signs of sarcoidosis

A 
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
71
Q

Identify appropriate investigations for sarcoidosis

A

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)

72
Q

What are the diagnostic tests for sarcoidosis?

A

Biopsy and Histology

Shows non-ceseating granulomas

73
Q

How is sarcoidosis staged? And what are the stages.

A

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

74
Q

What do you expect to find on LP results following a Multiple sclerotic clinical history?

A

Oligoclonal bands on electrophoresis

75
Q

Define multiple sclerosis

A

• Inflammatory demyelinating disease of the CNS

76
Q

What are the types of MS?

A

• 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

77
Q

What are the RF/aetiolofy of MS?

A

Aetiology:
UNKOWN

RF:
o EBV exposure
o Prenatal vitamin D levels

78
Q

Summarise the epidemiology of multiple sclerosis

A
  • UK prevalence: 1/1000
  • 2 x as common in FEMALES
  • Age of presentation: 20-40 yrs
79
Q

Recognise the presenting symptoms of multiple sclerosis

A

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
80
Q

Recognise the signs of multiple sclerosis on physical examination

A

• 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

81
Q

What should happen for MS diagnosis?

A

Diagnosis is based on the finding of two or more CNS lesions with corresponding symptoms, separated in time and space M McDONALD CRITERIA

82
Q

What investigations should you perform for MS?

A

• 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

83
Q 
What should you suspect with a pt presenting with:
acute onset RUQ pain
tender hepatomegaly
ascites
no jaundice
history of polycythaemia vera
A

Budd Chiari syndrome

Sudden onset ascites with tender hepatomegaly in the absence of jaundice should hold a high degree suspicion of budd chiari syndrome

84
Q

What is Budd Chiari syndrome?

A

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

85
Q

Define TB

A

Granulomatous disease caused by Mycobacterium tuberculosis

86
Q

What are the 3 stages of TB?

A

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

87
Q

Summarise the epidemiology of tuberculosis

A

Annual mortality = 3 million (95% in developing countries) Annual UK incidence = 6000
ASIAN IMMIGRANTS** are the highest risk group in the UK

88
Q

Recognise the symptoms and signs of tuberculosis

A 
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

89
Q

Identify appropriate investigations for tuberculosis

A

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

90
Q

What are the findings on CXR of TB?

A

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
91
Q

Which drug commonly causes thrombocytopenia?

A

Heparin

92
Q

Define meningitis

A

Inflammation of the leptomeningeal (pia and arachnoid mater) coverings of the brain, most commonly due to infection

93
Q

What’s the most common causing organisms of meningitis in adults and elderly?

A

o Adults
• Neisseria meningitidis
• Streptococcus pneumoniae
• Tuberculosis

o Elderly
• Streptococcus pneumoniae
• Listeria monocytogenes

94
Q

What are the RF for meningitis?

A 
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
95
Q

Summarise the epidemiology of meningitis

A

Summarise the epidemiology of meningitis

• UK: 2500 notifications/yr

96
Q

Recognise the presenting symptoms of meningitis

A
  • Acute onset Severe headache *
  • Photophobia *
  • Neck or backache NECK STIFNESS
  • Irritability
  • Drowsiness
  • Vomiting
  • High-pitched crying or fits (common in children)
  • Reduced consciousness
  • Fever
97
Q

What are signs of meningism on examination?

A

• 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
98
Q

Identify appropriate investigations for meningitis

A

• Bloods
o Two sets of blood cultures

• Imaging
o CT scan - exclude mass lesion or raised ICP before LP

•  Lumbar Puncture 
o  MC&amp;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
99
Q

Generate a management plan for meningitis

A

• 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

100
Q

Identify possible complications of meningitis

A
  • 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)
101
Q

What could an inverted T wave indicate on ECG?

A 
LBBB
Left ventricular hypertrophy
Myocardial infarction
Myocardial ischaemia
Hypokalemia
102
Q

How does hyperkalemia present on an ECG?

A

Tented T waves

103
Q

How does hypokalemia present on an ECG?

A

U waves

104
Q

How does overflow diarrhoea present?

A

Elderly immobile pt
Suffering from constipation
Then watery diarrhoea episodes
No indication of infection or anything else.

105
Q

Constipation management

A 
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
106
Q

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?

A

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.

107
Q

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?

A

b12 deficiency
60yo + tiredeness + neurological symptoms = b12

OE: 
angular stomatitis* 
glossitis* 
peripheral neuropathy
pale
subacute combined degeneration of the spinal cord.
108
Q

How is b12 absorbed in the body?

A 
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)

109
Q

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?

A

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.

110
Q

What is the most common type of gastric cancer?

A

Adenocarcinoma

111
Q

Where is gastric cancer more prelevant in the world?

A

Japan

112
Q

How does a typical gastric cancer pt present?

A

History of reflux
Epigastric pain
FLAWS

Usually they present at a quite late stage unfortunately.

113
Q

What are the signs of gastric cancer OE?

A
  • 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)
114
Q

What are some NSAID contraindications

A

History of gi ulcers
Asthma
Aspirin use
Congestive heart failure

(can be used along steroids though)

115
Q

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?

A

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

116
Q

What is acute pericarditis?

A 
•  Inflammation of the pericardium 
o  It may be acute, subacute or chronic  
its uncommon
Its idiopathic
Can follow an infection
117
Q

What do you expect to see on an ECG of pericarditis?

A

Widespread saddle shaped ST elevation

in sinus rhythm

118
Q

What do you expect to find OE of pericarditis?

A

• Bi-basal crackles = Pleural effusion
• Fever
• Pericardial friction rub
o Heard best at lower left sternal edge, with patient leaning forward during expiration

119
Q

Current hospitalised patient with catheter in has normal basic observations but severely decreased urine output. What’s the first thing you do

A

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.

120
Q

Elderly alcoholic woman is admitted post fall due to hip pain. She starts geting impaired GCS and focal neurology. What do you expect?

A

Recent possible head trauma = cranial haemorrhage
Alcoholic = Subdural

SUBDURAL HAEMATOMA

121
Q

How are subdural haematomas classified?

A

Classification
o ACUTE: < 72 hrs
o SUBACUTE: 3M 20 days
o CHRONIC: > 3 weeks

122
Q

Typical presentation of subdural haematoma

A

Trauma in elderly

Preceding decreased consciousness

123
Q

40yo Female pt presents with weight loss, irritability, blurred vision, lid lag

What are you thinking?

A

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

GET AHEAD medicine (6 decks)

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