Practice Paper 5 Flashcards
What are the 3 types of dementia
ALZHEIMER’S DISEASE (50%) - degeneration of the cerebral cortex, with cortical atrophy and reduction in acetylcholine production
VASCULAR DEMENTIA (25%) - brain damage due to several incidents of cerebrovascular disease (e.g. strokes/TIAs)
LEWY BODY DEMENTIA (15%) - deposition of abnormal proteins (Lewy bodies) within the brain stem and neocortex
PC of alzheimer’s
insidious onset
PC of lewy body dementia
Fluctuating levels of consciousness, hallucinations, falls and Parkinsonian symptoms
Which system in the liver do quinolone AB use?
they inhibit cytochrome p450
Which other drug uses cyt p450 system and hence can’t be sued with quinolones?
warfarin
Define T1DM
Metabolic hyperglycaemia
Caused by absolute insufficiency of pancreatic insulin production
What causes T1DM
autoimmune destruction of b cells (insulin producing cells of the pancreas)
due to genetic susceptibility combined with an environmental trigger
PC of T1DM
Juvenile onstet <30yo Polyuria Polydipsia Nocturia Tiredness Weight loss
Investigations of T1DM
Blood glucose:
- fasting >7
OR
- random >11.1
Hba1c, U&E’s (hyperkalemia prone)
Whats the MX of T1DM
Conservative - advice and pt education
Short acting insulin 3/day before meails
- Lispro, Aspart, Detemir
Long acting insulin 1/day
- Isophane, Glargine, Detemir
Insulin pumps
Monitoring capillary blood glucose levels
Monitoring HbA1C every 3-6months
Screening for complications
Hypoglycaemia mx
If reduced consciousness:
50ml of 50% glucose IV
OR
1mg glucagon IM
If consciousness is normal:
50g oral glucose + starchy meal
What are the complications of T1DM
DKA
Microvascular: retinopathy, neuropathy, nephropathy
Macrovascular: peripheral vascular disease, IHD, Stroke/TIA’s
Increased risk of infections
What are the complications of mx of T1DM
Weight gain
Fat hypertrophy at injection sites
Hypo’s
How do hypoglycemic episodes present
Fits Confusion Coma Tachycardia Palpitations Tremor Hunger Personality changes
What is the prognosis for T1DM
good when early diagnosis, good mx, good glucose control and good compliance
Main causes of morbidity+mortality are vascular disease and renal failure
How does DKA present?
Nausea Vomiting Abdominal pain Polyuria/Polydipsia Drowsiness Confusion Coma Kussmaul breathing Ketotic breath Dehydration
What causes DKA?
Infections
Errors in mx
Newly diagnosed T1DM
Idiopathic
What ix do you need to do for DKA?
WCC (might be raised) U&E's: High urea, High Creatinine *** (due to dehydration) LFT CRP Glucose Amylase ABG - metabolic acidosis with high anion gap Blood&Urinary ketones
What does an ABG show in DKA?
Metabolic acidosis with high anion gap
Whats the mx of DKA? **
50U soluble insulin in 50ml of normal saline
Use insulin sliding scale
Continue with this until: capillary ketone are <0,3, venous pH is above 7.30 and venous HCO3- is above >18mmol
Then change to SC Insulin
(but continue IV for 1-2hrs)
500ml normal saline over 15-30mins until SBP is >100
K+ replacement
Monitori: BG, capillary ketones, urine output = catheterise, U&E’s, VBG.
Broad spectrum AB if there’s infection
Thromboprophylaxis
NBM for atleast 6 hrs
NG tube if GCS is reduced
Define T2DM
Increased peripheral resistance to insulin action, impaired insulin secretion, increased hepatic glucose output
What causes T2DM
Genetic + Environment (MODY)
Obesity
2’ to pancreatic disease, endocrine disease, drugs.
Whats the PC of T2DM pts
Incidental finding sometimes Polyuria Polydipsia Tiredness Infections - Balantis*, Foot ulcers, Candidiasis Hyperosmolar Hyperglycaemic State - HHS
What are the signs OE for T2DM
Increased BMI usually
Increased waist circumference
BP
Diabetic foot: dry skin, loss of SC tissue, ulceration, gangrene, charcot’s arthropathy, weak foot pulses.
SKIN CHANGES (rare): o Necrobiosis lipoidica diabeticorum (well-demarcated plaques on shins or arms with shiny atrophic surface and redMbrown edges)
o Granuloma annulare (flesh-coloured papules coalescing in rings on the back of hands and fingers)
o Diabetic dermopathy (depressed pigmented scars on shins)
What IX do you do for T2DM
1 or more of the following is required to diagnose T2DM:
- Symptomatic patient + random plasma glucose >11.1
- Fasting plasma glucose >7
- 2hr plasma glucose >11.1 after 75g OGTT
What things need to be monitored in T2DM
HbA1C U&E's Lipid profile eGFR Urine albuime: Creatinine ratio
Whats the medication steps in T2DM
At diagnosis: Lifestyle + Metformin (step 1)
If HbA1C >7% after 3 months: step 1 + sulphonylurea
If HbA1C >7% after 3 months: step 1 + basal insulin
If HbA1C >7% after 3 months: add premeal rapid acting insulin
Whats the mx of T2DM
Medicines
Screening for: retinopathy, nephropathy, diabetic foot, vascular disease, CVD - bp, chol.
Pregnant women need strict glycemic control
Whats the mx of HHS
Similar to DKA
+ use 0,45% saline if serum Na+ is >170mmol
- 50 U insuline in 50ml normal saline
- SC insulin
- 500ml normal saline bolus
- Thromboprophylaxis
- K+ replacement
- NBM
What are the complications of T2DM
HHS (due to insulin deficiency, dehydration, raised sodium, raised glucose, raised osmolality, no acidosis though)
Nephropathy: microalbuminuira, proteinuria, renal failure, UTI recurrence.
Retinopathy: background, pre-proliferative, proliferative, more prone to glaucoma and cataracts.
Macrovascular: IHD, stroke, Peripheral vascular disease
What tests do you run on a pre diabetic pt
IFG - impaired fasting blood glucose is 5,6-6,9
IGT - impaired glucose tolerance gives plasma 7.8-11 2hrs after 75mg OGTT.
Whats the triad of cardinal biochemical features for DKA
Hyperglycaemia
Hyperketonaemia
Metabolic Acidosis
Whats the pathophysiology of DKA
The hyperglycaemia causes dehydration and electrolyte loss especially Na+ and K+ through osmotic dieresis.
Ketosis is caused by insulin deficiency and it is exacerbated by elevated catecholamines and other stress hormones resulting in unrestrained lipolysis to free fatty acids for ketogenesis in the liver.
The resulting metabolic acidosis causes the exchange of hydrogen ions for IC K+ although there is also K+ loss through the kidney and intestine.
What are prelevant RF for atherosclerosis?
Smoking LDL cholesterol Hypertension Lack of exercise Obesity (preventable RF)
Secondary causes:
Poor mx of diabetes
Alcohol consumption causes
both cause hypertension
What TFT’s results do you expect normally in a hypothyroidism pt?
Low t4 and high TSH
What are you suspecting if a pt presenting with classic hypothyroidism symptoms has TFT’s of low t4 and low TSH and has bitemporal hemianopia
What test do you want to do?
Suspect central hypothyroidism (2’ hypothyroidism)
Due to a pituitary adenoma
Request an MRI
Define sickle cell disease
A chronic condition with sickling of red blood cells caused by inheritance of haemoglobin S (HbS)
Explain the pathophysiology of sickle cell disease
• Autosomal recessive
• Caused by a point mutation in the beta-globin gene resulting in the substitution of glutamic acid in position 6 by valine
• This results in the formation of abnormal haemoglobin S
• Deoxygenation of HbS alters the conformation resulting in sickling of red cells
• Sickling makes the red cells more fragile and inflexible
• These sickled red cells are prone to:
o Sequestration and destruction (reduced red cell survival ~ 20 days)
o Occlusion of small blood vessels causing hypoxia, which leads to further sickling and occlusion
What factors precipitate sickling
o Infection
o Dehydration
o Hypoxia
o Acidosis
Summarise the epidemiology of sickle cell disease
- Rarely presents before 4-6 months (because HbF can compensate for the defect in adult haemoglobin)
- Common in Africa, Caribbean, MiddleMEast and other areas with a high prevalence of malaria
Recognise the presenting symptoms of sickle cell disease
Symptoms secondary to VASO-OCCLUSION or INFARCTION: o Autosplenectomy (splenic atrophy or infarction) = Leads to increased risk of infections with encapsulated organisms (e.g. pneumococcus, meningococcus)
o Abdominal Pain
o Bones
• Painful crises affect small bones of the hands and feet causing dactylitis in CHILDREN
• Painful crises mainly affect the ribs, spine,
pelvis and long bones in ADULTS
o Myalgia and Arthralgia
o CNS
• Fits and strokes
o Retina
• Visual loss (proliferative retinopathy)
Symptoms of SEQUESTRATION CRISIS
o NOTE: sequestration crises occur due to pooling of red cells in various organs (mainly the spleen)
o Liver –> exacerbation of anaemia
o Lungs --> acute chest syndrome • Breathlessness • Cough • Pain • Fever
o Corpora cavernosa
• Persistent painful erection (priapism)
• Impotence
Recognise the signs of sickle cell disease on physical examination
Signs secondary to VASO-OCCLUSION, ISCHAEMIA or INFARCTION
o Bone - joint or muscle tenderness or swelling (due to avascular necrosis)
o Short digits - due to infarction in small bones of the hands
• Retina - cotton wool spots due to retinal ischaemia
• Signs secondary to SEQUESTRATION CRISES
o Organomegaly
• The spleen is ENLARGED in early disease
• Later on, the spleen will reduce in size due to splenic atrophy
o Priapism
• Signs of anaemia
Identify appropriate investigations for sickle cell disease
BLOODS: o FBC • Low Hb * • Reticulocytes: - HIGH - in haemolytic crises - LOW - in aplastic crises o U&Es
• Blood Film o Sickle cells o Anisocytosis (variation in size of red cells) o Features of Hyposplenism: • Target cells • Howell-Jolly bodies
• Sickle Solubility Test
o Dithionate is added to the blood
o In sickle cell disease you get increased turbidity *
• Haemoglobin Electrophoresis
o Shows HbS
o Absence of HbA (if homozygous HbS)
o High HbF
• Hip X-Ray
o Femoral head is a common site of avascular necrosis *
• MRI or CT Head
o If there are neurological complications
What do you expect a blood film of a sickle cell disease pt to look like
o Sickle cells o Anisocytosis (variation in size of red cells) o Features of Hyposplenism: • Target cells • Howell-Jolly bodies
Generate a management plan for sickle cell disease
• Infection Prophylaxis
o Penicillin V
o Regular vaccinations (particularly against capsulated bacteria e.g. pneumococcus)
• Folic Acid
o If severe haemolysis or in pregnancy
• Hydroxyurea/Hydroxycarbamide *
o Increases HbF levels
o Reduces the frequency and duration of sickle cell crisis
• Red Cell Transfusion
o For SEVERE anaemia
o Repeated transfusions (with iron chelators) may be required in patients suffering from repeated crises
• Advice
o Avoid precipitating factors, good hygiene and nutrition, genetic counselling, prenatal screening
• Surgical
o Bone marrow transplantation
o Joint replacement in cases with avascular necrosis
Whats the mx for acute painful crisis of sickle cell disease
• ACUTE (PAINFUL CRISES) o Oxygen o IV Fluids o Strong analgesia (IV opiates) o Antibiotics
Identify the possible complications of sickle cell disease
- Aplastic crises
- Haemolytic crises
- Pigment gallstones
- Cholecystitis
- Renal papillary necrosis
- Leg ulcers
- Cardiomyopathy
Whats an aplastic crisis
• Aplastic crises
o Infection with Parvovirus B19 can lead to a temporary cessation of erythropoiesis (which can cause red cell count to plummet in sickle cell patients because their red cells have a shortened life span and can’t tolerate a cessation of erythropoiesis)
Summarise the prognosis for patients with sickle cell disease
• Most patients with sickle cell disease who manage their disease well will survive until around the age of 50 yrs
• Mortality is usually the result of:
o Pulmonary or neurological complications in ADULTS
o Infection in CHILDREN
What are the symptoms of sedative withdraw?
Nausea Vomiting Autonomic hyperactivity Insomnia Delirium Seizures
Known coeliac disease pt comes in with itchy rash on both forearms with evidence of blistering
What is it
Dermatitis Herpetiformis
• Intense, itchy blisters on elbows, knees or buttocks
What are the cutaneous features of Crohn’s?
Perianal abscess
Fistulae
Skin tags
Apthous ulcers
What are the cutaneous features of UC?
Erythema nodosum
Pyoderma gangrenosum
What are the cutaneous features of Sarcoidosis?
Erythema nodosum Lupus pernio (purple indurated lesions)
Identify the possible complications of Crohn’s disease
• GI: o Haemorrhage o Strictures o Perforation o Fistulae (between bowel, bladder, vagina) o Perianal fistulae and abscesses o GI cancer o Malabsorption
• Extraintestinal Features: o Uveitis o Episcleritis o Gallstones o Kidney stones o Arthropathy o Sacroiliitis o Ankylosing spondylitis o Erythema nodosum o Pyoderma gangrenosum o Amyloidosis
What is the chronic mx of crohn’s?
Long-Term
o Steroids - for acute exacerbations
o 5-ASA analogues - decreases the frequency of relapses (useful for mild to moderate disease)
• NOTE: more commonly used in UC
o Immunosuppression: using steroid-sparing agents (e.g. azathioprine, 6-mercaptopurine, methotrexate) reduces the frequency of relapses
o Anti-TNF agents: (e.g. infliximab and adalimumab) - very effective at inducing and maintaining remission. Usually reserved for refractory Crohn’s.
• General Advice:
o Stop smoking
o Dietician referral (low fibre diet necessary if there are stricture present)
• Surgery indicated it:
o Medical treatment fails
o Failure to thrive in children in the presence of complications
o Involves resection of affected bowel and stoma formation M NOTE: there is a risk
of disease recurrence
Recognise the presenting symptoms of ulcerative colitis
- Bloody or mucous diarrhoea (stool frequency depends on severity of disease)
- Tenesmus and urgency
- Crampy abdominal pain before passing stool
- Weight loss
- Fever
- Extra-GI manifestations (e.g. uveitis, scleritis, erythema nodosum, pyoderma gangrenosum)
Recognise the presenting symptoms of Crohn’s disease
- Crampy abdominal pain (due to inflammation, fibrosis or bowel obstruction)
- Diarrhoea (may be bloody or steatorrhoea)
- Fever, malaise, weight loss
- Symptoms of complications
- Sometimes right iliac fossa pain* due to inflammation of terminal ileum
Why should you not administer high flow o2 in type 2 respiratory failure with respiratory acidosis?
It will lead to worsening of the hypercapnic respiratory failure
What is chronic bronchitis
Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years
Narrowing of the airways resulting in bronchiole inflammation (bronchiolitis) Bronchial mucosal oedema Mucous hypersecretion Squamous metaplasia
What is emphysema
Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles
Destruction and enlargement of alveoli
Leads to loss of elasticity that keeps small airways open in expiration
Progressively larger spaces develop called bullae (diameter > 1 cm)
Recognise the presenting symptoms of COPD
Chronic cough Sputum production Breathlessness Wheeze Reduced exercise tolerance
Recognise the signs of COPD on physical examination
INSPECTION Respiratory distress Use of accessory muscles Barrel-shaped over-inflated chest Decreased cricosternal distance Cyanosis
PERCUSSION Hyper-resonant chest Loss of liver and cardiac dullness Auscultation Quiet breath sounds Prolonged expiration Wheeze Rhonchi - rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions Sometimes crepitations
SIGNS OF O2 RETENTION
Bounding pulse
Warm peripheries
Asterixis
LATE STAGES: signs of right heart failure (cor pulmonale)
Right ventricular heave
Raised JVP
Ankle oedema
What might you expect in the FBC of a COPD pt
Increased Hb and haematocrit due to secondary polycythaemia
What is cor pulmonale
Abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels.
If a young pt presents with classic COPD symptoms and signs what investigation should you do?
a1 antitrypsin levels - useful in young patients who have never smoked
Though this is rare, consider it in young patients, who have never smoked, presenting with COPD type symptoms (and may have accompanying symptoms
of cirrhosis)
Whats the mx for acute COPD exacerbation?
**24% O2 via Venturi mask
Increase slowly if no hypercapnia and still hypoxic (do an ABG)
Corticosteroids
Start empirical antibiotic therapy if evidence of infection
Respiratory physiotherapy to clear sputum
Non-invasive ventilation may be necessary in severe cases
Whats the chronic mx for COPD?
STOP SMOKING
Bronchodilators
SABA = Short-acting beta-2 agonists (e.g. salbutamol)
Anticholinergics (e.g. ipratropium bromide)
LABA = Long-acting beta-2 agonists (if > 2 exacerbations per year)
Steroids
Inhaled beclamethasone - considered in all patients with FEV1 < 50% of predicted OR > 2 exacerbations per year
Regular oral steroids should be avoided if possible
Pulmonary rehabilitation
Oxygen therapy
Only for those who stop smoking
Indicated if:
PaO2 < 7.3 kPa on air during a period of clinical stability
Define PKD
Autosomal DOMINANT inherited disorder characterised by the development of multiplerenal cysts that gradually expand and replace normal kidney substance, variably
associated with extrarenal (liver and cardiovascular) abnormalities
What mutations cause PKD?
85% caused by mutations in PKD1 on chromosome 16
This is a membrane-bound multidomain protein involved in cell-cell and cell-matrix interactions
15% caused by mutations of PKD2 on chromosome 4
What’s the pathophysiology of PKD?
Proliferative/hyperplastic abnormality of the tubular epithelium
Early on, the cysts are connected to the tubules from which they arise and the fluid content is glomerular filtrate
When cyst diameter >2 mm, they detach from the tubule and the fluid content isderived from secretion of the lining epithelium
With time, the cysts enlarge and cause progressive damage to adjacent functioning nephrons
Summarise the epidemiology of polycystic kidney disease
MOST COMMON inherited kidney disorder
Responsible for 10% of end-stage renal failure
Recognise the presenting symptoms of polycystic kidney disease
Present at 30-40 yrs **
20% have no family history
May be asymptomatic
Flank Pain - may result from cyst enlargement/bleeding, stone, blood clot migration, infection
Haematuria
Hypertension
Associated with Berry aneurysms so it may present with a SAH !!!!
Recognise the signs of polycystic kidney disease on examination
Abdominal distension Enlarged cystic kidneys Palpable liver Hypertension Signs of chronic renal failure (if end stage) Signs of associated AAA
Identify appropriate investigations for polycystic kidney disease
US/CT
- Will show multiple cysts bilaterally and enlarged kidneys*
- Might show liver cysts
What complications can arise from PKD?
Cerebral aneurysms - Berry SAH due to ruptured aneurysms Hepatic cysts Pancreatic cysts Mitral valve prolapse Mitral regurgitation
What are bladder diverticuli associated with?
Usually secondary to urinary outflow obstruction and can become infected due to stagnant urine or obstruction in the outlet.
Define polymyalgia rheumatica
• An inflammatory condition of unknown cause, which is
characterised by severe BILATERAL pain and morning STIFFNESS* of the shoulder, neck and pelvic girdle.
o NOTE: polymyalgia rheumatica does NOT cause weakness
With what is polymyalgia rheumatica associated with?
Temporal Arteritis
- 40-50% of people with temporal arteritis have polymyalgia rheumatica
- 15% of people with polymyalgia rheumatica will go on to develop temporal arteritis
- Both conditions respond to corticosteroids
Summarise the epidemiology of polymyalgia rheumatica
- Relatively common
- Occurs in people aged > 50 yrs
- Peak age of onset: 73 yrs
- 3 x more common in FEMALES **
Recognise the presenting symptoms and signs of polymyalgia rheumatica
• Tend to be relatively non-specific
• Usual inclusion criteria for polymyalgia rheumatica:
o Age > 50 yrs
o Duration of symptoms > 2 weeks
o Bilateral shoulder or pelvic girdle aching, or both
o Morning stiffness lasting > 45 mins
o High ESR/CRP*
- The characteristic clinical picture of polymyalgia rheumatica: bilateral shoulder pain and stiffness of acute or subacute onset with bilateral arm tenderness
- NO WEAKNESS
- Symptoms are worst when walking
- Morning stiffness may be so bad that they find it difficult to get out of bed, or raise their arms enough to brush their hair *** BUZZ
- May be flu-like symptoms at onset
Identify appropriate investigations for polymyalgia rheumatica
- ESR/CRP - raised **
- FBC
- U&Es
- LFTs
- Bone profile
- Protein electrophoresis
- TFTs
- Creatine kinase
- Others: urinary Bence Jones proteins, autoantibodies (e.g. anti-CCP antibodies)
Generate a management plan for polymyalgia rheumatica
- CORTICOSTEROIDS **
- Steroid- sparing agents (e.g. methotrexate) are sometimes used
- Assistance from physiotherapy and occupational therapy
- Monitor for adverse effects of steroids (e.g. osteoporosis)
Which drug is used in cardiac arrest management to improve coronary perfusion pressure?
Adrenaline
What drug do you give in hyperkalemia to protect the heart?
Calcium gluconate
Define cardiac arrest
• Acute cessation of cardiac function
What are the 8 reversible causes of cardiac arrest?
The REVERSIBLE causes of cardiac arrest can be summarised as the 4 Hs and 4 Ts
• FOUR Hs o Hypothermia o Hypoxia o Hypovolaemia o Hypokalaemia/Hyperkalaemia
• FOUR Ts o Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis)) o Thromboembolic o Tamponade o Tension pneumothorax
PC of cardiac arrest
Cardiac arrest is usually sudden but some symptoms that may preceded by fatigue, fainting, blackouts, dizziness
Recognise the signs of cardiac arrest on physical examination
- Unconscious
- Not breathing
- Absent carotid pulses
Identify appropriate investigations for cardiac arrest
Identify appropriate investigations for cardiac arrest
• Cardiac Monitor
o Allows classification of the rhythm
• Bloods o ABG * o U&E o FBC o X-match o Clotting o Toxicology screen o Blood glucose
US - for cardiac tamponade
Generate a management plan for cardiac arrest
• SAFETY IS IMPORTANT
o Approach any arrest scene with caution
o The cause of the arrest may pose a threat
o Defibrillators and oxygen are hazards
• Basic Life Support
o If the arrest is witnessed and monitored, consider giving a precordial thump (thump the sternum of the patient with the ulnar aspect of your fist)
o Clear and maintain the airway with head tilt, jaw thrust and chin lift
o Assess breathing by look, listen and feel
• If they are not breathing, give two rescue breaths
o Assess circulation at carotid pulse for 10 seconds
• If absent M give 30 chest compressions at around 100/min
• Continue cycle of 30 chest compressions for every 2 rescue breaths
o Proceed to advanced life support as soon as possible
Then ALS
What steps are in ALS?
• Advanced Life Support
o Attach cardiac monitor and defibrillator
o Assess rhythm
• If pulseless ventricular tachycardia or ventricular fibrillation (SHOCKABLE RHYTHM)
- Defibrillate once (150-360 J biphasic, 360 J monophasic)
• Make sure no one is touching the patient or the bed
- Resume CPR immediately for 2 minutes and then reassess rhythm, and shock again if still in pulseless VT or VF
- Administer adrenaline (1 mg IV) after second defibrillation and again ever 3-5 mins
- If shockable rhythm persists after 3rd shock - administer amiodarone 300 mg IV bolus (or lidocaine)
• If pulseless electrical activity (PEA) or asystole (NON-SHOCKABLE RHYTHMS)
- CPR for 2, and then reassess rhythm
- Administer adrenaline (1 mg IV) every 3-5 mins
- Atropine (3 mg IV, once only) if asystole or PEA with rate < 60 bpm
o During CPR:
• Check electrodes, paddle positions and contacts
• Secure airway
- Once secure, give continuous compressions and breaths
• Consider magnesium, bicarbonate and external pacing
• Stop CPR and check pulse only if change in rhythm or signs of life
What’s the treatment of the reversible causes of cardiac arrest?
• Treatment of REVERSIBLE causes
o Hypothermia - warm slowly
o Hypokalaemia and Hyperkalaemia - correction of electrolyte levels
o Hypovolaemia - IV colloids, crystalloids and blood products
o Tamponade - pericardiocentesis
o Tension Pneumothorax - aspiration or chest drain
o Thromboembolism - treat as PE or MI
o Toxins - use antidote for given toxin
What is the first line treatment for hypothyroidism?
Carbimazole or Propylthiouracil
Antithyroid drugs
These drugs reduce the synthesis of new thyroid hormones by inhibiting the iodination of tyrosine
26yo female pt from sub-Saharan Africa presents with 2 months of haemoptysis and lethargy
In the last month she lost hald a stone and she frequently soaks the bedsheets with sweat
She has a negligible smoking history
Pulmonary TB
not cancer because = age and non smoking history
Define sjogrens’ syndrome
• Characterised by inflammation and destruction of exocrine glands (usually salivary and lacrimal glands).
o NOTE: when associated with other autoimmune diseases, Sjogren’s syndrome is termed secondary
With which conditions is sjogren’s associated with
• Associated autoimmune diseases: o Rheumatoid arthritis o Scleroderma o SLE o Polymyositis o Organ-specific autoimmune diseases (e.g. PBC, autoimmune hepatitis, myasthenia gravis)
Explain the aetiology/risk factors of Sjogren’s syndrome
• UNKNOWN
• Genetic associations:
o HLAMB8
o HLAMDR3
Recognise the presenting symptoms of Sjogren’s syndrome
- Dry eyes (keratoconjunctivitis sicca) - they will be gritty and sore **
- Dry mouth - leads to secondary dysphagia **
- Fatigue
- Fever
- Weight loss
- Depression
- Dry upper airways - leads to a dry cough and recurrent sinusitis
- Dry skin or hair
- Dry vagina M-may cause dyspareunia
- Reduced GI mucus secretions leads to reflux oesophagitis, gastritis and constipation
Recognise the signs of Sjogren’s syndrome on physical examination
- Parotid or salivary gland enlargement
- Dry eyes
- Dry mouth or tongue
- Signs of associated conditions
Identify appropriate investigations for Sjogren’s syndrome
• Bloods
o High ESR
o High amylase (if salivary glands involved)
• Autoantibodies
o Rheumatoid factor *
o ANA *
o AntiMENA (extractable nuclear antigens)
• Schirmer’s Test *
o A strip of filter paper is placed under the eyelid
o Positive for Sjogren’s syndrome if < 10 mm of the strip is wet after 5 mins
• Fluorescein/Rose Bengal Stains
o May show punctate or filamentary keratitis
• Other Investigations
o Reduced parotid salivary flow rate
o Reduced uptake or clearance on isotope scan
• Biopsy - of salivary or labial glands
Define anaphylaxis
• Acute life-threatening multisystem syndrome caused by sudden release of mast cell and basophil-derived mediators into the circulation
What are the causes of anaphylaxis?
- Immunogenic - IgE-mediated* or immune complex/ complement-mediated
- Non-Immunogenic - mast cell or basophil degranulation WITHOUT the involvement of antibodies (e.g. reactions caused by vancomycin, codeine, ACE inhibitors)
What is the pathophysiology of anaphylaxis?
o Inflammatory mediators such as histamine are released leading to bronchospasm, increased capillary permeability and reduce vascular tone
o This leads to tissue oedema
What are common allergens of anaphylaxis?
• Common Allergens o Drugs (e.g. penicillin) o Latex o Peanuts o Shellfish
o NOTE: anaphylaxis can be caused by the repeat administration of blood products in a patient with selective IgA deficiency (due to the formation of antiMIgA antibodies)
Recognise the presenting symptoms of anaphylaxis
- Wheeze
- Shortness of breath and a sense of choking
- Swelling of lips and face
- Pruritus
- Rash
• NOTE: patients may have a history of other hypersensitivity reactions (e.g. asthma, allergic rhinitis)
Recognise the signs of anaphylaxis on physical examination
- Tachypnoea
- Wheeze *
- Cyanosis
- Swollen upper airways and eyes
- Rhinitis
- Conjunctival infection
- Urticarial rash
- Hypotension
- Tachycardia
Generate a management plan for anaphylaxis
- ABCDE
- High flow O2
- IM Adrenaline (NOT IV)
- Chlorpheniramine (antihistamine) **
- Hydrocortisone
- If continued respiratory deterioration, may require bronchodilator therapy
- Monitor pulse oximetry, ECG and BP
Define haemophilia
• Bleeding diatheses resulting from an inherited deficiency of a clotting factor
What are the 3 subtypes of haemophilia?
- Haemophilia A: MOST COMMON - deficiency in factor 8
- Haemophilia B: deficiency in factor 9
- Haemophilia C: RARE - deficiency in factor 11
Explain the aetiology/risk factors of haemophilia
- Haemophilia A and B have X-linked recessive inheritance
- 30% of cases are new mutations
- Due to its inheritance pattern, Haemophilia is mainly seen in MALES
Recognise the presenting symptoms of haemophilia
- Symptoms usually begin in early childhood
- Swollen painful joints occurring spontaneously or with minimal trauma (haemarthroses)
- Painful bleeding into muscles
- Haematuria
- Excessive bruising or bleeding after surgery or trauma
- FEMALE carriers are usually asymptomatic, but may experience excessive bleeding after trauma
–> Generally speaking, bleeding in haemophilia is DEEP (into muscles and joints)
Recognise the signs of haemophilia on physical examination
Recognise the signs of haemophilia on physical examination • Multiple bruises • Muscle haematomas • Haemarthroses (right) • Joint deformity • Nerve palsies (due to nerve compression by haematomas) • Signs of iron deficiency anaemia
Identify appropriate investigations for haemophilia
- Clotting screen (high APTT)
- Coagulation factor assays (low factor 8, 9 or 11 (depending on type of haemophilia))
- Other investigations may be performed if there are complications (e.g. arthroscopy)
Differences between UC and Crohns histollogically
Crohns
Transmural
Patchy
UC
Submucosa or mucosa
Cotinuous
What is the string sign of Kantor
On small bowel barium follow through in Crohn’s you get:
String sign of Kantor - part of the intestine looks like a piece of string, showing incomplete filling of the intestinal lumen.
Which disease has an leucoerythroblastic picture on blood film?
Haemolytic anemia
55yo woman presents with sob and weakness in her legs.
She has a 15pack year history and is diabetic
There is reduced air entry on the left lower lung zone
CXR shows a mass lesion on the left lower lobe
She has metabolic alkalosis on ABG
She is hypokalemic
What are you thinking
Firstly its very clear she has lung cancer
Due to metastatic disease she was derranged hormone levels.
This caused her to be hypokalemic
Hypokalemia is responsible for myopathy - weakness in her legs
Which cranial nerves will be affected by pathology in the cavernous sinus?
3,4,6 and opthalmic division of 5
75yo man presents with hisotry of episodes of congitive impairment.
Some days he is entirely normal though.
He claims to see faces
OE: slow tremor, rigif tone of arms
What are you thinking?
Lewy body dementia
The 2nd most common cause of dementia after alzheimers.
Classic: fluctuating pattern, hallucinations, tremors (Parkinsonian symptoms)
Upper respiratory infection in an HIV patient
Pneumocystitis
Define neurofibromatosis
• An autosomal dominant genetic disorder affecting cells of neural crest origin, resulting
in the development of multiple neurocutaneous tumours
Type 1 neurofibromatosis characteristics
- Peripheral and spinal neurofibromas
- Multiple café au lait spots
- Freckling (axillary/inguinal)
- Optic nerve glioma
- Lisch nodules (on iris)
- Skeletal deformities
- Phaeochromocytomas
- Renal artery stenosis
Type 2 neurofibromatosis characteristics
- Schwannomas (often bilateral vestibular schwannomas) • Meningiomas
- Gliomas
- Cataracts
Whats the cause of neurofibromatosis
• Associated with multiple mutations in tumour suppressor genes NF1 (type 1) and NF2 (type 2)
Recognise the presenting symptoms of type 1 neurofibromatosis
• Type 1
o Skin lesions
o Learning difficulties (40%)
o Headaches
o Disturbed vision (due to optic gliomas)
o Precocious puberty (due to lesions of the pituitary gland from an optic glioma involving the chiasm)
• Positive family history (however, 50% are caused by new mutations)
Recognise the presenting symptoms of typ 2 neurofibromatosis
• Type 2 o Hearing loss o Tinnitus o Balance problems o Headache o Facial pain o Facial numbness
Recognise the signs of type 1 neurofibromatosis on physical examination
o 5+ café au lait macules of > 5 mm (prepubertal)
o 5+ café au lait macules of > 15 mm (post-pubertal)
o Neurofibromas (may appear as cutaneous nodules or complex plexiform neuromas)
o Freckling in armpit or groin
o Lisch nodules (hamartomas on the iris)
o Spinal scoliosis
Recognise the signs of type 2 neurofibromatosis on physical examination
o Few or no skin lesions
o Sensorineural deafness with facial nerve palsy or cerebellar signs (if the schwannoma is large)
What characteristic is suggestive of malignant melanoma in a newly appeared pigmented skin lesion which is raised
Irregular pigment network
Other characteristics: • A - asymmetry • B - border irregularity • C - colour variation • D - diameter > 6 mm • E - elevation/evolution
What’s the best prognostic indicator of malignant melanoma - following excision
Invasive depth of the lesion
What is CURB65 score used for?
COMMUNITY ACQUIRED pneumonia
Cutaneous feature of meningitis
Non blanching purpuric rash
What disgnostic tests are required for COPD?
Spirometry !! to get fev1 and fvc
and pulmonary function tests
46yo female comes to a&e with reduced consciousness. Blood glucose =9
She is hypothermic - 33 C
She has non-pitting oedema on the skin of her hands feet and eyelids
She has a thyroidectomy scar on her neck
What are you thinking
Myxoedema coma
Severe hypothyroidism
You would usually present this in an elderly pt
What are the symptoms of myxoedema comma
o Hypothermia o Hypoventilation o Hyponatraemia o Heart failure o Confusion o Coma / Decreased consciousness
How does non-pitting oedema present
Some people with severe or advanced hypothyroidism develop a condition called myxedema.
It tends to cause swollen legs and feet, but it can also cause swollen eyelids and lips.*
In some cases, it can also cause tongue swelling.
This causes non-pitting oedema
Whats the mx of myxoedema coma
o Oxygen o Rewarming o Rehydration o IV T4/T3 * o IV hydrocortisone o Treat underlying cause (e.g. infection)
Is HbA1C a diagnostic test for diabetes?
No
It’s rather a measure of glycaemic control further down the line - to monitor management.
Diagnostic tests are:
For symptomatic pts: fasting glucose of >7 or random glucose of >11
For asymptomatic pts: 2 samples needed
Urine should be tested for glucose and ketones (glycosuria ketonuria)
OGTT
When is OGTT indicated for diagnosis of diabetes?
When fasting glucose is just within the limits 6.1-6.9
When random glucose is just within the limits 7.8-11.0
Complications of MI
DARTH VADER o Death o Arrhythmias o Rupture o Tamponade o Heart failure o Valve disease o Aneurysm o Dressler's syndrome o Embolism
Acute coronary syndrome mx
MONABASH • Morphine • Oxygen • Nitrates • Anticoagulants (aspirin + clopidogrel) • Beta-blockers • ACE inhibitors • Statins • Heparin
Whats the mx for Unstable Angina / NSTEMI
o Admit to coronary care unit
o OXYGEN
o IV access, monitor vital signs and serial ECG
o GTN infusion
o MORPHINE
o Metoclopramide (to counteract the nausea caused by morphine)
o ASPIRING (300 mg initially, followed by 75 mg indefinitely)
o CLOPIDOGREL (300 mg initially, followed by 75 mg for at least 1 year if troponin positive or high risk)
o LMWH (e.g. enoxaparin)
o BETA-BLOCKER (e.g. metoprolol)
o Glucose-insulin infusion if blood glucose > 11 mmol/L
o GlpIIb/IIIa inhibitors may also be considered (e.g. tirofiban) in patients:
• Undergoing PCI
• At high risk of further cardiac events
o If little improvement, consider urgent angiography with/without revascularisation
When are b-blockers contraindicated?
- Acute heart failure
- Cardiogenic shock
- Bradycardia
- Heart block
- Asthma
Mx of stable angina - chronic mx
CONSERVATIVE:
Minimise cardiac risk factors (e.g. blood pressure, hyperlipidaemia, diabetes)
MEDICAL:
o All patients should receive ASPIRIN 75 mg/day unless contraindicated
o Immediate symptom relief - GTN SPRAY
o Long-term management:
• Beta-blockers
• Calcium channel blockers
• Nitrates
INVASIVE PROCEDURES:
o Percutaneous coronary intervention (PCI)
- Performed in patients with stable angina despite maximal tolerable medical therapy
o Coronary artery bypass graft (CABG)
- Occurs in more severe cases (e.g. three-vessel disease)
What are the side effects of methotrexate?
Liver cirrhosis - monitor LFT’s
Macrocytic anemia - becase its a dihydrofolate reductase inhibitor
Aplastic anemia
Pulmonary fibrosis - baseline CXR to monitor since start of treatment.
Neutropenia
Myelosupression
It shouldn’t be used with alcohol - can worsten liver cirrhosis risk
Shouldn’t be taken during pregnancy - blocks the action of folate (neural tube defects)
Where is methotrexate used?
Crohn’s
Rheumatoid arthritis
Polymyalgia rheumatica
Which is the most common histological type of lung cancer
Squamous cell carcinoma
What is a common associated symptom with squamous cell lung carcinoma
Hypercalcaemia
Because the carcinoma stimulates the secretion of parathyroid like peptides which vause a rise in blood ca levels
Which nerve is compressed in carpal tunnel syndrome
Median nerve
Whats the cause of carpal tunnel syndrome?
Usually IDIOPATHIC
May be SECONDARY to:
o Tenosynovitis (e.g. in rheumatoid arthritis)
o Infiltrative diseases of the canal/increased soft tissue (e.g. amyloidosis, acromegaly)
o Bone involvement in the wrist (e.g. osteoarthritis, fracture)
o Fluid retention states (e.g. pregnancy, nephrotic syndrome)
o Other (e.g. obesity , menopause, diabetes*)
Recognise the presenting symptoms of carpal tunnel syndrome
• Tingling and pain in the hand and fingers
• Weakness and clumsiness of the hand
UNILATERAL !!!!
Recognise the signs of carpal tunnel syndrome on physical examination
- Sensory impairment in the median nerve distribution
- Weakness and wasting of thenar eminence (below the thumb)
- Tinel’s Sign - tapping the carpal tunnel causes symptoms
- Phalen’s Test - flexion of the wrist for 1 min may cause symptoms
• Look out for signs of the underlying cause (e.g. acromegaly, hypothyroidism)
Recognise the signs of rheumatoid arthritis on physical examination - Early signs
• Arthritis - most common in the HANDS
EARLY SIGNS: o Spindling of fingers o Swelling of MCP and PIP joints o Warm, tender joints o Reduction in range of movement
Recognise the signs of rheumatoid arthritis on physical examination - Late signs
LATE SIGNS:
o Symmetrical deforming arthropathy
o Ulnar deviation of fingers as a result of subluxation (partial dislocation) of the MCP joints
o Radial deviation of the wrist
o Swan neck deformity
o Boutonniere deformity
o Z deformity of the thumb
o Trigger finger (inability to straighten the finger, tendon nodule palpable)
o Tendon rupture
o Wasting of small muscles of the hand
o Palmar erythema
• Rheumatoid Nodules (right) - firm subcutaneous
nodules (usually found on the elbows, ulnar margin,
palms and over extensor tendons)
• Signs of complications
Identify appropriate investigations for rheumatoid arthritis
• Bloods
o FBC - low Hb, high platelets
o High ESR and CRP *
o Rheumatoid factor * (found in 70% of RhA patients)
• The presence of rheumatoid factor is associated with rheumatoid nodules and extra-articular manifestations
o Antinuclear antibodies (30%)
• Joint Aspiration
o May be performed in the acute setting to rule out septic arthritis
• Joint X-Ray
What do you expect to see on the joint xray of rheumatoid arthritis
o Deformity
o Osteopaenia
o Narrowing of joint space
o Soft tissue swelling
Define MODS
• A clinical syndrome characterised by the development of progressive and potentially reversible physiologic dysfunction of 2 or more organs or organ systems that is induced by a variety of insults, including sepsis.
• MODS is the final stage in a continuum beginning with SIRS + infection:
o SIRS + infection –> sepsis –> severe sepsis –> MODS
What is SIRS
Systemic Inflammatory Response Syndrome
What is the triad for nephrotic syndrome
Proteinuria (> 3 g/24 hr)
Hypoalbuminaemia (<30g/L)
Oedema
Hypercholesterolaemia is also a common feature
Risk factors for nephrotic syndrome
Most commonly caused by: minimal change glomerulonephritis in children
However, ALL forms of glomerulonephritis can cause nephrotic syndrome
Other causes: Diabetes mellitus Sickle cell disease Amyloidosis Malignancies (lung and GI adenocarcinomas) Drugs (e.g. NSAIDs) Alport's syndrome HIV
Recognise the signs of nephrotic syndrome on physical examination
Oedema: periorbital*, peripheral, genital
Ascites: fluid thrill, shifting
