Odds and Odds ratio

Odds = Number : total - number

Odds ratio = ratio of odds.

Haemorrhoids

Haemorrhoidal tissue is part of the normal anatomy which contributes to anal continence. These mucosal vascular cushions are found in the 3,7,11 positions. Haemorrhoids are said to exist when they become large, congested, and symptomatic.

Clinical features:

Painless rectal bleeding is the most common symptom
Pruritus
Pain: usually not significant unless piles are thrombosed
Soiling may occur with third or fourth degree piles


Types of haemorrhoids (EXTERNAL and INTERNAL)

External: Originate below the dentate line, prone to thrombosis, and may be painful

Internal: Originate above the dentate line, do not generally cause pain

Grading: 1 - does not prolapse. 2 - prolapses but reduces. 3 - remains out but manually replaceable. 4 - can't even manually put it back

Management: Soften stools - increase dietary fibre and increase fluid intake. Topical local anaesthetics and steroids may be used to help symptoms. Outpatient treatments: rubber band ligation superior to injection sclerotherapy. Surgery is reserved for large symptomatic haemorrhoids which do not respond to outpatient treatments. Newer treatments: Doppler guided haemorrhoidal artery ligation, stapled haemorrhoidopexy

Acutely thrombosed external haemorrhoids: typically present with significant pain, examination reveals purplish, oedematous, tender subcutaneous perianal mass. If patient presents within 72 hours then referral should be considered for excision. Otherwise, patients can be managed with stool softeners, ice packs, and analgesia. Symptoms usually settle within 10 days.

Gastric Adenocarcinoma

Epigastric pain is non-specific symptoms of upper-gastrointestinal pathology, but weight loss and anorexia are more sinister, with anaemia implying chronic gastrointestinal bleeding. The endoscopic appearance of a thickened rigid gastric wall suggests 'linitis plastica' (leather bottle stomach), a term used for gastric adenocarcinoma that diffusely infiltrates all layers of the gastric wall. The findings of numerous signet ring cells on biopsy confirms poorly differentiated (or diffuse) adenocarcinoma.

Patent ductus arteriosus

Overview

Acyanotic congenital heart defect, with a connection between the pulmonary trunk and descending aorta. More common in premature babies, born at high altitude or maternal rubella infection in the first trimester.

Features

Left subclavicular thrill
Continuous 'machinery' murmur
Large volume, bounding, collapsing pulse
Wide pulse pressure
Heaving apex beat

Management

Indomethacin closes the connection in the majority of cases. If associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful in keeping the duct open until after surgical repair.

Ankylosing spondylitis

Ankylosing spondylitis is a HLA-B27 associated spondyloarthropathy. It typically presents in males (sex ratio 5:1) aged 20-30 years old.

Features:

Young man with lower back pain and stiffness of insidious onset
Stiffness usually worse in the morning and improves with exercise
The patient may experience pain at night which improves on getting up

Clinical examination

Reduced lateral flexion
Reduced forward flexion - Schober's test - a line drawn 10cm above and 5cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5cm when the patient bends as far forward as possible
Reduced chest expansion


Other features

Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis
Cauda equina syndrome
Peripheral arthritis (25%, more common if female)

Drugs - taking a drug history

Ask about each individual substance

• Quantity
• Frequency
• Pattern of usage
• Age of onset when taking drugs
• When was the most recent use
• Method of administration
• Money spent on drugs
• Risky behaviours
• TOLERANCE
• DEPENDANCE
• WITHDRAWAL
• Motivation to quit
• Physical problems: cellulitis, hepatitis, aneurysms, abscesses, infection, other drug related medical issues
• Trigger factors to use drugs
• Understanding and insight

Clinical features of drug use:
Opiates - pinpoint pupils, low BP, venepuncture marks
Benzodiazepines - disinhibited or gives the impression of intoxicated, but is not drunk
Psychostimulants - rapid speech, large pupils, agitation, restlessness, high BP

Subarachnoid Haemorrhage - SAH

Sudden onset headache at back of head

Due to:
Rupture of aneurysm, AV malformation, maybe trauma but not true

8/100000

Atherosclerotic risk factors

Signs and symptoms

Headache
Neck stiffness - Kernig's sign - chemical meningitis
Impaired consciousness
Cranial nerve signs
Hemiplegia
Sentinel headache - before actual headache


Grade 1-5
5 = 100% (prolonged coma)
1 = 0% (no signs)

Prognosis
Overall mortality 35-50%, most die within 1 month
Worse with aneurysm better with AV malformation
Rebleeding very common


Investigations

CT
Lumbar puncture for blood and xanthochromia (yellow CSF)


Treatment - Coiling > clipping

Subdural haemorrhage

Between arachnoid and dura mater
Acute, chronic, acute on chronic.

After trauma. Usually venous bleed


Elderly
Hypertension
Falls
Anticoagulant therapy



TRAUMA
INCREASED ICP
BRAIN METS


Elderly patients at risk due to shrinkage of brain with age as a result of atherosclerosis.
DAMAGE to bridging veins


Symptoms

Drowsiness
Consciousness
Personality change

Other signs

Increased ICP
Seizures

Late signs

ONSET OF INJURY TO TIME OF FOCAL SYMPTOMS IS 63 days!!!


Investigations
CT/MRI
Hypodense chronic bleed, Hyperdense acute bleed

Differential

Stroke
Dementia
Mass lesion

Treatment

Irrigation/evacuation/Burr hole craniostomy - via a burr twist drill. Basically a hole is drilled into the skull
Craniotomy - flap of bone cut and temproarily left open to relieve high ICP. Used less often than burr hole.
Try to find cause of trauma - e.g. cause of falls, cataracts

Neurofibromatosis

Two types. 1 and 2
SPONTANEOUS and AUTOSOMAL DOMINANT

Type 1

von Recklinghausen's disease
Much more common than type 2 - accounts for 90% of cases

Autosomal dominant
Chromosome17
1 in 2500
M:F 1:1


Diagnosis

Cafe-au-lait spots
Neurofibromas
Freckling
Optic glioma
Lisch nodules (on iris)
Bone lesions
1st degree relative with NF1

Complications

Learning disability
Mass effect of neurofibromas

Nerve compression
Gut obstruction
Hypertension - renal artery stenosis
Malignancy
Epilepsy

MRI can show changes


Management: Treat annoying lesions only. Genetic counselling


Type 2 neurofibromas

Genetics

Autosomal dominant
Gene on chromosome 22

Epidemiology and aetiology
Much more rare than NF1: affects 1 in 35000 individuals

Diagnosis

Bilateral vestibular schwannoma
Relative and has unilateral vestibular schwannoma or neurofibroma, meningioma, glioma, schwannoma, juvenile cataract


Management

No cure
Annual hearing tests
Surgery to remove schwannomas

Sleep apnoea

Sleep apnoea is a physical condition in which the upper respiratory tract becomes partially occluded during sleep. This can cause transient cessation in breathing, which causes the patient to wake repeatedly during the night, reducing the quality of sleep. Sleep apnoea results in daytime tiredness. It is more common in overweight males who snore. Treatment is by continuous positive airway pressure (CPAP) via facemask during sleep. 

Narcolepsy

Narcolepsy forms a part of the differential diagnosis. It is less common than somnambulism, affecting <0.1% of the population. It is a neurological condition caused by a loss of inhibition of rapid eye movement (REM) sleep. It has four main features: irresistible attacks of sleep at inappropriate times, cataplexy (sudden loss of muscle tone when intense emotion occurs, leading to collapse), hypnogogic/ hypnopompic hallucinations (hallucinations that occur on falling asleep and waking respectively) and sleep paralysis. Not all cases of narcolepsy have all four features. When forming a diagnosis, factors that point to hypersomnia are sleeps that have a gradual onset, are worse in the mornings and rarely occur in unusual places. Factors that suggest narcolepsy are a short duration of sleep (10-20 minutes), the inability to control sleep attacks and interrupted night-time sleep, as well as the four main features. Management falls under the remit of neurologists

Overvalued idea and Delusion

Delusion

A delusion is a belief held with absolute conviction, such that it is not changeable, even by compelling counterargument or proof to the contrary. A primary delusion has no obvious cause considering the patient's circumstances. Secondary delusions are more closely linked with the rest of the clinical picture; for example, grandiose delusions (the belief of inflated self-worth) are common in mania, and a persecutory delusion may be seen in paranoid schizophrenia. A bizarre delusion is one that would be seen as totally implausible within the patient's culture.


Overvalued idea

An overvalued idea is an unreasonable, sustained, intense preoccupation that is maintained with less than delusional intensity, i.e. the patient may accept that it might not be true. An obsession is a repetitive senseless thought that is recognised as irrational but is unsuccessfully resisted by the person. The motor equivalent of an obsessional thought is a compulsion - a repetitive, stereotyped, seemingly purposeful behaviour that is not actually useful and is recognised as such by the patient. Ideas of reference are thoughts that the events or objects in one's immediate environment have a particular or unusual significance. Monomania is a pathological preoccupation with a single subject, and egomania is a pathological preoccupation with oneself.

Quinsy

Quinsy (peritonsillar abscess) is a collection of pus outside the tonsil usually seen in older children as a complication of tonsillitis. Affected patients are unwell and may develop severe dysphagia, earache and trismus (lockjaw). As you inspect the pharynx, there will be a unilateral bulge of the soft palate, with deviation of the uvula to the opposite side. The tonsils will be inflammaed and there is associated halitosis. Rupture of the abscess can result in aspiration pneumonia. Treatment is with penicillin. There may be as many as five organisms in the pus found in the abscess. Six weeks after quinsy, it is conventional to perform tonsillectomy.

Itching during pregnancy

Pruritus in pregnancy is common (around 20% of pregnancies), but the prevalence of itching due to abnormal liver function tests (LFTs) is less than 1%. In obstetric cholestasis, bile acids accumulate in the blood, causing jaundice and pruritus. There is a 90% recurrence rate in pregnancy, and 35% have a positive family history. Itching typically involves the palms and soles, but can affect the whole body. It is important to rule out other causes of jaundice and pruritus, including hepatitis and gallstones. Screening blood tests include LFTs, bile acids, clotting screen, anti-smooth muscle antibody, anti-mitochondrial antibody and viral serology (hepatitis virus, Epstein-Barr virus and cytomegalovirus). In obstetric cholestasis, transaminases, bile acids, alkaline phosphatase and bilirubin may all be raised.

Treatment includes chlorphenamine (an antihistamine) for pruritus and topical emollients. The lack of bile salts in the gut results in malabsorption of fat-soluble vitamins, including vitamin K, increasing the risk of postpartum haemorrhage and fetal intracranial bleeds. Oral vitamin K supplements are therefore required. Ursodeoxycholic acid, although not licenced for use in pregnancy, has been found to reduce accumulation of bile acids and relieves pruritus. It is important to treat obstetric cholestasis, as there is a risk of premature birth (60%), fetal distress (30%) and intrauterine death by acute anoxia.

Transposition of the great arteries

The great vessels are reversed (transposed), with the aorta coming off the right ventricle and the pulmonary artery off the left ventricle. Affected children are therefore dependent on the ductus arteriosus (duct-dependent) to supply oxygenated blood to the systemic circulation. As the duct closes after birth, the baby will become profoundly cyanotic and acidotic. Chest X-ray shows a characteristic narrow mediastinum with an 'egg-on-side' appearance of the heart shadow. The switch operation is required as definitive management.

Bulimia nervosa

A diagnosis of bulimia nervosa requires all three of the following:

• Binge eating
• Methods to prevent gaining weight (e.g. vomiting, purging, laxatives, etc.)
• Morbid dread of fatness (overvalued idea, not a delusion)

The incidence of bulimia is 12 per 100000, with females being affected 10 times more commonly than males. Individuals tend to be of a normal or above-normal weight. Complications are caused by starvation and vomiting, and include hypokalaemia, dehydration, enlargement of the parotid glands, dental caries, Mallory-Weiss tear, osteoporosis and Russel's sign (thick skin on the dorsum of the hands due to repeated induced vomiting by stimulating the gag reflex with the fingers). Treatment is similar to that of anorexia, but selective serotonin reuptake inhibitors may improve bingeing behaviour. Seventy percent of cases recover within 5 years and there is no increase in mortality.

Second degree heart block - Mobitz type 2

Most beats are conducted with a constant PR interval. Occasionally there is an atrial contraction without a subsequent ventricular contraction, i.e. there is intermittent blocking of conduction either through the AV node or, more commonly, the His-Purkinje system. Disease of the His-Purkinje system is most often associated with a prolonged QRS duration.


Features of this ECG:

• Sinus rhythm, 90 b.p.m., normal QRS axis
• Features of Mobitz type 2 AV block:
• The PR interval is constant
• The first and seventh P waves on the rhythm strip are not followed by a QRS complex

• Features of left ventricular hypertrophy:
• SV2 + RV5 > 35mm
• Widespread ST depression and T wave inversion

Clinical note:

• Permanent pacemaker inserted.

• Unlike Wenckebach, Mobitz type 2 is usually due to disease of His bundle rather than the AV node and if it progresses to CHB the escape rhythm tends to be slow with wide QRS complexes

Common causes of Mobitz type 2 AV block

• Degenerative disease of the conducting system
• Anteroseptal infarction

Left bundle branch block (LBBB)

• QRS duration of 120 ms (3 small squares) or more
• No secondary R wave in lead V1
• No Q waves in the lateral leads (V5-6, I and aVL)
• Secondary ST-T changes:
• ST segment changes, opposite to the dominant (terminal) QRS component
• T wave changes in the same direction as the ST segments
• These changes can mask the primary changes of acute myocardial infarction

Features of this ECG

• Sinus rhythm, 66 b.p.m.
• Diagnostic features of LBBB:
• Broad QRS, 135 ms
• No secondary R wave in V1
• No Q waves in the lateral leads

• Other features of LBBB:
• ST elevation in leads V1-V4
• T wave inversion leads I and aVL

• Left axis deviation -30 degrees

Causes of LBBB, left anterior or posterior hemiblock

• Ischaemic heart disease
• Hypertension
• Fibrotic degeneration
• Calcific aortic stenosis
• Congestive or hypertrophic cardiomyopathy
• Congenital heart disease
• Following cardiac surgery

LBBB itself does not cause a change of QRS axis. LBBB with left axis deviation implies more extensive conduction system disease involving the main bundle proximally and the left anterior fascicle distally. It therefore carries a poorer long-term prognosis.

Right bundle branch block (RBBB)

• QRS duration of 120 ms (3 small squares) or more
• Secondary R wave (R') in lead V1
• Other features:
• Slurring of S wave in the lateral leads V4-6, I, and AVL
• The T wave tends to be opposite of the terminal QRS component i.e. T wave inversion in the septal leads (V1-3) may be seen

Features of this ECG

• Sinus tachycardia, 114 b.p.m. normal QRS axis
• Diagnostic features of RBBB:
• Broad QRS, 145 ms
• Secondary R wave in V1, rSR' pattern

• Other features of RBBB:
• T wave inversion
• Slurred S wave

• Terminal negative component of P wave in lead V1
• Possible left atrial abnormality

Causes of right bundle branch block

• May occur in the absence of heart disease
• Fibrotic degeneration
• Ischaemic heart disease
• Hypertension
• Cardiomyopathy
• Congenital heart disease
• Atrial septal defect
• Fallot's tetralogy

• Acute, massive, pulmonary embolus

Ventricular flutter

This is another form of VT which is characteristic for its rate and appearance

• Very rapid, regular, wide complex tachycardia
• Rate 300 b.p.m. or more
• Sine wave morphology
• No distinction between QRS and T wave

Features of this ECG

• Ventricular flutter, rate 300-340 b.p.m. left axis deviation
• Characteristic morphology
• Sine wave
• No distinction between QRS and T wave
• It is unclear where one complex finishes and the other starts
• It looks the same if viewed upside down

Clinical note

• Ventricular flutter is usually short lived, associated with a marked fall in blood pressure and progresses to ventricular fibrillation
• This man was started on amiodarone

Anorexia nervosa

A diagnosis of anorexia nervosa requires all four of the following:

• Body weight 15% below expected, or body mass index <17.5 kg/m^2
• Self-induced weight loss (by dieting, exercising, vomiting, etc.)
• Morbid fear of being fat (an overvalued idea rather than a delusion)
• Endocrine disturbance (e.g. amenorrhoea, pubertal delay or lanugo hair)

The incidence of anorexia is 4 per 100000, with a peak at age 18 years. Around 10% of cases of anorexia occur in males. Risk factors include being Caucasian, high social class, academic prowess, and interests such as ballet or modelling. Other common features are anaemia, expressing a high interest in preparing or buying food, feeling tired and cold, bradycardia, and hypotension. Treatment options include cognitive-behavioural therapy/supportive therapy and raising calorie intake. Hospitalisation is indicated if there is a weight loss of over 35%. Around 50% of people with anorexia nervosa eventually recover completely. The mortality rate is 5%, usually from starvation or suicide.

An = without

Orexe = appetite.

Cachexia or wasting syndrome is loss of weight, muscle atrophy, fatigue, weakness, and significant loss of appetite in someone who is not actively trying to lose weight.

Cushing's Syndrome

Pituitary cause = Cushing's Disease
Cushing's disease = everything

Cushing's syndrome is caused by prolonged exposure to elevated levels of

• Endogenous glucocorticoids
• Exogenous glucocorticoids

 The degree of cortisol is very variable. When presentation is florid, diagnosis is usually straightforward. May be subtle however and combination of nonspecific clinical manifestations and variable cyclical biochemical parameters often make diagnosis difficult.
Early diagnosis and prompt treatment are essential.


Causes

• Adrenocorticotropic hormone dependent causes
• Excessive ACTH from the pituitary (Cushing's disease)
• Ectopic ACTH producing tumours
• Excess ACTH administration
• Non-ACTH dependent causes
• Adrenal adenomas
• Adrenal carcinomas
• Excess glucocorticoid administration

Epidemiology

•  Incidence of Cushing's is 10 to 15 people per million increases with
• Diabetes
• Obesity
• Hypertension
• Osteoporosis

Risk factors

• Cushing's syndrome due to an adrenal or pituitary tumour is more common in females (5:1)
• Peak incidence 25-40 years
• Ectopic ACTH production is due to lung cancer

Common causes

•  The most common cause of Cushing's syndrome is the use of exogenous glucocorticoids. Endogenous Cushing's syndrome is divided into corticotropin-dependent and corticotropin-independent causes:
• Corticotropin-dependent causes account for about 80-85% of cases
• Pituitary adenomas (Cushing's disease)
• Small cell carcinoma and other endocrine tumour
• Corticotropin-independent Cushing's syndrome
• Adrenal adenoma and adrenal carcinoma
• McCune-Albright syndrome (polycystic fibrous dysplasia and cafe au lait spot pigmentation with autonomous endocrine hyperfunction) and primary pigmented nodular adrenal disease and macronodular adrenal hyperplasia

Presentation

• Truncal obesity, supraclavicular fat pads, buffalo hump, weight gain
• Facial fullness, moon facies, facial plethora
• Proximal muscle wasting and weakness
• Diabetes or impaired glucose tolerance
• Gonadal dysfunction, reduced libido
• Hypertension
• Nephrolithiasis
• Skin: skin atrophy, purple striae, easy bruising, hirsuitism, acne: pigmentation occurs with ACTH dependent causes
• Psychological problems: depression, cognitive dysfunction, and emotional lability
• Osteopenia and osteoporosis
• Oedema
• Woman may complain of irregular menses
• Thirst, polydipsia, polyuria
• Impaired immune function: increased infections, difficulty with wound healing
• Child: growth restriction
• Patients with an ACTH producing pituitary tumour may develop headaches, visual problems and galactorrhoea
• Destruction of the anterior pituitary may cause hypothyroidism and amenorrhoea

Differential diagnosis

• Pseudo-Cushing's syndrome: all or some of the clinical features of Cushing's syndrome combined with biochemical evidence of hypercortisolism (but not caused by pituitary adrenal axis problems)
• Chronic severe anxiety and/or depression
• Prolonged excess alcohol consumption, which can cause a cushingoid appearance
• Obesity
• Poorly controlled diabetes
• HIV infection

Investigations

• During referral
• Not when there is intercurrent illness

Confirm presence of disease

• 24 hour urinary free cortisol
• 1mg overnight dexamethasone suppression test
• late-night salivary cortisol
• Midnight cortisol levels
• CRH test

Identify cause

• Plasma ACTH
• High-dose dexamethasone suppression test
• Inferior petrosal sinus sampling (IPS)
• MRI of pituitary
• Chest and abdominal CT scans
• Plasma CRH

Treatment

• Drugs
• Metyrapone
• Ketaconazole
• Mitotane
• Surgery
• Trans-sphenoidal microsurgery
• Radiotherapy
• For tumour in pituitary

Complications

• Metabolic syndrome
• Hypertension
• Impaired glucose tolerance and diabetes
• Obesity
• Hyperlipidaemia: raised LDL, cholesterol and triglycerides
• Coagulopathy: thrombophilia
• Osteoporosis
• Perforated viscera
• Impaired immunity, including opportunistic fungal infections
• Nelson's syndrome, which may follow bilateral adrenalectomy for Cushing's disease
• A primary pituitary tumour, which may cause panhypopituitarism and visual loss

Prognosis

• 5x more mortality
• Vascular disease and diabetes (with complications of diabetes including infections) killing them
• Usual course is chronic, with cyclic exacerbations and rare remissions
• Better prognosis with surgery
• Adrenocortical carcinomas have 5 year survival rate of 30% or less

Renal replacement therapy and transplantation

Renal replacement therapy has a vital role in the treatment of

• ACUTE (AKI: acute kidney injury)
• CHRONIC (end-stage renal disease)

Most patients with chronic kidney disease stage 4-5 (estimated GFR <30ml/min/1.72 m^2) or with CKD stage 3 and rapidly deteriorating renal function should be referred for assessment by nephrologist.

Should be referred at least a year in advance

Three ways to deal with it

• Conservative care and symptom control
• Dialysis
• Renal transplant

Conservative care

• Erythropoietin
• Vitamin D analogues
• Dietary control
• Antipruritics
• Antiemetics
• STILL need MDT
• Patients are more comfortable and more likely to die at home

Dialysis

• Malnourished without this
• Peritoneal or haemodialysis
• Good for young, bad for old

• In AKI, if:
• Uraemia (pericarditis, gastritis, hypothermia, fits or encephalopathy)
• Pulmonary oedema
• Severe hyperkalaemia
• Hypo and hypernatraemia
• pH very acidic (below 7.0)
• Severe renal failure urea greater than 30mmol/L and creatinine greater than 500micromol/L
• Toxicity with drugs that can be dialysed

• Haemodialysis complications
• Access-related: local infection, endocarditis, osteomyelitis, creation of stenosis, thrombosis or aneurysm
• Hypotension (common), cardiac arrhythmias, air embolism
• Nausea and vomiting, headache, and cramps
• Fever: Infected central lines
• Dialyser reactions: anaphylactic reaction to sterilising agents
• Heparin-induced thrombocytopenia, haemolysis
• Disequilibrium syndrome: restlessness, headache, tremors, fits, and coma
• Depression

• Peritoneal dialysis contraindications and complications 

• Contraindications
• Intra-abdominal adhesions and abdominal wall stoma
• Obesity, intestinal disease, respiratory disease and hernias are relative contra-indications

• Complications of peritoneal dialysis
• Peritonitis
• Sclerosing peritonitis
• Catheter problems: infections, blockage, kinking, leaks, or slow drainage
• Constipation, fluid retension, hyperglycaemia, weight gain
• Hernias (incisional, inguinal umbilical)
• Back pain
• Malnutrition 
• Depression

Transplantation

• Best long-term outcome for patients with end-stage renal disease
• Cadaveric or living
• All patients with end-stage renal disease should be considered for a transplant
• Patients followed up
• Cancer
• Drug toxicity
• Cardiovascular disease

Complications of transplantation and subsequent immunosuppression

• Postoperative problems - e.g. deep vein thrombosis, pulmonary embolism and pneumonia
• Opportunistic infections: viral (particularly herpes simplex in the first four weeks and then cytomegalovirus (CMV) later), fungal and bacterial
• Malignancies (especially lymphomas and skin cancers)
• Drug toxicity, bone marrow suppression
• Recurrence of the original disease in the transplant
• Urinary tract obstruction
• Cardiovascular disease, hypertension, dyslipidaemia
• Graft rejection:
• Hyperacute: occurs within minutes of insertion. Is now rare due to more accurate cross-matching. Requires removal of graft.
• Accelerated: aggressive mainly T-cell mediated crisis can occur within a few days in patients previously sensitised. Presents with fever, swollen transplanted kidney and rapidly increasing serum creatinine. Can be salvaged with high-dose steroids plus antilymphocyte antibiotics but long-term survival is affected
• Acute cellular: occurs in around 25% of patients usually in 1-3 weeks but can occur up to 12 weeks. Clinical signs are fluid retention, rising blood pressure and rapid increase in creatinine. Treatment is with intravenous steroids after diagnosis by biopsy. Latest induction regimens can reduce incidence of acute rejection to 10%
• Chronic: presents with a gradual rise in serum creatinine and proteinuria, resistant hypertension. Graft biopsy shows vascular changes, fibrosis, and tubular atrophy. It is not responsive to increasing immunosuppression therapy

Prognosis

• The outcome of renal transplantation has steadily improved. 1 year and 10 year graft survival rates are 89% and 67% for adult kidneys from 'brain death donors' and 96% and 78% for kidneys from live donors. Survival of the transplant recipient at 10 year for cadaveric and live donor transplants in 71% and 89% respectively
• Acute rejection and early graft loss are becoming increasing less common
• Cadaveric donor renal transplantation, more human leukocyte antigen (HLA) mismatches, increasing donor age, cold ischaemia time greater than 24 hours, and a history of diabetic nephropathy all increase the risk of graft failure, return to dialysis and death

Acromegaly

Growth hormone stimulates the production of insulin-like growth factor-1 (IGF-1), which is produced in the liver and many other tissues. IGF-1 is the main mediator of the actions of growth hormone.

• Acromegaly is caused by excessive secretion of growth hormone from
• Pituitary macroadenoma
• Pituitary microadenoma
• Growth Hormone-Releasing Hormone (GHRH) from
• Hypothalamic tumours
• Non-endocrine tumours
• Lung
• Pancreas
• Thyroid (medullary)
• Carcinoid

Acromegaly causes an overgrowth of all organ systems, bones, joints, and soft tissues

Incidence

• 3-4 per million subjects per year
• 40-45 age range

Presentation

• Local effects of the tumour
• Headaches
• Bitemporal hemianopia
• Hypopituitarism
• Excess GH
• ENLARGEMENT - Gradual change of appearance due to the effects on cartilage and soft tissues: enlargement of hands and feet (increase in ring and shoe size), frontal bossing, thickening of the nose, enlarged tongue (macroglossia), growth of the jaw (prognathism), and coarsening of facial features
• OBSTRUCTIVE SLEEP APNOEA - Macroglossia may cause obstructive sleep apnoea
• EXCESSIVE SWEATING/HIRSUITISM - Excessive sweating and oily skin, with development of skin tags. Women may have slight hirsuitism
• OSTEOARTHRITIS - Articular overgrowth of synovial tissue and arthropathy leading to arthritis (widespread osteoarthritis of the weight-bearing joints), back pain and kyphosis
• VISCERAL HYPERTROPHY - Heart, liver, thyroid (with multinodular goitre), prostate and kidneys
• NERVE COMPRESSION SYMPTOMS - Carpal tunnel syndrome
• CARDIAC FEATURES - Hypertension, left ventricular hypertrophy, cardiomyopathy and arrhythmias
• Hyperprolactinaemia
• Amenorrhoea
• Galactorrhoea

Complications

• Ischaemic heart disease, cardiac failure and cerebrovascular disease
• Diabetes
• Acromegalic arthropathy, affecting both appendicular and axial skeleton
• Obstructive sleep apnoea
• Increased incidence of colonic polyps and adenocarcinoma of the colon
• Hypopituitarism after surgery
• Hyperprolactinaemia - mass effect causing deficiencies in glucocorticoids
• Gestational diabetes and gravid hypertension in pregnant women

Investigations

• Visual field defects
• Blood glucose, serum phosphate, urinary calcium and serum triglycerides may be raised
• Assessment of growth hormone
• Random growth hormone
• Glucose tolerance test (glucose normally inhibits GH)
• IGF-1
• IGF binding-protein 3
• GHRH concentration
• Assessment of other pituitary hormones
• MRI for pituitary
• CT for distant tumours secreting GH
• OctreoScan(R) (somatostatin) to aid localisation of the tumour
• Cardiac assessment: Electrocardiogram and echocardiogram
• Screen for colorectal cancer

Differentials

• Pseudo-acromegaly
• Insulin resistance
• Minoxidil treatment

Management

• Manage symptoms
• Manage cause
• Trans-sphenoidal first line
• Drug treatment
• Somatostatin analogues (Octreotide and Lanreotide)
• Dopamine agonists (Cabergoline and Bromocriptine)
• Pegvisomant (Genetically modified analogue of GH)
• Radiotherapy for residual disease

Prognosis

• High GH = 2-3 times more mortality
• Microadenoma > Macroadenoma
• Remission rates 80% for microadenoma and 50% for macroadenoma
• Hypertension, cardiovascular disease, diabetes and long duration of symptoms are also poor prognostic factors

Notes

COPD

·         FEV1/FVC lower and can’t be reversed well with bronchodilators

·         Treatment

o   Smoking cessation

o   Bronchodilators

o   Corticosteroids

o   Oxygen

o   Infection prevention/treatment

·         BODE index

o   BMI

o   Obstruction (airflow)

o   Dyspnoea

o   Exercise capacity

Obstructive sleep apnoea

·         Sleepiness due to waking up many times at night

·         Fall in arterial O2 sats many times (measured on pulse oximetry)

·         Treatment

o   CPAP

o   Weight loss

Bronchiectasis

·         Permanent dilation of airways caused by CF or post-infectious

·         Recurrent infections

·         High resolution CT for diagnosis

·         Treatment

o   Physiotherapy

o   Antibiotics

o   Bronchodilators

o   Inhaled or oral steroids

o   Surgery (lung or heart/lung transplantation

Cystic fibrosis

·         Autosomal recessive

·         CFTR on chromosome 7 (CF transmembrane conductance regulator)

·         Treatment

o   Bronchiectasis

o   Pancreatic insufficiency (exocrine)

Asthma

·         Airflow limitation, airway hyperresponsiveness and inflammation of the bronchi

·         Extrinsic (younger) or intrinsic (older)

·         Diagnosis: Demonstrate variability by measuring PEFR or FEV1 (15% minimum), and look at CXR and atopy (histamine challenge?)

·         Treatment

o   B2 agonist

o   Add inhaled corticosteroids

o   Add LABA or leukotriene receptor antagonist (monteleukast or oral theophylline

o   Increase corticosteroids to 2000 micrograms daily

o   Add 40mg oral prednisolone daily

o   Hospital

Tuberculosis

·         Notifiable

o   Test all relatives (Mantoux?)

o   Treat relatives

o   Look at CXR and cultures

·         Standard treatment

o   Rifampicin

§  Turns secretions pink

§  Increased LFT and induces liver enzymes

o   Isoniazid

§  Polyneuropathy

§  ADD pyridoxine to prevent this

o   Pyrazinamide

§  Rashes and arthralgia and hyperuricaemia and gout

o   Ethambutol

§  Optic neuritis (check regularly)

o   Streptomycin

·         Prevent

o   BCG (Bacille Calmette-Guerin)

Sarcoidosis

·         Multisystem granulomatous disorder of unknown cause

·         Affects

o   Chest

§  Cough, breathlessness, wheeze, crackles

o   Skin

§  Erythema nodosum, lupus pernio, infiltration of scars

o   Eye

§  Anterior and posterior uveitis, conjunctival nodules, lacrimal gland enlargement, uveoparotid fever (Heerfordt’s syndrome with uveitis, parotid gland enlargement and facial nerve palsy)

o   Bone

§  Arthralgias, bone cysts

o   Metabolic

§  Hypercalcaemia (sarcoid macrophages produce 1,25 dihydroxyvitamin D)

o   Liver

§  Granulomatous hepatitis, hepatosplenomegaly

o   Neurological

§  Meningeal inflammation, seizures, mass lesions, hypothalamic-pituitary infiltration, diffuse sensorimotor neuropathy

o   Cardiac

§  Ventricular arrhythmias, conduction defects, cardiomyopathy with cardiac failure

·         Managed by:

o   Usually nothing

o   Can give prednisolone or even methotrexate/azathioprine/cyclophosphamide

·         Kills by

o   Respiratory damage

o   Renal damage due to hypercalciuria

Acute lung injury/acute respiratory distress syndrome

Acute lung injury (ALI) and the more severe acute respiratory distress syndrome (ARDS) are defined as respiratory distress occurring with stiff lungs, diffuse bilateral pulmonary infiltrates, refractory hypoxaemia, in the presence of a recognised precipitating cause and in the absence of cardiogenic pulmonary oedema (i.e. no clinical evidence of left atrial hypertension)

Aetiology

The commonest precipitating factor is sepsis. Other causes include trauma, burns, pancreatitis, fat or amniotic fluid embolism, aspiration pneumonia or cardiopulmonary bypass.


Pathophysiology

The cardinal feature is pulmonary oedema as a result of increased vascular permeability caused by the release of inflammatory mediators. Oedema may induce vascular compression resulting in pulmonary hypertension, which is later exacerbated by vasoconstriction in response to increased autonomic nervous activity. A haemorrhagic intra-alveolar exudate forms, which is rich in platelets, fibrin, and clotting factors. This inactivates surfactant, stimulates inflammations and promotes hyaline membrane formation. These changes may result in progressive pulmonary fibrosis.


Clinical features

Tachypnoea, increasing hypoxia, and laboured breathing are the initial features. The chest X-ray shows diffuse bilateral shadowing, which may progress to complete 'white out'.


Management

This is based on the treatment of the underlying condition

Pulmonary oedema should be limited with fluid restriction, diuretics and haemofiltration. If these measures fail, aerosolized surfactant, inhaled nitric oxide and aerosolised prostacyclin are experimental treatments whose exact role in the management of ARDS is unclear. Repeated positional change, i.e. changing the patient from supine to prone may allow reductions in airway pressures and the inspired oxygen fraction in those with severe hypoxaemia.


Prognosis

Although the mortality has fallen over the last decade, it remains at 30-40% with most patients dying from sepsis. The prognosis is very dependent on the underlying cause, and rises steeply with age and with the development of multiorgan failure.

Supraventricular tachycardias

These arise from the atrium or the atrioventricular junction. Conduction is via the His-Purkinje system and the QRS shape during tachycardia is usually similar to that seen in the same patient during baseline rhythm

Sinus tachycardia

• Sinus tachycardia is a physiological response during exercise and excitement. It also occurs in fever, anaemia, heart failure, and thyrotoxicosis, acute pulmonary embolism, hypovolaemia and drugs (e.g. catecholamines and atropine). Treatment is aimed at correction of the underlying cause. If necessary, Beta-blockers may be used to slow the sinus rate, e.g. in hyperthyroidism

Atrioventricular junctional tachycardias

• Tachycardia arises as a result of re-entry circuits in which there are two separate pathways for impulse conduction. They are usually referred to as paroxysmal SVTs and are often seen in young patients with no evidence of structural heart disease.
• Atrioventricular nodal re-entry tachycardia (AVNRT) is the commonest type of SVT. It is due to the presence of a 'ring' of conducting pathway in the atrioventricular (AV) node of which the 'limbs' have differing conduction times and refractory periods. This allows a re-entry circuit and an impulse to produce a circus movement tachycardia. On the ECG, the P waves are either not visible or are seen immediately before or after the QRS complex. The QRS complex is usually of normal shape because the ventricles are activated in the normal way, down the bundle of His. Occasionally the QRS complex is wide, because of the rate-related bundle branch block, and it may be difficult to distinguish from ventricular tachycardia.
• Atrioventricular reciprocating tachycardia (AVRT) is due to the presence of an accessory pathway that connects the atria and ventricles and is capable of anterograde or retrograde conduction, or in some cases both. Wolff-Parkinson-White syndrome is the best known type of AVRT in which there is an accessory pathway (bundle of Kent) between atria and ventricles. The resting ECG in Wolff-Parkinson-White syndrome shows evidence of the pathway's existence if the path allows some of the atrial depolarisation to pass quickly tot he ventricle before it gets through the AV node. The early depolarisation of part of the ventricle leads to a shortened PR interval and a slurred start to the QRS (delta wave). The QRS is narrow. These patients are also prone to atrial and occasionally ventricular fibrillation.
• Symptoms
• The usual history is of rapid regular palpitations usually with abrupt onset and sudden termination. Other symptoms are dizziness, dyspnoea, central chest pain and syncope. Exertion, coffee, tea or alcohol may aggravate the arrhythmia
• Acute management
• The aim of treatment is to restore and maintain sinus rhythm:
• Unstable patient - emergency cardioversion is required in patients whose arrhythmia is accompanied by adverse symptoms and signs
• Haemodynamically stable patient - increase vagal stimulation of the sinus node by the Valsalva manoeuvre (ask the paitent to blow into a 20-mL syringe with enough force to push back the plunger) or right carotid sinus massage (contraindicated in the presence of a carotic bruit)
• Adenosine is a very short acting AV nodal blocking drug that will terminate most junctional tachycardias. Other treatments are intravenous verapamil or beta blockers, e.g. metoprolol, verapamil is contraindicated with beta lockers, if the QRS is wide and therefore differentiation from VT difficult or there is AF and an accessory pathway

Long term management

• Radiofrequency ablation of the accessory pathway via a cardiac catheter is successful in about 95% of cases. Flecainide, verapamil, sotalol and amiodarone are the drugs most commonly used.

Heart Block

The common causes of heart block are coronary artery disease, cardiomyopathy and, particularly in elderly people, fibrosis of conducting tissue. Block in either the atrioventricular (AV) node or the His bundle results in AV block, whereas block lower in the conduction system produces right or left bundle block.

Atrioventricular block

• There are three forms:
• First-degree AV block: This is the result of delayed atrioventricular conduction and reflected by a prolonged PR interval (>0.22s) on the ECG. No change in heart rate occurs and treatment is unnecessary
• Second-degree AV block: This occurs when some atrial impulses fail to reach the ventricles
• Mobitz type 1 block (Wenckebach block phenomenon) is progressive PR interval prolongation until a P wave fails to conduct, i.e. absent QRS after P wave. The PR interval then returns to normal and the cycle repeats itself
• Mobitz type 2 block occurs when a dropped QRS complex is not preceded by progressive PR prolongation. Usually the QRS complex is wide
• 2:1 or 3:1 advanced block occurs when every second or third P wave conducts to the ventricles
• Progression from second-degree AV block to complete heart block occurs more frequently following acute anterior myocardial infarction and in Mobitz type II block, and treatment is with a cardiac pacemaker. Patients with Wenckebach AV block or those with second-degree block following acute inferior infarction are usually monitored.
• Complete heart block occurs when all atrial activity fails to conduct to the ventricles. There is no association between atrial and ventricular activity; P waves and QRS complexes occur independently of one another on the ECG. Ventricular contractions are maintained by a spontaneous escape rhythm originating below the site of the block in the:
• His bundle - which gives rise to a narrow complex QRS (<0.12s) at a rate of 50-60 bpm and is relatively reliable. Recent onset block due to transient causes, e.g. ischaemia, may respond to intravenous atropine without need for pacing. Chronic narrow-complex AV block usually requires permanent pacing.
• His-Purkinje system (i.e. distally) gives rise to a broad QRS complex (>0.12s), is slow (<40 bpm), unreliable and often associated with dizziness and blackouts (Stokes-Adams attacks). Permanent pacemaker insertion is indicated.

Bundle branch block 

• Complete block of a bundle branch associated with a wide QRS complex (more than or equals to 0.12s) with an abnormal pattern and is usually asymptomatic. The shape of the QRS depends on whether the right or the left bundle is blocked:
• Right bundle branch block (RBBB) - the right bundle branch no longer conducts an impulse and the two ventricles do not receive an impulse simultaneously. There is sequential spread of an impulse (i.e. first the left ventricle then the right) resulting in a secondary R wave (RSR')  in V1 and a slurred S wave in V5 and V6. RBBB occurs in normal healthy individuals, PE, RVH, IHD, and congenital heart disease, e.g. atrial and ventricular septal defect and Fallot's tetralogy
• Left bundle branch block (LBBB) - the opposite occurs with an RSR' pattern in the left ventricular leads (I, AVL, V4-6) and deep slurred S waves in V1 and V2. LBBB indicates underlying cardiac pathology and occurs in IHD, LVH, and aortic disease and following cardiac surgery

Normal Cardiac Axis

Normal = -30 to +90
Left = < -30
Right = > 90

Alcohol relapse drugs

STOP CRAVING

• Acamprosate

STOP OPIOID EFFECT

• Naltrexone

ANTABUSE

• Disulfiram

Central pontine myelinolysis

Over-rapid correction of the sodium concentration by whatever means must be avoided, as this can result in a severe, neurological syndrome due to local areas of demyelination, called central pontine myelinolysis or the osmotic demyelination syndrome. Features of this include quadriparesis, respiratory arrest, pseudobulbar palsy, mutism, and, rarely, fits. The distribution of the areas of demyelination include most often the pons, but also, in some cases, the basal ganglia, internal capsule, lateral geniculate body and even the cerebral cortex. Diagnosis is by characteristic appearances on brain MRI.

4 reasons for oedema

• Hydrostatic pressure increase
• Oncotic pressure decrease
• Blocked lymph drainage
• Open capillary walls

SPELLS HOBO lol!!!!!

Hypernatraemia and hyponatraemia

Hypernatraemia

• Too much water loss in comparison to sodium loss (or no sodium change at all)
• Nephrogenic/pituitary diabetes insipidus
• Nausea, vomiting, fever, confusion
• Replace over 48 hours

Hyponatraemia

• Too little water loss in comparison to sodium loss (or no sodium change at all)
• SIADH
• Cerebral oedema causes headache, confusion, convulsions, coma
• Restrict water
• Vasopressin antagonists in the future?

Thrombotic thrombocytopenic purpura (TTP)

Widespread adhesion and aggregation of platelets lead to microvascular thrombosis and profound thrombocytopenia. This occurs due to deficiency of ADAMTS 13, a protease which is normally responsible for the degradation of vWF. ADAMTS 13 deficiency is congenital, sporadic, or autoantibody mediated (pregnancy, systemic lupus erythematosus, infection, drug treatment e.g. clopidogrel). There is florid purpura, fever, fluctuating cerebral dysfunction and haemolytic anaemia with red cell fragmentation, often accompanied by renal failure. The coagulation screen is usually normal but lactate dehydrogenase levels are markedly raised as a result of haemolysis. Treatment is with plasma exchange (to remove the antibody to ADAMTS13), methylprednisolone and rituximab. Platelet concentrates are contraindicated.