GP Conditions Flashcards
Type 2 Diabetes complications (3)
Infections e.g. candida
Macrovascular arterial e.g. coronary artery disease, stroke
Microvascular e.g. neuropathy, nephropathy, retinopathy
1st line medication to manage T2DM patients of any age with hypertension
ACE inhibitors
Medication started in T2DM when the patient has CKD with ACR above 30mg/mmol
SGLT-2 inhibitors
Type of medication used for erectile dysfunction
Phosphodiesterase-5 inhibitors e.g. sildenafil
4 options for neuropathic pain in diabetic neuropathy
Amitriptyline (TCA)
Duloxetine (SNRI)
Gabapentin (anticonvulsant)
Pregabalin (anticonvulsant)
Step-wise medical management of T2DM
1st line: Metformin, once settled ADD SGLT-2 inhibitor if the patient has CVD or HF or QRISK above 10%
2nd line: ADD sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor
3rd line: Triple therapy (metformin plus 2) or insulin therapy
Two side effects of SGLT-2 inhibitors
Increased frequency of UTIs and genital thrush more glucose in the wee due to inhibiting reabsorption
Diabetic ketoacidosis
T2DM diagnostic results (3)
HbA1c > 48
Fasting plasma glucose > 7
Random plasma glucose: > 11.1
Pre-diabetes HbA1c
42-47 mmol/mol
Pathophysiology of T1DM
Autoimmune disorder where the insulin producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system
Main side effects of insulin treatment
Hypoglycaemia
Weight gain
Lipodystrophy
MOA metformin (3)
- Increase insulin sensitivity
- Decreases hepatic gluconeogenesis
- Decreases intestinal absorption of glucose
Metformin side effects
GI upset
Lactic acidosis
Secondary hyperthyroidism definition
Pathology in the hypothalamus or pituitary producing too much TSH
Graves’ disease definition
Autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism
Most common cause of hyperthyroidism / thyrotoxicosis
Graves’ disease
Which condition causing hyperthyroidism is most common in patients over 50
Toxic multinodular goitre
nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones
Pathophysiology of exophthalmos (proptosis)
Bulging of the eyes caused by Graves’ disease
inflammation, swelling and hypertrophy of the tissue behind the eyeballs force them forward, causing them to bulge out of the sockets
Pretibial myxoedema definition
Skin condition caused by glycosaminoglycans under the skin on the anterior aspect of the leg (the pre-tibial area)
Gives the skin a discoloured, waxy, oedematous appearance over this area
Specific to Graves’ disease and is a reaction to TSH receptor antibodies
Causes of hyperthyroidism (4)
GIST:
Graves’ disease
Inflammation (thyroiditis)
Solitary toxic thyroid nodule
Toxic multinodular goitre
Thyroiditis (thyroid gland inflammation) disease pattern
Initial period of hyperthyroidism followed by hypothyroidism
4 causes of thyroiditis
De Quervain’s thyroiditis
Hashimoto’s thyroiditis
Postpartum thyroiditis
Drug-induced thyroiditis
Graves’ disease specific features
Diffuse goitre (w/o nodules)
Graves’ eye disease with exophthalmos
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)
Presentation of hyperthyroidism
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination
1st line anti-thyroid drug
Carbimazole, usually taken for 12 to 18 months
Methods of dosing:
- Titrate to maintain normal levels
- Block all production and replace with levothyroxine
2 complications of carbimazole use
Acute pancreatitis (look for severe epigastric pain radiating to back)
Agranulocytosis (look for susceptible to infections/sore throat)
Blood results of thyrotoxicosis (e.g. Graves’)
TSH: low
Free T4: high
Antibodies found in Graves’ disease
TSH receptor antibodies
Antibodies found in Hashimoto’s thyroiditis
anti-TPO antibodies
1st line symptomatic management of hyperthyroidism
Propranolol
Most common cause of hypothyroidism in the developed world
Hashimoto’s thyroiditis
Most common cause of hypothyroidism in the developing world
Iodine deficiency
Presentation of hypothyroidism
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation
Treatment of hypothyroidism
Oral levothyroxine (synthetic T4 which metabolises to T3)
Investigations following a hypertension diagnosis
Fundoscopy: to check for hypertensive retinopathy
U+Es, Urine dipstick: to check for renal disease (as a cause or consequence of)
ECG: left ventricular hypertrophy or IHD
HbA1c: check for co-existing DM (CVD RF)
Lipids: check for hyperlipidaemia (CVD RF)
Hypertension stage 1 definition
ABPM/HBPM monitoring = > 135 / 85 mmHg
Or
Clinic reading persistently = > 140 / 90 mmHg
Step 1 management for hypertension in patient who is <55 or T2DM
1st line: ACE inhibitor
2nd line (e.g. because of ACEi cough side effect): Angiotensin 2 Receptor blocker
Step 1 management for hypertension in patient who is >55 or Afro-Caribbean with NO T2DM
1st line: Calcium channel blocker
Step 2 management for hypertension
ACEi/A2RB + CCB
OR
ACEi/A2RB + thiazide-like Diuretic
Step 3 management for hypertension
ACEi/A2RB + CCB + thiazide-like D
Step 4 management of hypertension based on K+ results
K+ < 4.5 add low dose spironolactone
K+ > 4.5 add alpha or beta blocker
Stage 2 hypertension definition
Clinic BP > 160/100
ABPM/HBPM > 150/95
Severe hypertension definition
Clinic systolic > 180 mmHg
Clinic diastolic > 120 mmHg
What would indicate a same-day specialist review in BP 180/120 mmHg
Retinal haemorrhage or papilloedema
Life threatening symptoms (new onset confusion, chest pain, HF Sx, AKI)
Suspected phaeochromocytoma (labile or postural hypotension, headache)
Single most common cause of secondary hypertension
Primary hyperaldosteronism (Conn’s)
Renal conditions which would increase BP
Glomerulonephritis
Pyelonephritis
APKD
Renal artery stenosis
Drug causes of secondary hypertension
Steroids
MAOIs
COC
NSAIDs (by blocking prostaglandins)
Top differentials for a non blanching rash (bleeding under the skin)
Leukaemia
Meningococcal septicaemia
Henoch-schonlein purpura
ITP
TTP
Traumatic
Analgesia management in osteoarthritis
1st line: topical NSAIDs (particularly beneficial for OA of knee or hand)
2nd line: oral NSAIDs - a PPI should be co-prescribed e.g. omeprazole
Characteristic features of OA of the hand
Unsymmetrical
Carpometacarpal (CMC) and distal interphalangeal (DIP) joints
Heberden’s nodes at the DIP pints
Bouchard’s nodes at the PIP joints
Squaring of the thumbs (fixed adduction)
X-ray investigation results of OA
LOSS:
Loss of joint space
Osteophytes forming at joint margins
Subchondral sclerosis
Subchondral cysts
Diagnosis of OA w/o investigations
Over 45, typical pain associated with activity and has no morning stiffness (or stiffness lasting under 30 minutes)
Which patients is OA most commonly seen in
Post-menopausal women (due to loss of protective oestrogen)
Gout definition
A type of crystal athropathy associated with chronic hyperuricaemia
Urate crystals are deposited in the joint, causing it to become inflamed
Episodes last several days with symptom-free periods in between
Gout typical presentation
Single acute hot, swollen painful joint (key DDx: septic arthritis)
Gouty tophi (subcutaneous uric acid in the hands, elbows and ears)
Risk factors for gout
Male
FHx
Obesity
High purine diet (meat and seafood)
Alcohol
Diuretics
CVD
Renal disease
Most commonly affected joints in gout
Base of the big toe: metatarsophalangeal joint (MTP joint) - 70% of first presentations affect 1st MTP
Base of the thumb: carpometacarpal joint (CMC joint)
Wrist
Gout can also affect larger joints e.g. knee and ankle
Diagnosis of gout
Clinical diagnosis
- supported by a raised serum urate level on blood test (typically checked 2 weeks later as may be high, normal or low during acute attack)
Aspirated joint fluid 2 findings in gout that differentiate it from septic arthritis and pseudogout
- No bacterial growth (important to exclude septic arthritis)
- Monosodium urate crystals: needle shaped and negatively birefringent of polarised light (PseudOgOut = rhOmbOid shaped and Positively birefringent)
X-ray findings in gout
No loss of joint space
Lytic lesion in the bone
Punched out erosions
Erosions can have sclerotic borders with overhanging edges
Management of acute flares of gout
1st line: NSAIDs e.g. naproxen - co-prescribed with PPI
2nd line: colchicine (if renal impairment or significant heart disease)
3rd line: oral steroids e.g. prednisolone
Gout prophylaxis
Xanthine oxidase inhibitors which lower uric acid level e.g. Allopurinol (1st) or Febuxostat (2nd)
- offered to all patients after their first attack of gout
- Prophylaxis is not started until inflammation has settled after the acute attack (NSAIDs/colchicine can be continued)
- Once established on allopurinol, continue during future acute attacks
Main side effect of colchicine
Diarrhoea
4 causes of acute liver failure
Paracetamol overdose
Alcohol
Viral hepatitis (usually A or B)
Acute fatty liver of pregnancy
Features of acute liver failure
Jaundice
Coagulopathy: raised PT time
Hypoalbuminaemia
Hepatic encephalopathy
Renal failure is common (hepatorenal syndrome)
Differentiating features of Crohn’s disease
‘Crows’ NESTS:
N - No blood or mucus (PR bleeding is less common)
E - Entire GI tract (mouth to anus)
S - ‘Skip’ lesions on endoscopy
T - Terminal ileum most affects and Transmural inflammation
S - Smoking is a risk factor
+ strictures and fissures
Differentiating features of Ulcerative Colitis
You See (UC) CLOSE UP:
C - Continuous inflammation
L - Limited to the colon and rectum
O - Only superficial mucosa affected
S - Smoking may be protective (UC less common in smokers)
E - Excrete blood and mucus
U - Use Aminosalicylates
P - Primary sclerosing cholangitis
Blood tests for IBD investigations
FBC: Hb (anaemia), platelet count (raised w inflammation)
CRP
U&Es: electrolyte imbalance, kidney function
LFTs: low albumin in severe disease (protein lost in bowel)
TFTs: hyperthyroidism as DDx for diarrhoea
Anti-TTG: coeliac
IBD screening and diagnostic investigations
Screening: faecal calprotectin (90% sensitive and specific)
Diagnostic: colonoscopy with multiple intestinal biopsies
UC management
Mild to moderate:
1st line = Aminosalicylate e.g. mesalazine
2nd line = Corticosteroids e.g. oral/PR prednisolone
Acute severe:
1st line = IV steroids e.g. IV hydrocortisone
Maintaining remission: aminosalicylate, Azathioprine, mercaptopurine
Panproctocolectomy will remove the disase = patient will have ileostomy or J pouch
Crohn’s management
1st line in inducing remission: glucocorticoids e.g. oral pred or IV hydrocortisone
1st line in maintaining remission: Azathioprine, mercaptopurine
Most common cause of hyperthyroidism in pregnancy
Graves disease
Cushing’s disease
Cushing’s syndrome caused specifically by a pituitary gland tumour
Causes of Cushing’s syndrome
High/chronic doses of exogenous steroids (most common cause)
Pituitary gland tumour (Cushing’s disease) - most common endogenous/ACTH dependent cause
Adrenal tumour (excessive cortisol)
Paraneoplastic ectopic ACTH i.e. small cell carcinoma in the lungs
5 mechanisms of cortisol
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness
electrolyte imbalance associated with ectopic ACTH secretion
Hypokalaemia
1st line / Gold standard test to diagnose Cushing’s syndrome
Overnight (low-dose) dexamethasone suppression test
high-dose test can be used to localise pathology e.g. cortisol + ACTH suppressed = pituitary adenoma)
Most common cause of primary hyperaldosteronism (Conn’s)
bilateral idiopathic adrenal hyperplasia
Features of primary hyperaldosteronism (Conn’s)
Hypertension
Hypokalaemia e.g. muscle weakness
Hypernatraemia
Metabolic alkalosis
aldosterone causes sodium retention and resulting potassium excretion in the kidneys
1st line investigation in Conn’s
Plasma aldosterone:renin ratio
= high aldosterone/low renin: aldosterone causes sodium retention which has a negative feedback on renin
Management of Conn’s (bilateral adrenocortical hyperplasia)
Aldosterone antagonist e.g. spironolactone
Renal colic definition
Unilateral loin to groin pain
Colicky (flucuating in severity)
Investigation renal colic
CT KUB (CT of the kidneys, ureters and bladder) within 24 hours of presentation
Ultrasound should be used for pregnant women and children
Presentation of hypercalcaemia/hyperparathyroidism
Renal stones
Painful bones
Abdominal groans
Psychiatric moans
3 causes of hypercalcaemia
Calcium supplementation
Hyperparathyroidism
Cancer (e.g. myeloma, breast, lung)
Most common type of renal stone
Calcium oxalate
Complications of renal stones (2)
Obstruction (leading to acute kidney injury)
Infection (obstructive pyelonephritis)
Presentation of renal stones
Renal colic
Haematuria
Most effective type of analgesia for renal stones
NSAIDs e.g. IM diclofenac
2nd line: IV paracetamol
Renal stones <5mm management
Watchful waiting (50-80% will pass)
Tamsulosin (alpha blocker) can be used to help aid passing
Surgical intervention: stones >10mm, won’t pass, signs of infection
Thiazide diuretic MOA in prevention of renal stones
Prevention of hypercalciuria by increasing distal tubular calcium resorption
2 prerenal causes of AKI
Hypovolaemia (secondary to D+V)
Renal artery stenosis
both cause lack of blood flowing to the kidneys/ischaemia
2 renal causes of AKI
glomerulonephritis
rhabdomyolysis
2 postrenal causes of AKI
renal stones
benign prostatic hyperplasia
Nephrotoxic drugs (5)
NSAIDs e.g. ibuprofen, aspirin can be continued at a cardioprotective 75mg dose
amingolycoside antibiotics e.g. gentamicin
ACE inhibitors e.g. ramipril
Angiotensin II receptor antagonists (ARBs) e.g. candesartan
Diuretics e.g. furosemide
Stage 1 AKI
urine output of less than 0.5 ml/kg/hour for ≥ 6 hours
OR
Increase in creatinine to 1.5-1.9 times baseline
Stage 2 AKI
urine output of less than 0.5 mL/kg/hour for ≥ 12 hours
OR
Increase in creatinine to 2.0 to 2.9 times baseline
Stage 3 AKI
urine output of less than 0.3 mL/kg/hour for ≥24 hours
OR
Increase in creatinine to ≥ 3.0 times baseline
Bladder cancer features (5)
frequency
urgency
nocturia
weight loss
painless haematuria
1st line investigation bladder cancer
cystoscopy and biopsy
2 major risk factors for transitional cell carcinoma of the bladder
Smoking
Exposure to aniline dyes
H. pylori treatment
1 PPI + 2 antibiotics + lifestyle modifications
e.g. lansoprazole + clarithromycin + metronidazole + stop smoking/caffeine
gastric ulcer vs duodenal ulcer pain
gastric ulcer = pain IMMEDIATELY after eating
CKD stages
Stage 1: > 90 mL + abnormal kidney tests
Stage 2: 60-89 mL + abnormal kidney tests (-30)
Stage 3A: 45-59 mL (-15)
Stage 3B: 30-44 mL (-15)
Stage 4: 15-29 mL (-15)
Stage 5/ESRF: <15mL
Ratio investigating proteinuria in CKD
albumin:creatinine ratio (ACR)
Management of CKD patients where ACR >30
1st line: ACE inhibitors
other: SGLT-2 inhibitors
How does CKD impact bone health
high phosphate (not being excreted in kidneys) drags calcium from the bones resulting in osteomalacia
secondary hyperparathyroidism (low calcium, low vitamin D, high phosphate)
renal ultrasound differentiation of CKD and AKI
bilateral small kidneys in CKD
how does CKD lead to anaemia
reduced erythropoietin levels
COPD stepwise treatment pathway (steroid responsive)
i.e. asthmatic features/atopic illness/FEV1 variation
Step 1: SABA e.g. salbutamol or SAMA e.g. ipratropium bromide
Step 2: SABA + LABA + ICS e.g. beclomethasone (if they were originally on SAMA, discontinue and start SABA)
Step 3: SABA + triple therapy i.e. LABA + ICS + LAMA e.g. tiotropium
COPD stepwise treatment pathway (non-steroid responsive)
i.e. no asthmatic features/no atopic illness/no FEV1 variation
Step 1: SABA or SAMA
Step 2: SABA + LABA + LAMA (if they were originally on SAMA, discontinue and start SABA)
Drug classes in asthma/COPD treatment and examples
SABA = short acting beta 2 agonist e.g salbutamol
LABA = long-acting beta 2 agonist e.g salmeterol
SAMA = short-acting muscarinic antagonist e.g ipratropium
LAMA= long-acting muscarinic antagonist e.g tiotropium
ICS = inhaled corticosteroid e.g. beclometasone, fluticasone
Moderate asthma definition
PEFR 50-75% best or predicted
Speech normal
Severe asthma definition
PEFR 33 - 50% best or predicted
Can’t complete sentences
Life threatening asthma definition + signs
PEFR < 33% best or predicted
Oxygen sats < 92%
‘Normal’ pC02 (4.6-6.0 kPa)
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
Feature of ‘near-fatal asthma’
Raised pCO2 > 6 kPa
Management for life threatening asthma
1st line Nebulised SABA (salbutamol) delivered in O2
Nebulised ipratropium bromide
Oral prednisolone for 5 days
positive asthma reversibility test
Improvement in FEV1 of 12% or more after inhalation of SABA
QRISK score
Risk of developing a heart attack or stroke in the next 10 years
>10% = benefit from a prescribed statin
3 key investigations in MI
ECG
CXR
Cardiac enzymes (troponin, myoglobin and creatinine kinase)
Primary hyperparathyroidism
Excess secretion of PTH resulting in hypercalcaemia
most common cause of hypercalcaemia in outpatients
Cause of 85% of primary hyperparathyroidism
Solitary adenoma
Primary hyperparathyroidism investigations
Bloods: high calcium, low phosphate
X-ray: pepperpot skull
What has occurred when PTH still not corrected after correcting underlying cause of secondary hyperparathyroidism
Secondary has caused hyperplasia of parathyroid glands = tertiary
2 main causes of secondary hyperparathyroidism
- Low vitamin D
- CKD
= cause low calcium which causes high PTH
Acute bacterial endocarditis contraindicated medication
Heparin
Rheumatoid arthritis hand signs (4)
Z-shaped deformity
Swan neck deformity
Boutonniere deformity
Ulnar deviation
Causes of clubbing
Cardiac = atrial myxoma, cyanotic heart disease, endocarditis, pericarditis
Gastrointestinal = malabsorption, inflammatory bowel disease, liver cirrhosis
Respiratory = Cystic fibrosis, Tuberculosis, Pulmonary fibrosis, bronchiectasis, bronchial carcinoma
Immediate management MI
MONA
Morphine
Oxygen therapy (if sats are less than 94%)
Nitrates
Aspirin + Antiplatelet
Mechanism of action of beta agonists in asthma
e.g. salbutamol or salmeterol
Stimulation of G-protein coupled receptor causes smooth muscle relaxation and hence bronchodilation
Mechanism of action of antimuscarinics in asthma
e.g ipratropium bromide
competitive inhibitor of acetylcholine
muscarinic receptors = parasympathetic effects e.g. bronchoconstriction
blocking these receptors causes the opposite effect and result in bronchodilation (sympathetic response)
1st line test coeliac disease
Tissue transglutaminase (TTG) antibodies (IgA)
Remember you also need to look for selective IgA deficiency (endomyseal antibody)
Gold standard investigation for coeliac disease
Endoscopic intestinal biopsy
Biopsy findings coeliac disease
Villous Atrophy
Crypt Hyperplasia
Increase in intraepithelial lymphocytes
Key signs of gastric cancer (3)
Dysphagia + palpable mass in abdomen + ascites
Chronic heart failure: NYHA classification
1: no symptoms + no limitations
2: mild symptoms + comfortable at rest but ordinary activity = symptomatic
3: moderate symptoms + comfortable at rest but less than ordinary activity = symptomatic
4: severe symptoms + symptoms even at rest
Management if BNP is ‘high’ when investigating HF
Transthoracic doppler echo within 2 weeks
’raised’ = transthoracic doppler echo within 6 weeks
1st line investigation heart failure
NT-proBNP
Radiological findings in HF
ABCDE
Alveolar oedema
Kerley B lines
Cardiomegaly
Dilated upper lobe veins
Pleural effusion
Key treatment for acute pulmonary oedema (acute heart failure)
IV loop diuretics e.g. furosemide
1st line therapy chronic heart failure
ACE inhibitor and beta blocker e.g. ramipril and bisoprolol
2nd line therapy chronic heart failure
Aldosterone antagonist e.g. spironolactone
SGLT-2 inhibitors e.g. dapagliflozin
AUDIT-C score
3 Qs:
How often do you have a drink containing alcohol?
How many units of alcohol do you drink on a typical day when you are drinking?
How often have you had 6 or more units (female) / 8 or more units (male), on a single occasion in the last year?
When should you double your dose of hydrocortisone in adrenal insufficiency
temperature of > 38.0 degrees
cold, flu, diarrhoea or other infection
break a bone
IBS presentation
Abdominal pain relieved by defecation
Bloating
Change in bowel habit
+ Made worse by stress, menstruation
IBS pain relief
Buscopan (antispasmodic)
C diff management
Metronidazole
Charcot’s triad
Cholangitis: RUQ pain, jaundice, and fever
Cholecystitis = jaundice is absent
Most common cause of cholecystitis
Gallstones
Biliary colic vs other gallstone related conditions
No fever and LFTs/inflammatory markers are normal
Gallstones risk factors
4 F’s
Fat
Female
Fertile
Fourty
+ Crohn’s, DM, rapid weight loss, drugs (COC)
Management biliary colic
Elective laparoscopic cholecystectomy
common bacteria which are causative of COPD exacerbations
Moraxella catarrhalis
Haemophilus influenzae
Strep pneumoniae
Differentiating acute bronchitis from pneumonia
Hx: absent in acute bronchitis: sputum, wheeze, breathlessness
O/E: absent in acute bronchitis: no other focal chest signs (dullness to percussion, crepitations, bronchial breathing), systemic features (malaise, myalgia, fever)
Management acute bronchitis
Supportive (analgesia, good fluid intake)
Antibiotic therapy: if the patient is systemically very unwell, pre-existing co-morbidities, high CRP
* 1st line = doxycycline (unless pregnant or a child)
* 2nd line = amoxicillin
3 key points children’s influenza vaccine
It’s given intranasally
First dose is given at 2-3 years then annually after that
It is a live vaccine
Contraindications to intranasal flu vaccine in children
Immunosuppressed
Aged < 2 years
Current febrile illness or blocked nose
Current wheeze or history of severe asthma
Egg allergy
Aspirin (e.g. Kawasaki)
inactivated, injectable vaccine given
Who receives the annual influenza vaccine
All people over 65
Chronic disease
Diabetes Mellitus
Immunosuppression
Pregnant women
inactivated vaccine so cannot cause influenza
Majority of hiatus hernia types
Sliding (GI junction moves above the diaphragm)
Risk factors hiatus hernia
Obesity
Increased abdominal pressure e.g. ascites, multiparity
Features of a hiatus hernia (4)
Heartburn
Dysphagia
Regurgitation
Chest pain
Hiatus hernia investigation
1st line: endoscopy
Most sensitive: Barium swallow
Management of hiatus hernia
All patients benefit from conservative management e.g. weight loss
Medical management: PPI therapy
External haemorrhoids
Originate below the dentate line
Prone to thrombosis, may be painful
Internal haemorrhoids
Originate above the dentate line
Do not generally cause pain
Grading of internal haemorrhoids
I: do not prolapse
II: prolapse on defecation
III: manually reduced
IV: cannot be reduced
Management of haemorrhoids
GP:
Soften stools (increase dietary fibre and fluid intake)
Topical local anaesthetics and steroids
Outpatient:
Rubber band ligation (1st) or injection sclerotherapy
GORD management
PPI (-prazole) for 1 month (full dose)
- If response, low dose treatment of PPI as required
- If no response:
Endoscopically proven oesophagitis: double dose PPI for 1 month
Endoscopically negative reflux disease: H2RA or prokinetic for one month
Complications of GORD
Oesophagitis
Ulcers
Anaemia
Barrett’s oesophagus
Oesophageal carcinoma
Risk factors for developing GORD
Stress and anxiety
Smoking and alcohol
Coffee and chocolate (reduce LOS tone)
Obesity
Features of fibromyalgia
Chronic pain (multiple site, sometimes all over)
Lethargy
Cognitive impairment (fibro fog)
Sleep disturbance, headaches, dizziness
4 points on fibromyalgia management
Explanation
Aerobic exercise
CBT
Medication (pregabalin, duloxetine, amitriptyline)
Early features of Lyme disease (within 30 days)
Erythema migrans (‘Bulls-eye’ rash at site of tick bite), usually painless - pathognomic
Systemic features
Management of asymptomatic tick bites
Remove tick, no antibiotic treatment routinely recommended
Management of suspected/confirmed Lyme disease
Doxycycline
Polymyalgia rheumatica key features
Typical patient > 60 years old
Usually rapid onset (e.g. < 1 month)
Aching, morning stiffness in proximal limb muscles (weakness is not considered a symptom in polymyalgia)
Other: Mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
Investigations polymyalgia rheumatica
Raised inflammatory markers
Creatinine kinase and electromyography = normal
Treatment polymyalgia rheumatica
Prednisolone
patients typically respond rapidly to steroids, failure to do so should prompt DDx
Most important causative viral pathogen of COPD exacerbation
Human rhinovirus
Features of COPD exacerbation
Increased dyspnoea, cough, wheeze
Increase in sputum (yellow-green)
Hypoxia / acute confusion
Fever
Cyanosis
Peripheral oedema
Differentials COPD exacerbation
Pneumonia
Pneumothorax
Pleural effusion
Pulmonary embolism
Management of COPD exacerbation (3)
- Increase frequency of bronchodilator (consider nebuliser)
- Prednisolone 30mg daily for 5 days
- Antibiotics: amoxicillin, clarithromycin, doxycycline (give Abx if sputum is purulent or clinical signs of pneumonia)
Admission criteria for COPD exacerbation
Severe breathlessness
Acute confusion or impaired consciousness
Cyanosis
Oxygen saturation <90%
Social reasons (inability to cope at home)
Significant comorbidity (cardiac disease, insulin diabetes)
thiazide-like diuretic examples
metolazone, indapamide, chlorthalidone
Units of alcohol calculation
Vol (L) x % ABV
Management of male with UTI
Nitrofurantoin for 7 days
Atrial fibrillation 1st line rate control medication
beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem)
Bacterial conjunctivitis presentation
Purulent discharge (eyes make be ‘stuck together’ in the morning)
Viral conjunctivitis presentation
Serous discharge + recent URTI
Management of infective conjunctivitis
Self limiting condition - settles without treatment within 1-2 weeks
1st line = Topical antibiotic therapy e.g. chloramphenicol drops (topical fusidic acid is used for pregnant women)
Contact lens should not be worn during an episode of conjunctivitis
School exclusion is not necessary
Acute vs chronic anal fissure
Acute = less than 6 weeks
Chronic = more than 6 weeks
3 risk factors for anal fissures
Constipation
IBS
STIs e.g. HIV, syphilis, herpes
Presentation of anal fissures
Painful, bright red, rectal bleeding
Management of an acute anal fissure
Soften stool: dietary advice (high fibre, high fluid), bulk-forming laxatives
Lubricants
Topical anaesthetics
Analgesia
Chronic anal fissure management
Add to acute management: topical glyceryl trinitrate (GTN)
Most common form of prostate cancer
Adenocarcinoma
Other causes of raised PSA
Benign prostatic hyperplasia (BPH)
Prostatitis and UTI
Ejaculation
Vigorous exercise
Management of low-grade prostate cancer
Active monitoring and watchful waiting
Common complication of radical prostatectomy
Erectile dysfunction
Complications of radiotherapy for prostate cancer (2)
Proctitis
Increased risk of bladder, colon and rectal cancer
Classic triad reactive arthritis
Urethritis, conjunctivitis and arthritis
‘Can’t see, pee or climb a tree’
Time course of reactive arthritis
Typically develops within 4 weeks of initial infection (symptoms generally last around 4-6 months)
Most common STI associated with reactive arthritis
Chlamydia trachomatis
Management of reactive arthritis
Symptomatic: analgesia, NSAIDs, intra-articular steroids
Methotrexate for persistent disease
Common trigger for otitis externa
Recent swimming
1st line treatment otitis externa
Topical antibiotics with or without steroid
if the patient fails to respond then refer to ENT
End stage heart failure disease prognosis
High risk of dying within 6-12 months
Raised urea and creatinine
Renal failure
Blood tests to screen for alcohol dependence
Raised:
GGT
MCV
CDT
Hypertension 4 further investigations
Creatinine
Electrolytes
ECG
Urinary protein
4 causes of constipation
Advanced age
Inactivity
Low calorie intake
Low fibre diet
Medications
Female sex
Hypothyroidism
