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GP Flashcards

1
Q

Define type 2 diabetes mellitus

A

Insulin resistance and relative insulin deficiency causing persistent hyperglycaemia, due to loss of function of beta-cells/progressive insulin secretion failure

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2
Q

Describe the epidemiology of type 2 diabetes mellitus

A

Increasing to epidemic proportions, commonly diagnosed >40yrs old, but increasingly onset at younger ages (childhood)

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3
Q

What are the risk factors for type 2 diabetes mellitus?

A

Obesity + lack of exercise
Family history
Asian, African, Afro-Caribbean ethnicities
High glycaemic index diet (e.g. sugary drink/food)
Age >40yrs
Drug treatments (e.g. steroids)
PCOS

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4
Q

What are the signs/symptoms of type 2 diabetes mellitus?

A

Polydipsia
Polyuria
Glycosuria
Blurred vision
Unexplained weight loss
Recurrent infections
Tiredness
Acanthosis nigricans

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5
Q

What are the investigations needed for type 2 diabetes mellitus?

A

Random plasma glucose > 11.1 mmol/L
Fasting plasma glucose > 7mmol/L
HbA1c > 48 mmol/L (6.5%)

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6
Q

What information and advice can be given for type 2 diabetes mellitus?

A
  • Provide sources of information and support (e.g. diabetes uk website)
  • Give advice on lifestyle changes if appropriate (exercise, weight loss, diet, alcohol, smoking)
  • Assess for associated anxiety/depression
  • Offer immunizations against influenza and pneumococcal infection
  • Referral to education programme (DESMOND)
  • Advise about entitlement to free prescriptions if using antidiabetic medication
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7
Q

What are the step-wise treatments for type 2 diabetes mellitus?

A
  • 1st line = metformin
  • If ineffective = dual therapy by adding DPP-4 inhibitor, pioglitazone, sulfonylurea, or SGLT-2 inhibitor
  • If ineffective = triple therapy by adding another class, or consider insulin therapy
  • If ineffective = consider switching one drug to GLP-1 receptor agonist
  • If patient has cardiovascular risk factors = add SGLT-2 inhibitor at any point
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8
Q

What is metformin? (explain action, use, CI, and SE)?

A
  • Action: increases insulin sensitivity
  • Use: 1st line treatment
  • CI: metabolic acidosis, renal impairment
  • SE: decreased appetite, GI issues
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9
Q

What are SGLT-2 inhibitors? (action, example, use, CI, SE)

A
  • Action: blocks glucose reabsorption in kidney
  • Example: empagliflozin (ending -gliflozin)
  • Use: in patients with increased cardiovascular risk, or in dual/triple therapy if at risk of hypoglycaemia
  • CI: risk of metabolic acidosis, renal impairment, active foot disease
  • SE: vulvovaginitis, UTIs (due to increase glycosuria)
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10
Q

What are DPP-4 inhibitors? (action, example, use, CI, SE)

A
  • Action: extends duration of GLP-1, so stimulates insulin secretion
  • Example: sitagliptin (ending -gliptin)
  • Use: dual/triple therapy
  • CI: ketoacidosis, renal/hepatic impairment, heart failure
  • SE: GI issues, pancreatitis, increased risk of infections, ILD (sitagliptin)
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11
Q

What is pioglitazone? (action, use, CI, SE)

A
  • Action: activate glucose uptake gene, increases insulin sensitivity
  • Use: dual/triple therapy
  • CI: heart failure, bladder cancer, hepatic impairment
  • SE: weight gain, insomnia, increased risk of bone fractures, infection, bladder cancer, and liver failure
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12
Q

What are sulfonylureas? (action, examples, use, CI, SE)

A
  • Action: stimulate insulin release
  • Example: gliclazide (ending -ide)
  • Use: dual/triple therapy
  • CI: renal/hepatic impairment
  • SE: GI issues, hypoglycaemia, weight gain
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13
Q

What are GLP-1 receptor agonists? (action, use, example, CI, SE)

A
  • Action: assists weight loss
  • Use: if triple therapy is ineffective, and BMI is over 35, or significant obesity-related comorbidities
  • Example: semaglutide (ending in -tide)
  • CI: ketoacidosis, pancreatitis, renal/hepatic impairment, severe GI disease
  • SE: pancreatitis, GI issues (decreased appetite, delayed gastric emptying), headaches, fatigue, dizziness
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14
Q

How is insulin therapy used in type 2 diabetes mellitus? (action, use, examples, SE)

A

Action: replacing insulin made by pancreas to lower blood glucose
Use: poor glucose control despite maximum use of other antidiabetic drugs, or if they are not tolerated/contraindicated
Examples: short/intermediate/long acting
SE: weight gain, altered vision, oedema, injection site reactions, risk of hypoglycaemia

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15
Q

What are the complications of type 2 diabetes mellitus?

A

Macrovascular = increased risk of cardiovascular disease, stroke, and peripheral vascular disease (narrowing of blood vessels -> reduced blood flow -> slow wound healing -> diabetic foot disease)
Microvascular =
- retinopathy (damaged blood vessels of the retina -> vision loss)
- nephropathy (damaged vessels in the kidney -> proteinuria, increased CVD risk)
- neuropathy (nerve damage -> sensory loss, typically glove and stocking distribution, pain, diabetic foot disease, also autonomic neuropathy -> autonomic dysfunction)
HYPEROSMOLAR HYPERGLYCAEMIC STATE

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16
Q

Define hyperosmolar hyperglycaemic state

A

A medical emergency and serious complication of T2DM, characterised by hyperglycaemia and hyperosmolality

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17
Q

What are the risk factors for hyperosmolar hyperglycaemic state?

A

Infection
Inadequate insulin or non-adherence to insulin treatment
New onset of diabetes
Physiological stress (e.g. trauma, surgery)
Drugs (corticosteroids, diuretics)
Other medical conditions (e.g. hypothyroidism, pancreatitis)

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18
Q

What are the signs/symptoms of hyperosmolar hyperglycaemic state?

A

Extreme polydipsia and polyuria
Confusion/reduced mental state
Severe dehydration
Weakness + lethargy
Hypotension
Tachycardia

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19
Q

What are the investigations needed for hyperosmolar hyperglycaemic state?

A
  • Random plasma glucose >30mmol/L
  • Plasma osmolality >320mmol/L
  • Urine dipstick = glycosuria (normal or slightly elevated ketones)
  • U+E = dehydration and AKI - high urea, sodium and potassium
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20
Q

What are the treatments for hyperosmolar hyperglycaemic state?

A
  • Arrange hospital admission
  • ABCDE assessment
  • Rehydrate with 0.9% saline IV
  • Give low dose insulin only if glucose isn’t falling with IV fluids
  • Replace electrolytes (if not corrected by IV fluids)
  • Prophylactic anticoagulation
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21
Q

What are the complications of hyperosmolar hyperglycaemic state?

A

Ischemia or infarction of organs (e.g. MI, CVE)
Seizures or coma
Thromboembolisms
Cerebral oedema (if rehydrated too quickly)
Acute respiratory distress syndrome

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22
Q

Define hypertension

A

Persistently raised arterial blood pressure (clinic readings above 140/90, and ambulatory/home readings above 135/85)

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23
Q

What are the causes of hypertension?

A

Primary hypertension (90%) has no identifiable cause
Secondary hypertension (10%) has a known underlying cause

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24
Q

What are the risk factors for hypertension?

A

Older age
Sex (more likely to be higher in men, but opposite when older)
Diet (high salt)
Lack of exercise
Excessive alcohol
Obesity
Ethnicity
Emotional stress or anxiety
Social deprivation
Family history
Comorbidities (diabetes or kidney disease)

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25
Q

What are the signs/symptoms of hypertension?

A

Usually asymptomatic
Headaches are more common than in the general public
Signs of end organ damage in kidneys (AKI, proteinuria), heart (ACS, LVH), eyes (papilledema, retinopathy)

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26
Q

What are the investigations needed for hypertension?

A
  • blood pressure measurement in clinic
  • ambulatory blood pressure monitoring (or home blood pressure monitoring)
  • asses for target organ damage (check kidney function, HbA1C, ECG, retinopathy)
  • assess cardiovascular risk (measure cholesterol, estimate QRISK score)
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27
Q

What are the stages of hypertension?

A
  • Stage 1: clinic bp of 140/90 - 159/99 and ABPM/HBPM of 135/85 - 149/94
  • Stage 2: clinic bp of 160/100 - 180/120 and ABPM/HBPM of 150/95 or higher
  • Stage 3: clinic systolic bp of over 180 or clinic diastolic bp of over 120
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28
Q

What lifestyle advice should be given to someone with hypertension?

A
  • Encourage healthy diet and regular exercise
  • Avoid excessive caffeine consumption
  • Reduce dietary salt
  • Smoking cessation
  • Reduce alcohol intake
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29
Q

What is the treatment for hypertension?

A

If under 55 or has T2DM…
- step 1 = ACE inhibitor (if not tolerated e.g. due to cough = ARB)
- step 2 = add CCB or thiazide-like diuretic

If over 55 or of black African/Afro-Caribbean origin…
- step 1 = CCB (if not tolerated e.g. due to oedema = thiazide-like diuretic)
- step 2 = add ACE inhibitor, ARB (preferred in black African/Afro-Caribbean origins), or thiazide-like diuretic

For both groups…
- step 3 = add 3rd option
- step 4 = add further diuretic like spironolactone (if potassium<4.5), or a/b-blockers (if potassium>4.5)
- step 5 = specialist advice

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30
Q

What are ACE inhibitors? (example, action, CI, SE)

A
  • Examples: ramipril (ending-pril)
  • Action: stops angiotensin I being converted to angiotensin II, to stop RAAS pathway and lower bp
  • CI: pregnancy
  • SE: cough, renal impairment, angio-oedema, hyperkalaemia, dizziness (hypotension)
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31
Q

What are angiotensin-II receptor blockers (ARBs)? (example, action, CI, SE)

A
  • Examples: losartan (ending -artan)
  • Action: stops effects of angiotensin-II to reduce bp
  • CI: pregnancy
  • SE: renal impairment, angio-oedema, hyperkalaemia, dizziness (hypotension)
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32
Q

What are calcium channel blockers? (example, action, CI, SE)

A
  • Examples: amlodipine (ending -dipine)
  • Action: acts on cardiac muscle to reduce the force of contractions, and on vascular smooth muscle to reduce contraction of arteries
  • CI: heart failure, cardiac outflow obstruction, hepatic/renal impairment, pregnancy
  • SE: GI issues (constipation), peripheral oedema, dizziness (hypotension)
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33
Q

What are thiazide-like diuretics? (example, action, CI, SE)

A
  • Examples: indapamide
  • Action: acts on distal convoluted tubule and collecting ducts to increase salt and water excretion
  • CIs: electrolyte imbalances, renal impairment, pregnancy
  • SE: postural hypotension, increased glucose intolerance, electrolyte imbalances (hypokalaemia), erectile dysfunction, dehydration/thirst/increased urine
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34
Q

What are the causes of secondary hypertension?

A

RENAL
R - renal stenosis, glomerulonephritis
E - endocrine (Cushing’s disease . pheochromocytoma, hyperaldosteronism, corticosteroids, oral contraceptive)
N - neurological (raised ICP)
A - aortic coarctation
L - little people (pregnancy-induced)

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35
Q

What are the complications of hypertension?

A

Heart failure
Coronary artery disease
Myocardial infarction
Stroke
Vascular dementia
Chronic kidney disease
Peripheral arterial disease

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36
Q

Define primary and secondary headaches

A

Primary (not associated with underlying conditions):
- migraine
- tension
- cluster (trigeminal autonomic cephalgia)
Secondary (precipitated by another condition):
- trauma to head/neck
- cranial vascular disorders (stoke, giant cell arteritis)
- intracranial hypertension
- brain malignancy
- substance exposure (CO, alcohol, medication)
- infection (meningitis, encephalitis, abscess)
- psychiatric disorders

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37
Q

What things are asked about in a headache assessment?

A
  • Onset, duration, frequency, pattern
  • Location, spread, severity
  • Associated symptoms
  • Household contacts with similar symptoms
  • Triggers and relieving factors
  • Comorbidities
  • Family history
  • Medications used for symptom relief
  • Impact on daily activities
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38
Q

What examinations are needed for headaches?

A
  • Vital signs
  • General appearance and mental state
  • Extracranial structures (carotids, temporal arteries, sinuses)
  • Neck (range of movement, tenderness, crepitation)
  • Fundoscopy
  • Neurological examination (cranial and peripheral)
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39
Q

What are the red flags for a headache?

A
  • Sudden onset and severe (SAH)
  • New onset (GCA, space-occupying lesion)
  • Progressive or persistent headache (space-occupying lesion)
  • Associated features of fever, impaired consciousness, seizure, neck pain/stiffness (meningitis), papilloedema (space-occupying lesion, intracranial hypertension), new-onset focal neurological deficit, change in personality, (stroke, space-occupying lesion) atypical aura (stroke), dizziness (stroke), vomiting (CO poisoning, space-occupying lesion), visual disturbance (GCA)
  • Contact with similar symptoms (CO exposure)
  • Precipitating factors of head trauma (subdural haematoma), worsened by standing (cerebrospinal fluid leak) or lying (space-occupying lesion), triggered by Valsalva manoeuvre (space-occupying lesion)
  • Comorbidities of immunocompromise (CNS infection), malignancy (metastasis), pregnancy (pre-eclampsia)
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40
Q

What are the features of a migraine?

A
  • Often unilateral and pulsating
  • Associated with photophobia, phonophobia, nausea and vomiting
  • Occurs with or without aura: visual symptoms (zigzag lines, flickering lights), or sensory symptoms (numbness, pins and needles), or atypical aura (motor weakness, double vision, poor balance, decreased consciousness)
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41
Q

What are the features of a cluster headache?

A
  • Severe unilateral orbital, supraorbital, and/or temporal pain
  • Associated with restlessness or agitation
  • Associated with increased lacrimation, nasal congestion, eyelid swelling, forehead/facial sweating/flushing, full sensation in ear
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42
Q

What are the features of a tension headache?

A
  • Bilateral, mild/moderate pain
  • Pressing, tightening, non-pulsating quality, often spread to or from the neck
  • Associated with no more that one of photophobia, phonophobia, or mild nausea
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43
Q

What investigations are needed for headaches?

A

Diagnosis made using ICHD criteria
Fundoscopy
Blood/CSF cultures: exclude CNS infection
CT/MRI: exclude SAH, stroke, space-occupying lesion
ESR/CRP, biopsy: exclude GCA

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44
Q

What are the treatments for migraines?

A

Avoid identified triggers
Drug treatment during attack:
- simple analgesia (NSIAD/paracetamol/aspirin)
- oral triptan (sumatriptan)
- anti-emetic (metoclopramide)
Prophylactic drug treatment:
- propranolol
- topiramate (teratogenic)
- amitriptyline
- non-pharmacological therapies (relaxation, CBT, acupuncture)
- last resort = botulinum toxin type A injections

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45
Q

What are the treatments of cluster headaches?

A

Avoid identified triggers
Acute attack:
- sumatriptan (s/c or nasal spray)
- high flow oxygen in short bursts
Prophylaxis:
- verapamil (calcium channel blocker)

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46
Q

What are the treatments for tension headaches?

A

Acute attack:
- over-the-counter simple analgesia (paracetamol, NSAIDs)
Chronic:
- acupuncture
- CBT/relaxation
- prophylactic amitriptyline

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47
Q

Define dyspepsia

A

A complex of upper GI tract symptoms including upper abdominal pain or discomfort, heartburn, acid reflux, nausea and/or vomiting, caused by GORD, peptic ulcers etc.

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48
Q

What are the risk factors for GORD?

A
  • Stress and anxiety
  • Smoking and alcohol
  • Obesity
  • Trigger foods: coffee/chocolate (reduce LOS tone), fatty foods (delay gastric emptying)
  • Drugs that decrease LOS pressure (NAIDS, steroids, a/b-blockers, anticholinergics, benzos)
  • Pregnancy (hormonal changes decrease LOS pressure)
  • Hiatus hernia (lower LOS tone)
  • Family history
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49
Q

What are the mechanisms causing GORD?

A

Reflux of gastric contents into the oesophagus due to:
- Transient relaxation (reduced tone) of the lower oesophageal sphincter (e.g. drugs, trigger foods)
- Increased intra-gastric pressure (e.g. straining/coughing/pregnancy)
- Delayed gastric emptying (e.g. diabetes, drugs)

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50
Q

What are the clinical features of GORD?

A
  • Predominant symptoms of heartburn and acid reflux
  • Atypical symptoms such as cough, hoarseness, asthma, dental erosions
  • Endoscopic evidence (oesophagitis or non-erosive reflux disease)
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51
Q

What is the management of GORD?

A

Lifestyle changes:
- smoking cessation
- weight loss
- reduce trigger foods/drinks
- eat smaller meals, avoid eating <3h before bed
- reduce alcohol consumption
Pharmacological:
- antacids (e.g. gaviscon)
- PPIs (e.g. lansoprazole)
- H2 blocker (e.g. famotidine)
Surgical:
- laparoscopic fundoplication

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52
Q

What is the mechanism of dyspepsia caused by peptic ulcers?

A

A breach of the epithelium of the gastric or duodenal mucosa that penetrates the muscularis mucosae (confirmed on endoscopy)

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53
Q

What are the risk factors for peptic ulcers?

A
  • H. pylori infection
  • Drugs (NAIDS, steroids, SSRIs, bisphosphonates)
  • Smoking and alcohol
  • Stress
  • Zollinger-Ellison syndrome (overproduction of gastric acid)
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54
Q

What are the clinical features of gastric and duodenal ulcers?

A

Gastric..
- pain 1-2 hours after meals
- aggravated by food
- vomiting is common
- more likely to haemorrhage (as haematemesis)
- weight loss
Duodenal…
- pain 2-4 after meals
- relieved by food
- vomiting not common
- less likely to haemorrhage (as melaena)
- weight gain

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55
Q

What investigations are needed for peptic ulcers?

A

FBC: iron-deficiency anaemia
H. pylori testing (carbon-13 breath test, stool antigen, serology)
Endoscopy (if over 55 or alarm symptoms)

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56
Q

What is the management for peptic ulcers?

A

Lifestyle changes:
- avoid drug causes and food triggers
- smoking cessation and reduce alcohol
- eat smaller meals, avoid eating <3h before bed
- lose weight
Medications (reduce acid + heal ulcers):
- antacid (gaviscon)
- PPIs (lansoprazole)
- H2 blocker (ranitidine)
Treat H. pylori infection (triple therapy):
- PPI + amoxicillin + clarithromycin
Surgical:
- endoscopic intervention to treat bleeding ulcers

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57
Q

What are the red flag symptoms for upper GI cancers?

A
  • Unexplained appetite loss
  • Unexplained weight loss
  • Abdominal mass
  • New onset diabetes (with weight loss, age >60)
  • Back pain (with weight loss, age >60)
  • Jaundice (age >40)
  • Dysphagia
  • Haematemesis/melaena
  • Diarrhoea/constipation, nausea/vomiting (with weight loss, age >60)
  • Dyspepsia (treatment-resistant, weight loss, raised platelets, low haemoglobin, nausea/vomiting age >55)
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58
Q

Define erectile dysfunction

A

Persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance

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59
Q

What are the causes of erectile dysfunction?

A

Vasculogenic:
- cardiovascular disease
- hypertension
- peripheral arterial disease
- hyperlipidaemia
- diabetes
- pelvic surgery
Neurogenic:
- degenerative disorders (Parkinson’s, MS)
- stroke
- spinal cord trauma or disease
- diabetes
Anatomical/structural:
- abnormalities
- prostate/penile cancer
Endocrine:
- diabetes
- primary/secondary hypogonadism
- hyper/hypothyroidism
Psychogenic:
- lack of arousability
- performance anxiety
- relationship problems
Drugs:
- antihypertensives
- diuretics
- antidepressants
- antiepileptics

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60
Q

What is needed to asses erectile dysfunction?

A
  • Ask about psychosexual factors
  • Medical and surgical history (associated conditions and risk factors
  • Physical exam (BMI, genitalia, consider DRE)
  • Blood tests (assess cause, and cardiovascular risk = HbA1C, lipid profile, testosterone, PSA, TFTs)
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61
Q

How is erectile dysfunction managed?

A
  • Lifestyle advice (weight loss, alcohol reduction, smoking cessation, stop cycling)
  • Optimise management of risk factor conditions
  • Psychological therapy
  • PDE-5 inhibitors: sildenafil (Viagra), tadalafil (Cialis)
  • Testosterone replacement (if hypogonadism cause)
  • Specialist treatments (intraurethral suppository or intracavernosal injections, vacuum assisted device, penile implant)
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62
Q

Define LUTS

A

LUTS = lower urinary tract symptoms
Storage:
- frequency
- urgency
- nocturia
- incontinence
Voiding:
- poor flow (slow/splitting/spraying)
- hesitancy
- intermittency
- straining
- terminal dribble
Post-micturition:
- post-micturition dribble
- feeling of incomplete emptying

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63
Q

What are the common causes of LUTS in men?

A
  • Benign prostatic enlargement
  • Neurological conditions (diabetic neuropathy, stroke, MS, dementia)
  • Infection (UTI, STI)
  • Drugs (diuretics, antimuscarinics)
  • Injury/surgery to urethra/prostate/pelvis
  • Cancer (prostate, bladder)
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64
Q

What are the risk factors for LUTS?

A
  • Age
  • Obesity
  • High dihydrotestosterone
  • Diabetes
  • High fasting glucose
  • Inflammation
  • Increased size of prostate
  • Fat and red meat intake
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65
Q

What is needed in an assessment for LUTS?

A
  • Take history of symptoms and possible causes
  • Examine abdomen, genitalia, digital rectal exam
  • Ask patient to complete a urinary frequency-volume chart and/or international prostate symptom score
  • Dipstick urine (for blood, protein, leucocytes, and nitrates)
  • Measure creatinine and eGFR
  • Consider need for PSA (benign prostatic enlargement or prostate cancer)
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66
Q

What is involved in the management of LUTS?

A

Non-pharmacological:
- pelvic floor and bladder training
- advice on fluid intake (adequate amount, timings)
- advice on lifestyle measures (weight loss, diet, exercise, alcohol, caffeine)
- use containment products (absorbent pads/pants, catheters)
Pharmacological:
- alpha-blockers (tamsulosin, alfuzosin)
- if prostate enlarged: 5-alpha reductase inhibitor (finasteride)
- antimuscarinics (oxybutynin)
Specialist:
- catheterisation (intermittent or indwelling, urethral or suprapubic)
- prostate surgery

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67
Q

Describe the pathophysiology of prostate cancer

A
  • 95% are adenocarcinomas
  • Most commonly in peripheral prostate
  • Often multifocal, each foci can differ in genetic mutation, growth rate, and metastasis
  • Most are indolent and slow growing
  • Some are more aggressive and invade local tissue or metastasise (often to bone)
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68
Q

What are the risk factors for prostate cancer?

A
  • Increasing age
  • Black ethnicity
  • Family history
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69
Q

What are the signs/symptoms of prostate cancer?

A
  • LUTS (nocturia, frequency, urgency, hesitancy, retention, terminal dribble)
  • Weight loss/anorexia
  • Erectile dysfunction
  • Lethargy
  • Visible haematuria
  • Lower back or bone pain
  • On examination: hard irregular prostate
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70
Q

What investigations are needed for prostate cancer?

A
  • Consider PSA
  • Refer to suspected cancer pathway (2ww)
  • Secondary care assessment: biopsy + imaging
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71
Q

What can PSA levels indicate?

A

Increased serum PSA can be…
- prostate enlargement
- older age
- infection
- physical causes (vigorous exercise, DRE, catheterisation, prostate biopsy)
- prostate cancer
- normal prostate
Normal serum PSA can be…
- normal prostate
- prostate enlargement
- prostate cancer
- infection
Decreased serum PSA can be…
- obesity
- drugs (5-alpha reductase inhibitors, statins, thiazide diuretics)

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72
Q

Describe epididymo-orchitis

A
  • Inflammation of the epididymis and/or testis
  • Cause: chlamydia/N.gonorrhoea
  • Features: sudden-onset painful swelling, dysuria, fever
  • Treatment: antibiotics, analgesia, draining of abscesses
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73
Q

Describe hydrocele of the scrotum

A
  • Fluid within the tunica vaginalis
  • Cause: patent processes vaginalis, or testis trauma/tumour/infection
  • Treatment: usually resolves spontaneously, may need aspiration or surgery
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74
Q

Describe varicocele of the scrotum

A
  • Dilated blood vessels of pampiniform plexus
  • Features: visible as distended scrotal blood vessels that feels like ‘a bag of worms’, associated with subfertility
  • Treatment: surgery or embolisation
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75
Q

How is diarrhoea defined?

A

Increased stool frequency and volume, and decreased consistency

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76
Q

What pathophysiology contributes to diarrhoea?

A
  • Increased osmotic load in the gut lumen
  • Increased secretion/decreased absorption
  • Inflammation of the intestinal lining
  • Increased intestinal motility
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77
Q

What are the causes of diarrhoea?

A

Infection
IBS
IBD
Colorectal cancer
Drugs (laxatives, antibiotics, chemotherapy)
Food allergy/intolerance
Hyperthyroidism
Pancreatic insufficiency
Faecal impaction (overflow)

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78
Q

What infections commonly cause gastroenteritis?

A
  • Vibrio cholerae: e.g. travelling in south Asia, Africa
  • Escherichia coli: e.g. from animal products
  • Shigella, salmonella, campylobacter: e.g. food poisoning
  • Clostridium difficle: e.g. associated with antibiotic use and hospital admission
  • Norovirus: e.g. outbreaks in care homes, schools, cruise ships
  • Giardia: e.g. parasite from infected water
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79
Q

What are the investigations needed for diarrhoea?

A
  • Faecal sample for microbiology, calprotectin, and blood
  • FBC: anaemia
  • TFTs
  • LFTs
  • U&Es
  • ESR/CRP: raised in inflammation
  • Antibodies for coeliac disease (IgA, tTG, EMA)
  • Sigmoidoscopy/colonoscopy: detect malignancies/inflammation
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80
Q

What are the treatments of diarrhoea?

A
  • Treat the cause
  • Rehydration: oral is best, but IV if vomiting
  • Electrolyte replacement
  • Drugs: codeine phosphate or loperamide, avoid antibiotics unless infective diarrhoea causes systemic symptoms
  • Public health indication: high-risk people (food handlers, healthcare workers, care home residents), food poisoning, outbreaks in community or hospitals
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81
Q

What are the red flag features of colorectal cancer?

A
  • Unexplained weight loss
  • Unexplained or persistent rectal bleeding
  • Abdominal or rectal mass
  • Severe abdominal pain
  • Iron deficiency anaemia
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82
Q

Define irritable bowel syndrome

A

A mixed group of chronic abdominal symptoms often exacerbated by stress, for which no organic cause can be found, classified as a functional gut disorder/disorder of gut-brain-interaction

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83
Q

What are the possible pathophysiological mechanisms of irritable bowel syndrome?

A
  • Abnormal gut-brain interactions
  • Visceral hypersensitivity
  • Motility disturbances
  • Abnormal GI immune function
  • Changes in gut microbiome
  • Abnormal autonomic activity
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84
Q

What are the risk factors for IBS?

A
  • Enteric infection
  • Genetics
  • Inflammation (secondary to IDB)
  • Dietary factors
  • Drugs (antibiotics)
  • Psychological factors (stress, anxiety, depression)
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85
Q

What are the signs/symptoms of IBS?

A
  • Change in bowel habit
  • Altered stool passage (straining, urgency, incomplete evacuation)
  • Abdominal pain or discomfort
  • Abdominal bloating
  • Passing mucus in stools
  • Extraintestinal features: lethargy, nausea, headache, gynaecological/bladder symptoms
  • Alternative conditions have been excluded
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86
Q

What are the investigations needed for IBS?

A
  • FBC, B12, folate: normal (rules out anaemia)
  • CRP/ESR: normal (rules out inflammation/infection)
  • Coeliac serology: normal (rules out coeliac disease)
  • Faecal calprotectin: normal (rules out IBD)
  • Stool microbiology: normal (rules out infection)
  • In women, CA-125: normal (rules out ovarian cancer)
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87
Q

What is involved in the management of irritable bowel syndrome?

A

Non-pharmacological:
- patient education and lifestyle advice (diet, fluid intake, exercise, stress)
- psychological therapies: CBT, gut hypnotherapy
Pharmacological
- for constipation: laxatives
- for diarrhoea: loperamide (antimotility)
- for abdominal pain/spams: mebeverine hydrochloride (antispasmodic) or amitriptyline (2nd line)

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88
Q

Define inflammatory bowel disease

A

A chronic, relapsing-remitting inflammatory disease of the GI tract, categorised as ulcerative colitis or Chron’s disease (or unclassified)

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89
Q

Describe the pathophysiology of ulcerative colitis

A

Diffuse, continuous, superficial inflammation of the large bowel only

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90
Q

Describe the pathophysiology of Crohn’s disease

A

Patchy (skip lesions), full thickness inflammation of anywhere in the GI tract (most commonly terminal ileum)

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91
Q

What are the risk factors for ulcerative colitis?

A
  • Family history
  • Drugs (e.g. NSAIDs)
    *appendicectomy and smoking are protective
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92
Q

What are the risk factors for Crohn’s disease?

A
  • Family history
  • Smoking
  • Infectious gastroenteritis
  • Appendicectomy
  • Drugs (NSAIDs)
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93
Q

What are the signs/symptoms of inflammatory bowel disease?

A
  • Non-specific: fatigue, malaise, anorexia, fever
  • Diarrhoea (blood +/- mucus = UC more likely)
  • Faecal urgency and/or incontinence
  • Nocturnal defecation
  • Abdominal pain (lower left quadrant, may improve after defecation)
  • Abdominal distention/mass
  • Weight loss
  • Perianal fistulae/abscess
  • Extraintestinal: clubbing, arthritis, osteoporosis, mouth ulcers, uveitis, erythema nodosum, ankylosing spondylitis
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94
Q

What are the investigations needed for inflammatory bowel disease?

A
  • FBC: check for anaemia
  • CRP/ESR: raised with inflammation
  • U&E: asses electrolytes and dehydration
  • LFTs: low albumin reflects disease activity
  • TFTs: rule out hyperthyroidism causing diarrhoea
  • Serum ferritin, vit B12 and D, folate: check for nutritional deficiencies due to malabsorption
  • Coeliac serology: rule out coeliac disease
  • Stool microscopy and culture: rule out C. diff and others
  • Faecal calprotectin: raised with inflammation
  • Colonoscopy/endoscopy and biopsy: diagnosis, differentiate between Chron’s and UC, asses severity
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95
Q

What are the treatments of ulcerative colitis?

A
  1. Aminosalicylates (e.g. mesalazine): 1st line for remission induction/maintenance
  2. Corticosteroid (e.g. prednisolone): remission induction if not effective/tolerated with 5-ASA (not for maintenance)
  3. Calcineurin inhibitors (tacrolimus): added to corticosteroids to induce remission if inadequate response to steroids
  4. Immunosuppressants (e.g. thiopurines, or methotrexate 2nd line): maintain remission in more severe cases and if not maintained by 5-ASA
  5. Biologics (anti-TNFs e.g. infliximab): induce remission in severe active disease if conventional therapy is not effective/tolerated
  6. Surgery: colectomy/terminal ileostomy
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96
Q

What are the treatments for Chron’s disease?

A
  1. Corticosteroids (e.g. prednisolone): induce remission, gradually taper dose, not used to maintain remission
  2. Immunosuppressants (e.g. azathioprine, or methotrexate 2nd line): add to steroids, can be used for maintaining remission
  3. Biologics (anti-TNFs, e.g. infliximab): to induce remission in severe active disease or if conventional therapy is not effective/tolerated, and for maintenance
  4. Aminosalicylates (e.g. mesalazine): much less of a role than in UC, only used if steroids are contraindicated/not tolerated
  5. Surgery: colostomy/ileostomy (permeant/temporary)
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97
Q

What are the complications of inflammatory bowel disease

A
  • Psychosocial impact
  • Toxic dilation of the colon (risk of perforation)
  • Bowel obstruction
  • Intestinal strictures
  • Fistulae
  • Anaemia
  • Malnutrition
  • Colorectal cancer
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98
Q

What clinical features are suggested of colorectal cancer?

A
  • Change in bowel habits
  • Rectal bleeding
  • Weight loss
  • Loss of appetite
  • Abdominal pain
  • Anaemia
  • Abdominal/rectal/anal mass
  • Positive FIT
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99
Q

Define diverticular disease

A
  • Diverticular disease is the presence of symptomatic diverticula (outpouching of the gut wall), commonly in the sigmoid/descending colon
  • Diverticulosis is the presence of non-symptomatic diverticula
  • Diverticulitis refers to the inflammation of diverticula (usually due to infection)
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100
Q

Describe the pathogenesis of diverticular disease

A

High intra-luminal pressures (e.g. due to low-fibre diet) prompts the herniation of the mucosa through the muscle layers of the gut at weak points adjacent to penetrating vessels

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101
Q

What are the risk factors for diverticular disease?

A
  • Older age
  • Diet low in fibre or high in red meat
  • Smoking
  • Obesity
  • NSAIDs and opioids
  • Immunosuppression
  • Genetic factors
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102
Q

What are the signs/symptoms of diverticular disease?

A

Pain:
- often lower left quadrant
- intermittent
- triggered by eating
- relieved by passage of stool/flatus
Nausea
Bloating
Altered bowel habits
Rectal bleeding

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103
Q

What are the signs/symptoms of diverticulitis?

A

Pain:
- hypogastrium or lower left quadrant
- constant
Fever
Sudden change in bowel habits
Significant rectal bleeding or mucus in stools
Abdominal mass or distention

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104
Q

What are the investigations needed for diverticular disease/diverticulitis?

A
  • FBC: raised WBC in diverticulitis
  • CRP: raised in diverticulitis
  • Faecal occult blood test
  • Imaging: endoscopy, colonoscopy, CT (confirm diagnosis and exclude other causes)
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105
Q

What are the treatments of diverticular disease?

A
  • Lifestyle advice: high-fibre diet, adequate fluid intake, weight loss, stopping smoking
  • Avoid NSAIDs and opioids
  • Bulk-forming laxatives
  • Simple analgesia (e.g. paracetamol)
  • Antispasmodics (e.g. mebeverine)
  • Surgical resection (occasional)
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106
Q

What are the treatments for diverticulitis?

A

Mild attacks:
- bowel rest (fluid only)
- antibiotics (co-amoxiclav) if systemically unwell
- simple analgesia for pain
Managed in hospital (if pain not managed, oral hydration is not maintained, significant comorbidity)
- IV fluid and antibiotics
- surgical resection/drainage

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107
Q

What are the complications of diverticular disease?

A
  • Perforation
  • Haemorrhage
  • Fistulae
  • Abscesses
  • Obstruction (strictures)
  • Sepsis
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108
Q

Describe the categorisation of lower/upper and complicated/uncomplicated UTIs

A
  • Lower: cystitis, urethritis, epididymo-orchitis, prostatitis
  • Upper: pyelonephritis, ureteritis
  • Uncomplicated: non-pregnant women
  • Complicated: pregnant, men, children, catheterised, immunocompromised, structural abnormalities, recurrent/persistent infection
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109
Q

What are the most common pathogens to cause UTIs?

A

E.coli: > 50% = most common
Proteus: 10-15% (associated with renal stones)
Klebsiella: 10% (hospital/catheter associated)
Staph. saprophyticus: 5-8% (young women)
Pseudomonas: 4% (recurrent UTI/underlying pathology)

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110
Q

What are the risk factors for UTIs?

A
  • Recent instrumentation of the renal tract
  • Abnormality of the genitourinary tract
  • Incomplete bladder emptying (prostatic obstruction)
  • Urinary incontinence
  • Sexual activity
  • Diabetes
  • Pregnancy
  • Immunocompromised
  • Reduced functional status
  • History of UTI
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111
Q

What are the sings/symptoms of lower UTIs?

A
  • Dysuria (discomfort, pain, stinging, burning)
  • Increased frequency and nocturia
  • Visible cloudy urine or haematuria
  • Suprapubic pain
  • New/worsening delirium/lethargy (in >65)
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112
Q

What are the investigations needed for lower UTIs

A
  • Urine dipstick: positive for leukocytes and/or nitrates, +/- red blood cells
  • MSU: for culture and sensitivities
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113
Q

What are the treatments of uncomplicated lower UTIs?

A

Not always necessary to send sample and treat if mild-moderate symptoms
If treated:
- 3 day course of antibiotics (nitrofurantoin 100mg BD)
Adjunctive advice:
- simple analgesia
- increase fluid intake
- void pre – post intercourse
- hygiene

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114
Q

What are the treatments for complicated lower UTIs?

A
  • 7 day course of antibiotics
  • 1st line = nitrofurantoin 100mg BD (cannot be used in pregnancy at term, low renal function, and has side effects, alternative = amoxicillin or trimethoprim)
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115
Q

Define pyelonephritis

A
  • Infection of one or both of the kidneys, usually caused by bacteria from the bladder (a type of upper UTI)
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116
Q

What is the presentation of pyelonephritis?

A
  • Uni/bilateral loin, suprapubic, or back pain
  • Lower UTI symptoms (frequency, dysuria, haematuria, hesitancy)
  • Can have fever, nausea/vomiting, malaise
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117
Q

What investigations are needed for pyelonephritis?

A
  • Urinalysis: + for blood, protein, leukocytes, nitrite
  • MSU: + blood culture
  • CRP/ESR: raised
  • FBC: raised WBCs
  • Imaging (US/CT): identify structural abnormalities
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118
Q

What is the management for pyelonephritis?

A
  • Supportive measures (rest, adequate fluids, analgesia)
  • Admission if signs of sepsis, comorbid, severe dehydration, suspected complications
  • Antibiotics: cefalexin/co-amoxiclav for 7-10 days
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119
Q

Define urolithiasis/renal colic

A

The formation of stones anywhere in the renal tract (most commonly kidneys - renal colic), caused by structural abnormalities, infection, or supersaturated urine (increased calcium oxalate, urate etc.)

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120
Q

What are the signs/symptoms of stones in the urinary tract?

A

Often asymptomatic
Pain
- loin radiating to groin
- unilateral or bilateral
- colicky
- acute onset
- associated nausea/vomiting
UTI symptoms
- dysuria
- urgency
- frequency
- haematuria

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121
Q

What are the investigations needed for stones in the urinary tract?

A
  • Urinalysis (+ve blood, +ve nitrite/leukocytes suggests infection)
  • Bloods: FBC, U&E, calcium, phosphate
  • Imaging: non-contrast CT within 24 hours (US in pregnancy/children)
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122
Q

What is the management for stones in the urinary tract?

A
  • Admission if signs of sepsis, increased risk of AKI, inadequate fluid intake, anuria
  • Analgesia: NSAID, paracetamol, codeine
  • Antiemetics if needed
  • Encourage adequate fluids

Treatment of stone depends on size:
- small/asymptomatic/safe location = watchful waiting
- ESWL (extracorporeal shock wave lithotripsy - fragments stones to facilitate passage)
- PCNL (percutaneous nephrolithotomy - extraction of larger stones)
- ureteroscopy
- nephrectomy (rare)

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123
Q

What causes gout?

A

Hyperuricaemia caused by:
- breakdown of DNA into purines
- dietary purine absorption (beer, shellfish, offal, fructose, red meat)
- reduced excretion in kidney disease
Leads to urate crystal formation, clustering, and propagation
Exacerbated by cold and trauma (affects crystal solubility)
Symptoms caused by inflammatory response to urate deposition in joints

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124
Q

What are the risk factors for gout?

A
  • Comorbidities - CKD, hypertension, diabetes mellitus, hyperlipidaemia, osteoarthritis, myelo/lymphoproliferative disorders
  • Diet - consumption of excess alcohol, sugary drinks, meat, and seafoods
  • Obesity
  • Family history
  • Male sex
  • Menopausal status in women (more common postmenopausal)
  • Older age
  • Drugs (diuretics, aspirin, antihypertensives, cytotoxic)
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125
Q

What are the 4 clinical phases of gout?

A
  1. Asymptomatic hyperuricaemia
  2. Acute gout
  3. Intercritical gout - resolution of first attack with second often occurring within 1 year
  4. Chronic tophaceous gout - deposition of large crystals (tophi) causing irregular firm nodules and chronic joint damage
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126
Q

What are the sings/symptoms of gout?

A
  • Rapid onset of ‘podagra’ of 1st metatarsophalangeal joint (swelling, red and shiny overlying skin, and severe pain)
  • can also affect other joints
  • Low grade fever
  • General malaise
  • Nocturnal symptoms
  • Tophi (hard cutaneous nodules on extensor surfaces of affected joints) - suggest chronic untreated gout
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127
Q

What are the investigations needed for gout?

A
  • Serum uric acid: high, but can be low in acute gout, measure 2-4 weeks after flare up
  • Joint aspiration: strongly negatively birefringent needle shaped crystals on microscopy, culture
  • X-rays (show punched-out lesions, areas of sclerosis, and tophi in later stages)
  • Ultrasound/CT/MRI (identify urate deposition, structural joint damage and inflammation)
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128
Q

What are treatments for acute gout?

A

Nonpharmacological:
- ice packs
- rest and elevation
Pharmacological:
- NSAID +/- paracetamol
- Colchicine
- Corticosteroid (prednisolone): oral, intraarticular, or IM

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129
Q

What is the management for preventing gout?

A

Non-pharmacological:
- healthy and balanced diet (high protein, reduced alcohol, red meat, fructose)
- weight loss
Pharmacological:
- urate lowering therapy = allopurinol or febuxostat (if CI/not tolerated e.g. in CKD)
- gout prophylaxis = colchicine or (NSAID/corticosteroid if CI/not tolerated)

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130
Q

Define rheumatoid arthritis

A

A chronic inflammatory autoimmune disease characterised by symmetrical, deforming, peripheral arthropathy, as well as other extra-articular features

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131
Q

Which joints are most commonly affected by rheumatoid arthritis?

A

Small joints of the hands and feet:
- metacarpophalangeal (MCP)
- proximal interphalangeal (PIP)
- metatarsophalangeal (MTP)
Larger joints (e.g. knees) become involved in later stages
No spinal involvement

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132
Q

What are the signs/symptoms of rheumatoid arthritis?

A
  • Pain (worse at rest, eases with activity)
  • Swelling around joints (boggy feeling)
  • Stiffness of joints (lasting over an hour in the morning)
  • Later joint damage and deformities: e.g. ulnar deviation, swan-neck or Boutonniere deformities of fingers, z-deformity of thumb
  • Systemic features: malaise, fatigue, fever, weight loss
  • Extra-articular features: problems with the lungs, heart, and eyes, osteoporosis, vasculitis, depression, splenomegaly, and nodules
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133
Q

What investigations are needed for rheumatoid arthritis?

A
  • ESR/CRP (raised but not always)
  • FBC (normocytic anaemia of chronic disease and high platelets in active RA)
  • LFTs (mild elevation of alkaline phosphate)
  • Rheumatoid factor (+ve in 60-70% of RA)
  • Anti-CCP antibodies (+ve in 98% of RA, more specific that RF)
  • X-ray (LESS = loss of joint space, erosions, soft tissue swelling, see-through bones (osteopenia))
  • Ultrasound/MRI (detect swelling and erosions in more detail)
134
Q

What are the treatments for rheumatoid arthritis?

A
  • Disease-modifying anti-rheumatic drugs: DMARDs (e.g. methotrexate, sulphasalazine, hydroxychloroquine)
  • Biological agents: anti-TNF (e.g. adalimumab), anti-CD20/B cell (rituximab), JAK inhibitors
  • Steroids: systemic or injections to reduce inflammation
  • NSAIDs: symptom relief but no effect on disease progression
  • Physio and occupational therapy
  • Surgery
135
Q

Define spondyloarthritis

A

A range of inflammatory arthritis conditions, most commonly affecting the spine (axial spondyloarthritis), which can be associated with other inflammatory conditions such as psoriasis, anterior uveitis, and IBD

136
Q

What are the features of spondyloarthritis?

A

SPINEACHE
- Sausage digit (dactylitis)
- Psoriasis (personal/family history)
- Inflammatory back pain
- NSAID (good response)
- Enthesitis
- Arthritis
- Chron’s/colitis
- HLA-B27
- Eye (anterior uveitis)

137
Q

Define osteoarthritis

A

An age-related disorder of a joint, occurring when damage (insult/injury) triggers repair processes leading to structural changes, affecting all the tissues of the joint (most commonly the articular cartilage), initially as asymmetrical monoarthritis

138
Q

What are the risk factors of osteoarthritis?

A
  • Age (cumulative effect of traumatic insult)
  • Female
  • Genetic predisposition
  • Obesity
  • Occupation
  • Local trauma
  • Inflammatory arthritis
  • Low bone density
  • Abnormal biomechanics (hypermobility, congenital hip dysplasia, neuropathic conditions)
139
Q

Which joints are most commonly affected by osteoarthritis?

A

Hand:
- 1st carpometacarpal (CMC) at the base of thumb
- proximal and distal interphalangeal joints (PIP, DIP)
- may have Heberden’s (DIP)/Bouchard’s (PIP) nodes, deviation, fixed flexion/extension
Knee:
- typically bilateral and symmetrical
- may have restricted flexion/extension, antalgic gait, bony swelling, locking/giving way
Hip:
- pain in groin/buttocks/thigh
- may have painful and restricted internal rotation, Trendelenburg’s gait, fixed flexion

140
Q

What are the signs/symptoms of osteoarthritis?

A
  • Pain (may not be present despite X-ray changes, activity related, develops over months or years)
  • Joint stiffness lasting less than 30 mins only
  • Functional impairment (walking, daily living activities)
  • Alteration in gait
  • Joint and bony swelling
  • Limited range of movement
  • Muscle wasting and weakness
141
Q

How is osteoarthritis assessed?

A
  • Ask full history of pain, swelling, and stiffness, including functional limitations
  • Assess for risk factors
  • Ask what treatments have been tried
  • Examine joint for clinical features
  • Consider X-ray (in uncertainty/atypical features, or sudden worsening symptoms)
142
Q

What are the radiological features of osteoarthritis?

A

LOSS
- Loss of joint space
- Osteophyte formation (new bone formation at joint margins)
- Subchondral sclerosis
- Subchondral cysts

143
Q

What are the treatments of osteoarthritis?

A

Non-pharmacological:
- weight loss
- physio/occupational therapy (muscle strengthening, aerobic fitness)
- footwear
- walking aids
Pharmacological:
- topical (NSAIDs)
- oral (NSAIDs, or paracetamol/weak opioids)
- Intra-articular steroid injections
- DMARDs in inflammatory/erosive OA
Surgical:
- arthroscopy
- osteotomy
- arthroplasty (whole joint replacement)
- fusion (usually ankle and foot)

144
Q

Define COPD

A

Chronic obstructive pulmonary disease, characterised by persistent respiratory symptoms (such as breathlessness, cough, and sputum) and airflow obstruction (usually progressive and not fully reversible)

145
Q

What are the risk factors for COPD?

A
  • Smoking
  • Occupational exposures (dusts, fumes, chemicals)
  • Air pollution
  • Genetic factors (alpha-1 antitrypsin)
  • Lung development in-utero/childhood
  • Asthma
146
Q

What are the pathological causes of COPD?

A
  • Bronchitis (clinical = cough, sputum production)
  • Emphysema (histological = destruction of alveolar walls, enlarged air spaces)
  • Chronic inflammation caused by exposure to noxious particles or gases (usually tobacco smoke but also from environmental and occupational exposures)
147
Q

What are the signs/symptoms of COPD?

A

Breathlessness (progressive, on exertion)
Cough (recurrent)
Sputum production
Frequent LRTI
Wheeze
Accessory muscle use
Hyperinflation of chest
Cyanosis
Cor pulmonale (raised JVP, peripheral oedema)
Weight loss

148
Q

What investigations are needed for COPD?

A
  • Spirometry: FEV1/FVC ratio < 0.7 or 70% (little or no reversibility after bronchodilator)
  • CXR: hyperinflated lungs, excludes other causes
  • Sputum culture (if purulent and persistent)
  • Serial home peak flow measurements: to exclude asthma
  • CT: more detail of structural damage (bronchial wall thickening, increased air spaces)
  • Serum alpha-1-antitrypsin: detects deficiency
    FBC: may show anaemia, high platelets
149
Q

What are the treatments for COPD?

A

Non-pharmacological:
- smoking cessation
- physiotherapy
- pulmonary rehabilitation
- psychological support
- optimise comorbidities
- offer vaccinations
Pharmacological:
- 1st = SABA (e.g. salbutamol) or SAMA (e.g. ipratropium) as a reliever
- 2nd + LABA (e.g. salmeterol) and LAMA (e.g. tiotropium)
- 3rd + inhaled corticosteroid (e.g. beclomethasone) if asthmatic features
- 4th = refer to specialist (oral steroids, theophylline, mucolytics, prophylactic antibiotics, long-term oxygen)

150
Q

What features suggest an acute exacerbation of COPD?

A
  • Worsening breathlessness
  • Increased sputum volume and purulence
  • Fever without obvious source
  • URTI
  • Increased respiratory/heart rate
  • Pursed lip breathing/use of accessory muscles
  • Confusion/drowsiness
  • Reduction in ALDs
  • New onset cyanosis or peripheral oedema
151
Q

What are the treatments of an acute exacerbation of COPD?

A
  • Consider need for hospitalisation (oxygen, IV steroids/antibiotics, intubation)
  • Increased dose of relievers
  • Nebulised bronchodilators (salbutamol + ipratropium)
  • Oral prednisolone 30mg for 5 days
  • Antibiotics (e.g. amoxicillin 500mg TDS for 5 days)
152
Q

What symptoms are suggestive of lung/pleural cancer?

A
  • Cough
  • Chest pain
  • Breathlessness
  • Recurrent chest infections
  • Persistent hoarse voice
  • Haemoptysis
  • Finger clubbing
  • Fatigue
  • Weight loss
  • Lymphadenopathy
  • Loss of appetite
153
Q

What investigations are needed for lung/pleural cancer?

A
  • FBC: anaemia, high platelets
  • CXR
  • 2ww referral
154
Q

Define asthma

A

A chronic respiratory condition associated with inflammation and airway hyper-responsiveness, leading to episodic bronchospasm due to triggers

155
Q

What are the risk factors for asthma?

A
  • Personal/family history of atopic disease (asthma, eczema, allergic rhinitis)
  • Male sex (children)/female sex (adult)
  • Premature birth/low birth weight
  • Respiratory infections in infancy
  • Obesity
  • Social deprivation (exposure to damp housing, pollution, smoking)
  • Workplace exposures (dust, spray paints etc.)
  • Exposure to allergens at home (pets, feather pillows/duvets etc.)
156
Q

What are the features of asthma?

A
  • Episodic symptoms of (cough, breathlessness, wheeze, chest tightness)
  • Diurnal variation (worse at night/early morning)
  • Exacerbated by exercise, infection, exposure to cold air or allergens
  • Occupational asthma: symptoms improve when not at work
157
Q

What investigations are needed for asthma?

A
  • Spirometry: FEV1/FVC < 0.7 (obstructive), reversible improvement by 12% or increase in volume of at least 200ml after using bronchodilator
  • Peak flow meter: taken x2 daily for 1-2 weeks, shows 20% diurnal variability
  • FeNO testing (detects eosinophilic airway inflammation): 40 ppb or more
  • Detect allergens: measure total/specific IgE in blood, or skin prick testing
158
Q

What are the treatments for asthma?

A

Non-pharmacological:
- smoking cessation
- weight loss
- physio/speech therapy
- allergen/air pollutant avoidance
Pharmacological:
- 1st = SABA (e.g. salbutamol) reliever inhaler
- 2nd + low-dose inhaled corticosteroid (e.g. beclomethasone)
- 3rd + leukotriene receptor antagonist (e.g. montelukast)
- 4th + LABA (e.g. salmeterol) +/- LTRA
- 5th = change to maintenance and reliever therapy (ICS + fast-acting LABA)
- 5th = specialist input (+ oral steroids/theophylline/biologics)

159
Q

How do the treatments for asthma/COPD work?

A
  • beta agonists = relax bronchial smooth muscle by increasing cAMP, acting within minuets (short acting) or overnight (long acting)
  • corticosteroids = decrease bronchial mucosal inflammation, acting over days
  • leukotriene receptor antagonists = block the effects of cysteinyl leukotrienes in the airways to reduce inflammation
  • muscarinic antagonists = decrease bronchial smooth muscle spasm, can be short or long acting (used for COPD not asthma)
  • theophylline = inhibits phosphodiesterase, so decreases bronchoconstriction by increasing cAMP
  • biologics (e.g. omalizumab) = anti-IgE monoclonal antibody
160
Q

How is the severity of an acute exacerbation of asthma graded?

A
  • Moderate: PEFR > 50-75% best, normal speech and no acute features
  • Acute severe: PEFR 33-50% best, or RR > 25, or PR > 110, or inability to complete sentences/use of accessory muscles
  • Life threatening: PEFR < 33% best, or O2 < 92%, or altered consciousness/poor respiratory effort/hypotension/silent chest
161
Q

What are the treatments for an acute exacerbation of asthma?

A
  • Nebulised bronchodilators (e.g. salbutamol + ipratropium if severe)
  • Oxygen (if low sats)
  • Oral steroids (prednisolone)
  • Antibiotics (only if infective cause)
  • Specialist: IV magnesium sulphate, steroids, intubation/ventilation
162
Q

Define occupational lung disease?

A

A wide-range of respiratory conditions caused by inhaling a harmful substance in the workplace or exposures which may aggravate the symptoms of any pre-existing lung disease

163
Q

What are the most common occupational lung diseases?

A
  • Asthma
  • Non-malignant pleural disease
  • Pneumoconiosis
  • Inhalation accidents
  • Bronchitis/emphysema
  • Lung cancer
  • Mesothelioma
164
Q

Define bronchiectasis?

A

Chronic inflammation of the bronchi and bronchioles leading to permanent dilatation and thinning of these airways

165
Q

What are the causes of bronchiectasis?

A
  • Previous severe lower respiratory tract infection (pneumonia, pertussis, TB, influenza)
  • Aspiration or inhalation injury
  • COPD or asthma
  • Disorders of mucociliary clearance (cystic fibrosis, primary ciliary dyskinesia)
  • Associated conditions: connective tissue disorders (rheumatoid arthritis), IBD
166
Q

What are the signs/symptoms of bronchiectasis?

A
  • Persistent cough
  • Copious purulent sputum
  • Haemoptysis
  • Dyspnoea
  • Wheeze
  • Coarse crackles
  • Finger clubbing
  • Systemic: fever, fatigue, weight loss
167
Q

What are the investigations needed for bronchiectasis?

A
  • Sputum culture: often colonise Pseudomonas aeruginosa, or S. aureus
  • FBC: raised WBC in infection
  • CXR: exclude other pathology, may show abnormalities in severe disease
  • Spirometry: asses airflow obstruction, identify co-existent COPD/asthma
  • High-resolution CT: DIAGNOSTIC, asses extent and distribution of disease
  • Immunoglobulins: test for IgG, IgA, and IgM deficiency
  • Bronchoscopy: exclude obstruction, obtain sample for culture
  • Other tests: CF testing, IgE/skin prick test for Aspergillus, RF/anti-CPP/ANCA for RA
168
Q

What are the treatments for bronchiectasis?

A

Physiotherapy:
- airway clearance
- exercise
Antibiotics:
- for acute exacerbations, depends on sensitivities (e.g. Pseudomonas = oral ciprofloxacin)
- long-term, for recurrent exacerbations, depends on sensitivities
Bronchodilators:
- beta agonists (e.g. nebulised salbutamol)
- muscarinic antagonists
- theophylline
- corticosteroids (only if also asthmatic)
Surgery: (in severe disease)
- resection

169
Q

What ABG results are seen in type 1 respiratory failure?

A

O2 = low
CO2 = normal/low
HCO3 = normal

170
Q

What ABG results are seen in type 2 respiratory failure?

A

O2 = low
CO2 = high
HCO3 = normal (acute), high (chronic)

171
Q

What are some common causes of type 1 respiratory failure?

A

Pneumonia
Pulmonary embolism
Altitude
Lung fibrosis

172
Q

What are some common causes of type 2 respiratory failure?

A

Obstruction (COPD/severe asthma)
Muscle weakness (motor neuron disease)
Reduced respiratory drive (e.g. opiate SE)
Obesity

173
Q

What are the common causes of upper respiratory tract illnesses?

A

Viral illness:
- Rhinoviruses (45-50%)
- Influenza A virus (25-30%)
- Coronaviruses (10-15%)
- Adenoviruses (5-10%)
- Respiratory Syncytial viruses (5%, immunocompromised or children )

174
Q

Describe pharyngitis and laryngitis (infectious)

A
  • Symptoms: sore throat, runny nose, cough, headache, difficulty swallowing, fever, swollen lymph nodes, hoarse voice
  • Time course: last 3-5- days but sometimes longer
  • Viral causes (most common): rhinovirus, adenovirus, EBV, acute HIV
  • Bacterial causes: most commonly Strep. pyogenes, also Strep. pneumoniae, H. influenzae, Corynebacterium diphtheriae, Neisseria gonorrhoea, Mycoplasma pneumoniae
  • Diagnosis: throat swab for PCR or culture
175
Q

What are the chronic causes of laryngitis?

A
  • Smoking
  • Allergies
  • Acid reflux
  • Autoimmune disorders (rheumatoid arthritis, sarcoidosis)
  • TB
176
Q

What is the treatment of upper respiratory tract infections?

A

Viral:
- vocal rest
- high fluid intake
- paracetamol
- home remedies (e.g. tea and honey)
Bacterial:
- depends on causes/sensitivities etc.
- 1st line amoxicillin
- also clarithromycin

177
Q

Describe bronchitis

A
  • Inflammation of the bronchi epithelium due to lower respiratory tract infection
  • Causes: mostly viral
  • Symptoms: cough (1-3 weeks), SOB, wheeze, runny nose, sore throat, fever
  • Diagnosis: viral swab for PCR, CXR = normal
  • Treatment: usually none (self-limiting), antibiotics if bacterial
178
Q

Define pneumonia

A

Inflammation of the lung parenchyma caused by infections (usually bacteria), categorised as community-acquired (CAP) or hospital-acquired (HAP)

179
Q

What are the most common causes of community-acquired pneumonia?

A
  • Streptococcus pneumoniae (most common)
  • Haemophilus influenzae
  • Moraxella catarrhalis
  • Strep. pyogenes
  • Staphylococcus aureus
  • Atypical (Mycoplasma pneumoniae, Legionella, Chlamydia)
  • Viruses (influenza A/B, RSV, coronaviruses)
180
Q

What are the signs/symptoms of pneumonia?

A

Local:
- cough
- sputum (rusty sputum suggests S. pneumoniae)
- shortness of breath
- pleuritic chest pain
- tachypnoea
- signs of consolidation (reduced expansion, dull percussion, increased vocal resonance)
Systemic:
- malaise
- weakness
- fever, sweats, rigors
- tachycardia
- hypotension
- hypoxia, cyanosis

181
Q

What are the red flags for a respiratory infection?

A
  • Delirium/confusion
  • Renal impairment (high urea)
  • Increased oxygen demand (high resp rate, high lactic acid from anaerobic respiration)
  • Low blood pressure
    *all signs of sepsis
182
Q

What is the CURB65 score?

A

Asses the severity of community-acquired pneumonia, predicts mortality, and need for admission
One point for each:
- confusion
- respiratory rate > 30/min
- blood pressure < 90/60
- age > 65
0 = mild
1-2 = moderate
3-4 = severe

183
Q

What is the empirical antibiotic treatment for pneumonia?

A

Mild severity (CURB65 = 0):
- oral amoxicillin or clarithromycin if allergic
Moderate severity (CURB65 = 1-2):
- oral amoxicillin + clarithromycin
Severe (CURB65 = 3-5):
- IV co-amoxiclav/cefuroxime + clarithromycin

184
Q

How is pneumonia prevented?

A

Pneumococcal vaccination to…
- adults over 65
- infants
- immunocompromised
- co-morbidities

185
Q

Describe the copper IUD (method, time course, SE)

A
  • Method: prevents fertilisation and implantation of egg in the womb
  • Time course: 5-10 years
  • Unwanted effects: periods may become heavier or more painful, higher risk of ectopic pregnancy, insertion risk
186
Q

Describe levonorgestrel-releasing IUS (Mirena coil) (method, time course, SE)

A
  • Method: slowly releases progesterone (prevents ovulation and implantation of egg)
  • Time course: 5-8 years, effective immediately if started in days 1-5, or after 7 days if not
  • Unwanted effects: can have irregular bleeding, hormonal effects (acne, mood swings, breast tenderness), higher risk of ectopic pregnancy, insertion risk
187
Q

Describe the progesterone injections (Depo) (method, time course, SE)

A
  • Method: progesterone inhibits ovulation
  • Time course: repeat every 8-12 weeks, effective immediately if started in days 1-5, or after 7 days if not
  • Unwanted effects: irregular or persistent periods, may gain weight, can cause osteoporosis, can take up to 1 year after stopping to become fertile
188
Q

Describe the contraceptive implant (method, time course, SE)

A
  • Method: slowly releases progesterone (inhibits ovulation)
  • Time course: lasts 3 years, effective immediately if started in days 1-5, or after 7 days if not
  • Unwanted effects: 1/3 have heavier periods, 1/3 have irregular periods, hormonal changes (acne, mood swings, breast tenderness)
189
Q

Describe the progesterone-only pill (method, time course, SE)

A
  • Method: progesterone inhibits ovulation
  • Time course: no limit on course duration, effective after 48 hours
  • Unwanted effects: 1/3 have heavier periods, 1/3 have irregular periods, hormonal changes (acne, mood swings, breast tenderness)
190
Q

Describe the combined oral contraceptive pill (method, time course, SE)

A
  • Method: progesterone (inhibits ovulation) and oestrogen (maintains endometrial thickness)
  • Time course: no limit on course duration, effective immediately if started in days 1-5, or after 7 days if not
  • Unwanted effects: increased risk of blood clots and breast cancer, hormonal changes (acne, mood swings, breast tenderness)
191
Q

What screening questions are needed before starting the combined oral contraceptive pill?

A
  • Personal/family history of blood clots/clotting disorders
  • Personal/family history of breast cancer
  • Check BMI (CI in > 35)
  • Check smoking status (CI in smoker aged over 35)
  • Check BP (risk of increased BP on pill, CI in uncontrolled hypertension)
  • Ask if they have a history of migraines with aura (CI in severe migraines, or under 25)
192
Q

Describe eczema

A
  • A chronic inflammatory skin condition due to defects in the normal continuity of the skin barrier
  • Affects people of all ages but frequently presents in early childhood
  • Characterised by dry, red, itchy patches of skin on the flexor surfaces that is episodic with flares and remission
193
Q

What are the associations of eczema?

A
  • Asthma
  • Hay fever
  • Food allergies
  • Family history
194
Q

What are some triggers of eczema?

A
  • Irritant allergens (soap/detergents)
  • Irritant clothing (wool/silk)
  • Skin infections (staph. aureus)
  • Contact allergens (medications/perfumes)
  • Inhaled allergens (pollen/pets)
  • Hormonal triggers (premenstrual/pregnancy)
  • Climate (winter/sweating)
  • Concurrent illness (stress/ill health)
  • Dietary factors (associated food allergy)
195
Q

How is the severity of eczema categorised?

A
  • Clear: normal skin, no evidence of active eczema
  • Mild: areas of dry skin and infrequent itching (w/wo redness)
  • Moderate: areas of dry skin, frequent itching, redness (w/wo excoriation or local skin thickening)
  • Severe: widespread areas of dry skin, incessant itching, and redness (w/wo excoriation, extensive skin thickening, bleeding, oozing, cracking)
  • Infected: eczema that is weeping, crusted, with pustules, fever or malaise
196
Q

How is eczema managed?

A
  • Maintenance: as often as possible, generous amounts
  • Flares: short-course steroids, sparing amounts
  • Emollients (E45, diprobase, oilatum, aveeno)
  • Soap/shampoo substitutes
  • Topical steroids
  • Antihistamine for itch (e.g. cetirizine)
  • Others: systemic immunosuppressants, topical tacrolimus, bandages
197
Q

Describe the steroid creams used in dermatology

A

From weakest to strongest:
- hydrocortisone (0.5-2.5%)
- clobestaone (eumovate)
- betamethasone (betnovate, or fucibet with antibiotic)
- mometasone (elocon - mainstay treatment of eczema from neck down)
- clobetasol (dermovate, only on thick skin)

198
Q

Describe bacterial infected eczema

A
  • Signs/symptoms = weeping, pustules, crusts, rapidly worsening eczema, fever, and malaise
  • Most common organism = staphylococcus aureus
  • Treatment = flucloxacillin (clarithromycin if allergic)
199
Q

Describe eczema herpeticum

A
  • Presentation: widespread, painful, vesicular rash with systemic symptoms (fever, lethargy, lymphadenopathy)
  • Causing organisms: herpes simplex virus, varicella zoster virus
  • Management: acyclovir
200
Q

Define psoriasis

A

Systemic, immune-mediated, inflammatory skin disease, typically with a chronic relapsing-remitting course, characterised by well-defined, erythematous, scaly skin lesion, and may have nail and joint involvement

201
Q

What is the management of psoriasis?

A
  • Lifestyle advice; smoking cessation, weight loss, reduce stress
  • Emollients (creams, lotions, ointments)
  • Topical corticosteroids (to only treat localised areas, for no longer than 8 weeks in the same areas)
  • Vitamin D preparation (e.g. dovobet - contains betamethasone and vitamin D analogue)
  • Coal tar preparation
  • Specialist treatment: phototherapy, topical calcineurin inhibitors, systemic therapy, biologic therapy
202
Q

What are the different forms of psoriasis?

A
  • Chronic plaque psoriasis: most common, often affects extensor surfaces of elbows/knees, trunk, or scalp, ranges from mild to very extensive
  • Scalp psoriasis: often the first or only site, can have very thick plaques, can have alopecia
  • Nail psoriasis: nail pitting, discolouration, onycholysis (detachment from nail bed)
  • Palmoplantar psoriasis: lesions on the palms and/or soles, associated thickening of skin, can cause painful fissures
  • Guttate psoriasis: widespread small scattered papules, particularly on trunk and limbs, first occurs after streptococcal infection
  • Flexure (inverse) psoriasis: affects skin folds (e.g. groin, axillae, sacral/gluteal cleft), well-defined and itchy with little/no scaling
  • Pustular psoriasis: generalised or localised, rapidly developing widespread pustules with systemic illness, may or may not be preceded by another form, medical emergency
  • Erythrodermic psoriasis: widespread and affecting more than 90% of body surface area, may or may not be preceded by another form, can cause systemic illness, medical emergency
203
Q

What are some potential triggers of psoriasis?

A
  • Streptococcal infection
  • Drugs (NSAIDs, ACEi, beta-blockers, antibiotics, lithium, anti-malarial drugs)
  • UV light exposure
  • Trauma (scratching, burns, surgery, tattoos)
  • Hormonal changes (puberty, post-partum, menopause)
  • Psychological stress
  • Smoking and alcohol
  • Obesity
204
Q

What conditions are associated with psoriasis?

A
  • Inflammatory arthritis
  • Metabolic syndrome (obesity, hyperlipidaemia, hypertension, T2DM, NAFLD)
  • Ischemic heart disease
  • Inflammatory bowel disease
  • Anxiety and depression
  • Venous thromboembolism
  • Lymphoma
  • Coeliac disease
  • Ophthalmic conditions (e.g. uveitis)
205
Q

Describe the childhood vaccination program

A
  • 8 weeks: 6-in-1 (diphtheria, tetanus, pertussis, polio, HiB, HepB), meningococcal B, rotavirus
  • 12 weeks: 6-in-1, pneumococcal, rotavirus
  • 16 weeks: : 6-in-1, meningococcal B
  • 1 year: HiB, meningococcal B and C, pneumococcal, MMR
  • 2-11 years: influenza each year from September
  • 3 years and 4 months: diphtheria, tetanus, pertussis, polio, MMR
  • 12-13 years (school year 8): HPV
  • 14 years (school year 9): diphtheria, tetanus, polio, meningococcal A, C, W, Y
206
Q

What are the antibiotics and antifungals used for skin infections?

A

Antibiotics:
- flucloxacillin
- clarithromycin

Antifungals:
- clotrimazole (canesten - genital)
- miconazole (daktarin - athletes foot)
- fluconazole (oral - if resistant to topicals)

207
Q

What percentage level of vaccination is needed for herd immunity, and what are the current UK trends and targets?

A
  • Level needed for herd immunity = 90%
  • UK target = 95%
  • Current trend = decreasing, none above 95%, some below 90%
208
Q

What are the complications of a child not being vaccinated?

A
  • They have an increased risk of life-threatening conditions (meningitis, measles, polio)
  • They are putting other people at risk (immunocompromised, very young/elderly)
  • The community infection risk increases with the more people who are unvaccinated
209
Q

Describe the rash appearance and additional symptoms of meningitis

A
  • Rash = non-blanching, purpuric or petechial, mostly on trunk/extremities
  • Symptoms = fever, neck stiffness, headaches
210
Q

Describe the rash appearance and additional symptoms of measles

A
  • Rash = erythematous maculopapular, begins on face/behind ears then spread over trunk/extremities, also Koplik spots (white papules on oral mucosa)
  • Other symptoms = cough, coryza, conjunctivitis, fever, malaise
211
Q

Describe the rash appearance and additional symptoms of rubella

A
  • Rash = light-pink/red maculopapular, often not as widespread as measles, also Forchheimer spots (petechiae on soft palate)
  • Other symptoms = tender/swollen glands, slight fever/malaise
212
Q

Describe the rash appearance and additional symptoms of scarlet fever

A
  • Infection = strep. A
  • Rash = erythematous, pin-point rash, rough like sand paper, also Pastia lines (linear rash in skin folds), white/strawberry tongue
  • Other symptoms = sore throat, fever, swollen/tender lymph nodes, peeling extremities
213
Q

Describe the rash appearance and additional symptoms of ‘slapped check’

A
  • Infection = parvovirus B19
  • Rash = bright red cheeks, then lace-like rash on trunk/extremities, can last weeks
  • Other symptoms = mild fever, flu-like illness
214
Q

Describe the rash appearance and additional symptoms of urticaria/hives

A
  • Rash = erythematous, superficial swelling (wheals), itching/burning
  • Caused by histamine reaction to allergies, viral/bacterial infection, etc.
215
Q

Describe the rash appearance and additional symptoms of roseola

A
  • Infection = herpes virus
  • Rash = rose-pink, raised, usually start on trunk after fever has resolved
  • Other symptoms = high fever, upper respiratory symptoms
216
Q

Describe the rash appearance and additional symptoms of impetigo

A
  • Infection = commonly staph. aureus
  • Rash = red/yellow, macule progressing to pustules/vesicles, crusted edges, may be weeping, often on face or extremities
  • Other symptoms = none
217
Q

Describe the rash appearance and additional symptoms of Kawasaki disease

A
  • Cause = autoimmune vasculitis
  • Rash = erythematous maculopapular, strawberry tongue, red cracked lips, red/swollen hands/feet with later skin flaking
  • Other symptoms = persistent fever for over 5 days, unilateral large lymph nodes, conjunctivitis
218
Q

Describe the rash appearance and additional symptoms of chicken pox

A
  • Infection = varicella zoster virus
  • Rash = red papules progressing to vesicles, itchy, often begins of trunk/face, spreads rapidly, clears after 1-3 weeks but can leave scars
  • Other symptoms = fever, cold-like symptoms, vomiting, diarrhoea
219
Q

Describe the rash appearance of molluscum

A
  • Raised ‘pearl’ lesion, small white dimple in centre
  • May have a secondary infection and require antibiotics, otherwise self limiting
220
Q

Describe the rash appearance and additional feature of hand foot and mouth disease

A
  • Infection: commonly coxsackie virus A16
  • Rash: progression from pink macules to small oval blisters on tops/palms/soles of hands and feet, and in/around the mouth
  • Additional features: fever, lethargy, sore throat
221
Q

Describe the rash appearance and additional features of shingles

A
  • Infection: reactivation of varicella zoster virus
  • Rash: vesicular or pustular rash, dermatomal distribution, unilateral (cut off at midline)
  • Additional features: localised pain, fever, headaches, local lymph node enlargement
222
Q

How are skin lesions assessed for melanoma?

A

ABCDE(FG for nodular melanoma)
A - asymmetry (not symmetrical)
B - border (irregular)
C - colour (multipigmented, or very dark)
D - diameter (larger than 6mm)
E - evolving (changing in size, shape, colour, elevation)
F - firm
G - growing rapidly

223
Q

Describe the skin lesion seen in actinic keratosis (and treatment)

A
  • Found on sun damaged skin (e.g. scalp, face, back on hands)
  • Thickened scaly plaques, can be red, skin coloured, white or pigmented
  • If becomes ‘coned’ or ‘horned’ with a tender base, suspicion of underlying squamous cell carcinoma
  • Often treated with diclofenac (anti-inflammatory), or photodynamic therapy
224
Q

Describe the skin lesion seen in seborrhoeic keratosis

A
  • Aging related warty lesion
  • ‘Stuck on’ and well demarcated, raised or flatter, smooth or warty surfaces, can be skin coloured, brown, black, or mixed colours
  • Often fragile and crusty
225
Q

Describe the skin lesion seen in basal cell carcinoma

A
  • Locally invasive skin tumour, mostly seen on sun exposed areas
  • Slow growing plaque or nodule, can be skin coloured, pink, pigmented
  • Most common type is nodular: raised shiny edge with central depression/ulceration, prominent blood vessels
226
Q

What is the feverPAIN criteria?

A

Criteria for prescribing antibiotics for a sore throat, 1 point given for:
- Fever (in last 24 hours)
- Purulence (pus on tonsils)
- Attend rapidly (within 3 days of onset)
- Inflamed tonsils (severely)
- No cough or coryza
Higher score = more likely to be bacterial cause

227
Q

What are the causes of hyperthyroidism?

A

Primary: abnormal overproduction of thyroid hormones / increased thyroid function
- grave’s disease (autoimmune) = 75% of hyperthyroidism
- toxic multinodular goitre
- toxic adenoma
- metastatic follicular thyroid cancer
- iodine excess (e.g. contrast media)
Secondary: abnormal overproduction of TSH
- TSH-secreting pituitary adenoma

228
Q

What are the risk factors for hyperthyroidism?

A
  • Female sex
  • Smoking
  • Family history
  • Other autoimmune conditions
  • Low or sudden increase in iodine intake
229
Q

What are the signs/symptoms of hyperthyroidism?

A
  • Weight loss
  • Hyperphagia (increased appetite)
  • Tachycardia
  • Sweating
  • Heat intolerance
  • Diarrhoea
  • Menstrual disturbances
  • Reduced libido
  • Tremor
  • Irritability
  • Anxiety/restlessness
  • Lid lag/retraction/eye bulging in Graves disease
230
Q

What investigations are needed in hyperthyroidism?

A
  • TFTs = high T4/T3, low TSH (secondary = high for both)
  • Thyroid antibodies = TSH-receptor Abs or thyroid peroxidase Abs (indicate Grave’s disease)
  • US of neck = image enlargement or nodularity if malignancy is suspected
231
Q

What are the treatments for hyperthyroidism?

A

Pharmacological:
- beta-blockers (symptom control)
- antithyroid drugs (e.g. carbimazole - blocks T4 synthesis)
Specialist treatments:
- radioiodine = radiation damages DNA of thyroid cells, first line in Grave’s disease
- surgery = usually total thyroidectomy

232
Q

What causes hypothyroidism?

A

Primary: abnormal underproduction of thyroid hormones / decreased thyroid function
- hashimoto’s thyroiditis (autoimmune: inflammation -> goitre)
- primary atrophic hypothyroidism (autoimmune: no goitre)
- iodine deficiency (dietary, common cause world wide)
- drugs (anti-thyroids, iodine, lithium)
- post-thyroidectomy/radioiodine
- postpartum hypothyroidism
Secondary: abnormal low TSH production
- pituitary/hypothalamic dysfunction

233
Q

What are the risk factors for hypothyroidism?

A
  • Female sex
  • Family history
  • Other autoimmune conditions
  • Tuner’s or Down’s syndrome
  • Radiation/surgery to head or neck
  • Pregnancy
234
Q

What are the signs/symptoms of hypothyroidism?

A
  • Weight gain
  • Bradycardia
  • Cold intolerance
  • Constipation
  • Menstrual disturbances/infertility
  • Non-specific weakness/fatigue
  • Dry skin/hair loss
  • Depression
  • Impaired concentration/memory
235
Q

What investigations are needed for hypothyroidism?

A
  • TFTs = low T4/T3, high TSH (secondary = low for both)
  • Thyroid antibodies = thyroid peroxidase Abs (indicate autoimmune cause)
  • US of neck: image enlargement or nodularity if malignancy is suspected
  • Consider also checking for pernicious anaemia, diabetes, coeliac disease
236
Q

What is the treatment for hypothyroidism?

A

Pharmacological:
- synthetic T4 (levothyroxine)
Specialist input if:
- suspected secondary cause
- associated endocrine disease
- goitre, nodule, or structural changes
- female and planning pregnancy
- atypical TFTs

237
Q

Describe type 1 diabetes

A
  • Insulin deficiency causing persistent hyperglycaemia
  • Caused by autoimmune destruction of beta-cells of the pancreas
  • Usually presents aged 5-15 but can be any age
238
Q

What are the risk factors for type 1 diabetes?

A
  • Genetic (a heritable polygenic disease)
  • Environmental (diet, vitamin D deficiency, early-life exposure to certain viruses)
  • Personal and family history of autoimmune diseases
239
Q

What are the signs/symptoms of type 1 diabetes mellitus?

A
  • Polydipsia (increased thirst)
  • Polyuria (increased urination)
  • Weight loss (BMI < 25)
  • Excessive tiredness
  • May present with DKA (+ vomiting, abdominal pain, lethargy/confusion, rapid/deep breathing)
240
Q

What investigations are needed for type 1 diabetes mellitus?

A

Random plasma glucose > 11mmol/L
Fasting plasma glucose > 7mmol/L

241
Q

What are the treatments of type 1 diabetes mellitus?

A

Insulin (or analogues): short-acting (4-6h) to long-acting (12-24h)
Different regimens…
- multiple injection basal-bolus = short-acting before meals + once (or more) daily long-acting
- mixed (biphasic) = 1/2/3 injections of short/intermediate mix of insulin
- continuous subcutaneous infusion (insulin pump) = programmed to deliver insulin through needle/cannula, gives personalised basal rate + higher infusion at meal times

242
Q

What are the complications of type 1 diabetes mellitus?

A

Macrovascular = increased risk of cardiovascular disease, stroke, and peripheral vascular disease (narrowing of blood vessels -> reduced blood flow -> slow wound healing -> diabetic foot disease)
Microvascular =
- retinopathy (damaged blood vessels of the retina -> vision loss)
- nephropathy (damaged vessels in the kidney -> proteinuria, increased CVD risk)
- neuropathy (nerve damage -> sensory loss, typically glove and stocking distribution, pain, diabetic foot disease, also autonomic neuropathy -> autonomic dysfunction)
DIABETIC KETOACIDOSIS

243
Q

Describe diabetic ketoacidosis

A

A medical emergency and serious complication of T1DM, characterised by…
- hyperglycaemia
- raised plasma ketones
- metabolic acidosis

244
Q

What are the causes of diabetic ketoacidosis?

A
  • Treatment errors (stopped/reduced insulin dose)
  • Infection/illness (e.g. myocardial infarction)
  • Undiagnosed/untreated T1DM
245
Q

What are the signs/symptoms of diabetic ketoacidosis?

A
  • Extreme polydipsia and polyuria
  • Nausea + vomiting
  • Hyperventilation (Kussmaul breathing)
  • Weight loss
  • Confusion
  • Abdominal pain
  • Dehydration
  • Tachycardia
  • Hypotension
246
Q

What are the investigations needed in diabetic ketoacidosis?

A
  • Random plasma glucose > 11mmol/L
  • Plasma ketone > 3mmol/L
  • Blood pH < 7.35 / HCO3- < 15mmol/L
  • Urine dipstick showing glycosuria and ketonuria
  • Serum U+E = raised urea and creatinine
  • Decreased total K+, increased serum K+
247
Q

What is the treatment for diabetic ketoacidosis?

A
  • Hospital admission
  • ABC emergency management
  • 1st = rehydrate with 0.9% saline IV
  • Then give IV insulin
  • Then replace electrolytes (K+)
  • Treat underlying cause
248
Q

What are the signs/symptoms of anaemia?

A

Systemic:
- fatigue
- pallor
- dyspnoea
- anorexia
Head:
- faintness
- headache
- tinnitus
- cognitive dysfunction
Heart:
- palpitations
- angina
- tachycardia
- heart murmurs
Neurological symptoms in B12 deficiency:
- weakness
- neuropathy
- psychiatric
Koilonychia (curved nails)
Angular cheilitis (ulcers in corner of mouth)

249
Q

List the 4 types of anaemia and their causes

A

Microcytic anaemia (low MCV):
- iron-deficiency anaemia (most common)
- thalassaemia (decreased Hb production)
Normocytic anaemia (normal MCV):
- acute blood loss
- renal disease
- chronic disease
- bone marrow failure
Macrocytic anaemia (high MCV):
- folate deficiency
- B12 deficiency
- alcohol excess/liver disease
Haemolytic anaemias (can be normocytic or macrocytic):
- sickle cell (normocytic)
- bone marrow disorders
- autoimmune
- infection (e.g. malaria)

250
Q

What are the causes of iron deficient anaemia?

A
  • Blood loss: common = GI, menstrual, rare = haematuria, donation
  • Increased demand (pregnancy)
  • Impaired absorption (e.g. coeliac disease, IBD, gastrectomy, H.pylori)
  • Dietary deficiency (rare in adults)
251
Q

What blood results are found in iron-deficient anaemia?

A
  • Low haemoglobin (>130 in men, >120 in women/children, >110 in pregnancy)
  • Low MCV
  • Low ferritin (>30 is diagnostic)
  • High total iron binding capacity
  • High transferrin
  • Low transferrin saturation
252
Q

What are the causes of folate deficiency?

A
  • Poor nutrition (found in green veg, common in poverty and elderly)
  • Malabsorption (coeliac, Crohn’s)
  • Increased demand (pregnancy, malignancy)
  • Drugs (alcohol, methotrexate)
253
Q

What is the management of iron-deficiency anaemia?

A
  • Investigate/treat source of bleeding or underlying cause
  • Urgent referral is over 50 with family history of colorectal cancer, or positive FIT
  • Advise to maintain adequate balanced intake of iron-rich foods (dark green veg, meat, etc.)
  • Replace iron - ferrous sulphate OD (continue 3 months after Hb is normal to replenish stores)
254
Q

What are the causes of vitamin B12 deficiency?

A
  • Pernicious anaemia (autoimmune reduction of intrinsic factor)
  • Dietary (found in meat/dairy, common in vegans)
  • Malabsorption (due to ileal resection, coeliac, Chron’s, or bacterial overgrowth)
  • Drugs (PPIs, H2-receptor antagonists, colchicine
255
Q

What are the causes of acute liver disease?

A
  • viral (hepatitis A, B, EBV)
  • drugs (antibiotics e.g. co-amoxiclav, paracetamol overdose)
  • alcohol
  • vascular (Budd-Chiari syndrome, veno-occlusive disease, ischemia)
  • obstruction
  • congestion (congestive cardiac failure)
256
Q

What investigations suggest folate/vitamin B12 deficiency anaemia?

A
  • Low haemoglobin
  • High MCV
  • Low folate/B12
  • Anti-intrinsic factor antibodies (pernicious anaemia)
257
Q

What is the management of folate deficiency anaemia?

A
  • Asses underlying cause
  • Dietary advice for good sources of folate (broccoli, brown rice, chickpeas)
  • Oral supplements of folic acid (5mg/day)
    *if combined with B12 replacement, start B12 replacement first
258
Q

What is the management of vitamin B12 deficiency anaemia?

A

Vitamin B12 replacement (hydroxocobalamin):
- given frequently, then less as maintenance
- intramuscular if due to malabsorption
- oral if due to dietary causes
Dietary advice for good sources of vitamin B12: eggs, fortified cereals/bread, meat)
*if combined with folate replacement, start vitamin B12 replacement first

259
Q

What are the signs/symptoms of acute liver failure?

A
  • may be asymptomatic
  • generalised symptoms (malaise, nausea, anorexia)
  • jaundice as disease progresses
  • rare: confusion, bleeding, RUQ pain, hypoglycaemia
260
Q

What are the causes of chronic liver disease?

A
  • viral (hepatitis A, B, EBV)
  • drugs (antibiotics and common)
  • autoimmune (primary biliary cholangitis, primary sclerosing cholangitis)
  • metabolic (iron or copper overload)
  • neoplastic
  • fatty liver disease (alcoholic and non-alcoholic)
261
Q

What are the signs/symptoms of chronic liver failure?

A
  • ascites/oedema
  • jaundice/pruritis
  • bleeding (easy bruising, haematemesis)
  • gynaecomastia
  • spider naevi
  • clubbing
  • palmar erythema
  • hepatosplenomegaly
  • hepatic encephalopathy
262
Q

Define fatty liver disease

A

The accumulation of fat in the liver (steatosis) which can progress and be associated with inflammation (steatohepatitis), divided into:
- alcoholic fatty liver disease (AFLD)
- non-alcoholic fatty liver disease (NAFLD)

263
Q

What investigations are suggestive of fatty liver disease?

A
  • LFTs: raised ALT/AST (hepatocellular injury), AST:ALT > 2:1 or raised GGT in alcohol cause
  • FBC: low platelets in advanced liver fibrosis
  • Hepatitis viral serology
  • Auto-antibodies: check for autoimmune hepatitis (raised ANA and ASMA) or PBC (raised AMA)
  • Ultrasound: detects steatosis
  • Liver biopsy: diagnostic
264
Q

What is the management of fatty liver disease?

A
  • Use FIB-4 score to assess risk of advance liver fibrosis
  • Lifestyle changes (weight loss, regular exercise, healthy diet, avoid alcohol)
  • Control risk factors (hypertension, T2DM)
  • Drugs: for non-diabetic patients - vitamin E supplements (can improve histology), pioglitazone (increase insulin sensitivity)
265
Q

Describe biliary colic

A
  • Definition: gallstones obstructing cystic or common bile duct
  • Presentation: intermittent RUQ/epigastric pain, often worse after eating (can have jaundice if stone passes into CBD)
  • Investigations: normal FBC and LFTs, US shows stone
  • Treatment: analgesia, outpatient surgical removal
266
Q

Describe cholecystitis

A
  • Definition: gallstone obstruction causing distention and inflammation of the gallbladder
  • Presentation: continuous RUQ/epigastric pain, worse on inspiration (Murphy’s sign), fever (can have nausea, or jaundice if stone moves to CBD)
  • Investigations: raised white blood cells, can have raised bilirubin and liver enzymes, US shows thickened wall +/- stone
  • Treatment: analgesia, antibiotics, surgical removal (within 1 week), or drainage
267
Q

Describe ascending cholangitis

A
  • Definition: bacterial infection of the biliary system due to partial/complete obstruction of ducts
  • Presentation: RUQ pain, fever, jaundice (Charcot’s triangle), also hypotension, altered mental state (Reynold’s pentad)
  • Investigations: high WBC, CRP, and liver enzymes, US or CT, ERCP is diagnostic
  • Treatment: analgesia, resuscitation if needed, antibiotics, ERCP for stone removal or drainage
268
Q

Define angina, and the difference between stable and unstable angina

A

Angina is the mismatch of oxygen demand an supply to the heart muscle, causing chest pain
- Stable angina is described as a chronic coronary syndrome, when the associated chest pain occurs predictably, for a short time (less than 5 mins), and is relieved with rest/GTN spray
- Unstable angina is described as new onset angina, or abrupt deterioration of stable angina, often occurring at rest, and is an acute coronary syndrome requiring emergency admission

269
Q

What are the causes and triggers of angina?

A

Causes:
- CHD/atherosclerosis (narrowing of lumen)
- Valvular disease, cardiomyopathy (rare)
Triggers:
- physical exertion
- emotional stress
- heavy meals
- cold weather

270
Q

What are the risk factors for IHD (causing chronic/acute coronary syndromes)?

A
  • Age
  • Cigarette smoking
  • Family history
  • Diabetes mellitus
  • Hyperlipidaemia
  • Hypertension
  • Kidney disease
  • Obesity
  • Physical inactivity
  • Stress
  • Male
271
Q

Describe the presentation of stable angina?

A
  • Constricting pain/tightness/discomfort in chest, shoulder, arm, neck, or jaw
  • Induced by exertion, etc.
  • Relieved by rest/GTN spray
  • Lasts less than 5 minutes
  • Can have breathlessness, sweating/pale, nausea
    *no fluid retention (unlike heart failure)
    *palpitations and syncope are rare
272
Q

What investigations are needed for stable angina?

A
  • ECG = abnormalities can’t confirm confirm diagnosis
  • Exercise testing (continuous ECG with exertion, relies on patient’s ability)
  • Stress echo (pharmacological stressor)
  • CT coronary angiography
273
Q

What are the treatments for stable angina?

A

Lifestyle changes (stop smoking, weight loss, exercise, diet)
Medication:
- nitrates (GTN spray for rapid-relief and long acting tablet - vasodilation to reduce BP which can be side effect)
- beta-blocker or calcium channel blocker (first line treatment, symptomatic relief, reduce oxygen demand of the heart)
- aspirin (secondary prevention, COX inhibitor to reduce platelet aggregation), or clopidogrel if intolerant
- ACE inhibitor (consider for patient who also have diabetes, less vasoconstriction to lower BP)
- also offer statin and antihypertensive if indicated

274
Q

What are the red flag symptoms of an acute coronary syndrome?

A
  • Pain at rest or minimal exertion
  • Pain that is continuous or prolonged (more than 15 mins)
  • Pain associated with dizziness, palpitations, tingling, nausea, sweating, breathlessness
  • Associated with haemodynamic instability (systolic BP < 90)
  • New onset or abrupt deterioration of stable angina
275
Q

What investigations are needed for an acute coronary syndrome?

A
  • ECG = STEMI will show ST elevation and pathological Q waves after a few days, unstable angina may show T wave inversion or ST depression, but normal ECG can’t exclude unstable angina or NSTEMI
  • Troponin = raised levels become detectable 3-6 hours after MI and stays elevated for several days, may be slightly elevated in unstable angina showing risk of cardiac events/death (not raised in stable angina)
  • GOLDSTANDARD = coronary angiography (shows presence and severity of coronary artery disease)
276
Q

What is the management for acute coronary syndromes?

A
  1. Arrange hospital admission for any suspected ACS
  2. Resuscitation if required
  3. Pain relief = GTN spray, opiate
  4. Immediate 300mg of aspirin (or clopidogrel is intolerant) if ST elevation on ECG
  5. Oxygen if hypoxic
  6. Revascularisation = immediate PCI in STEMI, consider angiography with follow-on PCI in NSTEMI (if troponin elevated)/unstable angina
  7. Fibrinolysis (if PCI is not possible within 2 hours, high risk of bleeding)
  8. Consider: nitrates, beta-blockers, calcium channel blockers, ACEi
277
Q

Define atrial fibrillation

A
  • A supraventricular tachycardia resulting from irregular electrical activity and ineffective conduction of the atria
  • Can be paroxysmal (lasts 30 seconds - 7 days), persistent (lasts more than 7 days, requires cardioversion), or permanent ( more than 1 year, or fails to terminate using cardioversion)
278
Q

What are the causes of atrial fibrillation?

A
  • Congestive heart failure
  • Atrial/ventricular dilation/hypertrophy
  • Valvular disease
  • Congenital heart disease
  • Inflammatory/infiltrative disease (e.g. pericarditis)
  • Non cardiac: acute infection, caffeine, smoking, alcohol, drugs (B2 agonists, thyroxine), metabolic imbalances, diabetes, metastasis from lung
279
Q

What are the signs/symptoms of atrial fibrillation?

A
  • Palpitations
  • Chest pain
  • Breathlessness
  • Syncope/dizziness
  • Reduced exercise tolerance
  • Can present with complication (stroke/MI)
    *some may be asymptomatic
280
Q

What are the investigations needed for arrhythmias?

A
  • Bloods: FBC, U&Es, TSH, HbA1C
  • ECG (simple 12 lead, 24hr, continuous monitoring)
  • Echocardiogram (if structural heart disease suspected)
281
Q

What is the management for atrial fibrillation?

A
  • Admit to hospital if haemodynamically unstable (high HR, low BP, LOC, syncope, chest pain, breathlessness) or signs of stroke, severe heart failure, PE
  • Refer to specialist if underlying cause identified
  • Assess risk of bleeding and need for anticoagulation (DOAC) with CHA2DS2VASc score
  • Offer support with weight loss, underlying diabetes, hypertension, anaemia, alcohol consumption to improve AF and reduce bleeding risk factors
  • Rate control: first line = beta-blockers or calcium channel blockers, if others ruled out or sedentary = digoxin, amiodarone = started in secondary care for severe cases, not long term
  • Rhythm control = if symptoms continue after rate control - electrical (for persistent AF) or pharmacological (using beta-blockers, dronedarone, flecainide) cardioversion
282
Q

Define cellulitis

A

Acute bacterial infection (strep. pyogenes, or staph. aureus) of the dermis and subcutaneous tissue, due to disruptions in the skin barrier, most commonly affecting lower limbs but also other areas such as upper limbs, face, and trunk

283
Q

What are the risk factors for cellulitis?

A
  • Increasing age
  • Trauma of the skin (bite, burn, laceration)
  • Increased risk of infection (diabetes, liver/renal disease, immunocompromised)
  • Contaminant skin condition (eczema)
  • Leg/foot ulceration
  • Lymphoedema
  • Leg oedema
  • Venous insufficiency
  • Obesity
  • Pregnancy
284
Q

What are the signs/symptoms of cellulitis?

A
  • Acute onset of red, painful, hot, swollen skin
  • Accompanied or preceded by fever, malaise, nausea, shivering, rigors
  • Blisters or bullae may be present
  • Can may inflamed reginal lymph nodes
  • May be systemically unwell/show signs of sepsis (tachycardia, hypotension, tachypnoea, confusion)
285
Q

What investigations are needed for cellulitis?

A

Not always necessary, but may consider:
- Swab for culture (if open wound, drainage, etc.)
- Ultrasound: identify underlying abscess for drainage
- Bloods: WBC, ESR, CRP to detect inflammation (non-specific)
- Other tests to exclude DVT, gout, septic arthritis

286
Q

Define stroke

A

A clinical syndrome caused by disruption of blood supply to the brain (due to infarction or haemorrhage), characterised by rapidly developing signs of focal or global disturbance of cerebral functions, lasting for more than 24 hours or leading to death

287
Q

What are the risk factors for stroke?

A

Lifestyle factors:
- smoking
- alcohol misuse
- physical inactivity
- poor diet
Established CVD:
- hypertension
- AF
- infective endocarditis
- IHD
- congestive heart failure
- structural defects
Other medical conditions:
- migraine
- hyperlipidaemia
- diabetes mellitus
- hypercoagulable disorders
- connective tissue disorders
Non-modifiable factors:
- older age
- male sex
- personal/family history of stroke/TIA
- lower level of education

288
Q

What are the signs/symptoms of a stroke in the anterior circulation?

A

Either hemisphere (symptoms contralateral):
- hemiparesis (upper limb = MCA, lower limb = ACA)
- hemisensory loss (upper limb = MCA, lower limb = ACA)
- visual field defect
Dominant hemisphere (usually LEFT hemisphere)
- language dysfunction (expressive/receptive dysphasia, dyslexia, dysgraphia)
Non-dominant hemisphere (usually RIGHT hemisphere)
- visuospatial dysfunction (geographical agnosia, dressing apraxia, constructional apraxia)
- anosognosia (impaired understanding of their illness, neglect of paralysed limb, denial of weakness)

289
Q

What are the signs/symptoms of a stroke in the posterior circulation?

A
  • Unsteadiness
  • Visual disturbance
  • Slurred speech
  • Disorder of perception
  • Headache
  • Vomiting
  • Others e.g. memory loss, confusion
290
Q

What investigations are needed for a stroke?

A
  • CT head (1ST LINE, without contrast, ideally within 1 hour)
  • MRI brain with diffusion weighted imaging (GOLDSTANDARD)
  • Blood tests (FBC, U&E, ESR, TFTs, glucose, lipids to asses general health and exclude other causes)
  • ECG (look for arrhythmias and cardiac causes)
  • ECHO (may show mural thrombus, valvular lesions)
  • Carotid Doppler ultrasound, or CT/MRI angiogram (asses carotid artery stenosis)
291
Q

What are the treatments for an ischemic stroke?

A
  • Admit to hospital urgently
  • ABCDE
  • Oxygen as needed
  • Maintain blood pressure and glucose
  • Antiplatelets (e.g. aspirin): only once haemorrhagic stroke is ruled out
  • Thrombolysis: only within 4.5 hours of onset, and if haemorrhagic stroke is ruled out, most effective in 1st 90 mins
  • Thrombectomy: for larger arterial occlusions
292
Q

What is the primary prevention for stroke/TIA?

A

Control risk factors:
- asses and treat hypertension, DM, hyperlipidaemia, cardiac disease
- smoking cessation
- exercise
Long term anticoagulants
- e.g. warfarin/DOAC
- in AF or prosthetic heart valves

293
Q

What is the secondary prevention for a stroke/TIA?

A
  • Lifestyle measures (exercise, stop smoking, healthy diet, restrict alcohol)
  • Antiplatelets: clopidogrel (or aspirin + dipyridamole)
  • Statin: atorvastatin
  • Anticoagulants if cardiac cause (warfarin/DOAC)
  • Optimise management of diabetes, hypertension, AF, obesity, heart failure
294
Q

Define TIA

A

Transient (less than 24 hours) neurological dysfunction caused by focal cerebral, spinal, or retinal infarction

295
Q

What are the signs/symptoms of TIA?

A

*symptoms come on suddenly and usually resolve after 1 hour but can persist up to 24 hours
- Unilateral weakness/sensory loss
- Dysphasia
- Ataxia, vertigo, or loss of balance
- Cranial nerve defects
- Amaurosis fugax (sudden transient loss of vision in one eye

296
Q

What is the management for a TIA?

A
  • Offer aspirin 300 mg immediately
  • Refer for specialist assessment within 24 hours
  • Antiplatelets: short-term aspirin, long-term (secondary-prevention) = clopidogrel
  • Statin: atorvastatin
  • Anticoagulants (warfarin/DOAC) is cardiac cause
  • Carotid endarterectomy (reduce stenosis)
297
Q

What are the long term complications of stroke/TIA?

A
  • Continence problems
  • Fatigue
  • Swallowing/nutrition/hydration issues
  • Cognitive dysfunction
  • Mood/wellbeing
  • Hearing difficulties
  • Oral health problems
  • Pain (neuropathic or MSK)
  • Sexual dysfunction
  • Spasticity
  • Communication difficulties
  • Difficulties with activities of daily living
298
Q

Define constipation

A

A heterogeneous symptom-based disorder, where defecation is problematic due to infrequent and/or hard stool, difficulty passing stool (often straining), or the sensation of incomplete emptying, classed as…
- functional/primary/idiopathic: chronic constipation (more than 3 months) without a known cause
- secondary/organic: constipation caused by underlying medical condition or medication

299
Q

What are the risk factors for constipation?

A

Social:
- low fibre or calorie intake
- difficulty accessing toilet
- changes in normal routine
- lack of exercise or reduced mobility
- family history
Psychological:
- anxiety/depression
- eating disorder
- somatization disorders
Physical:
- female
- older age
- poor fluid intake
- sitting position on toilet

300
Q

What are some of the secondary causes of diarrhoea?

A

Medications:
- analgesics: opiates and NSAIDs
- antispasmodics (e.g. hyoscine)
- diuretics (e.g. furosemide)
- iron or calcium supplements
- aluminium-containing antacids (e.g. gaviscon)
- antihistamines (e.g. hydroxyzine)
Endocrine/metabolic conditions:
- diabetes (with autonomic neuropathy)
- hypercalcaemia and hyperparathyroidism
- hypothyroidism
- hypermagnesemia
- hypokalaemia
Neurological conditions:
- multiple sclerosis
- Parkinson’s disease
- spinal cord injury
- cerebrovascular disease (stoke)
Structural abnormalities:
- anal fissures, strictures, haemorrhoids
- strictures of the colon (after diverticulitis, ischemia, or surgery)
- inflammatory bowel disease
- obstructive mass (e.g. malignancy)
- rectal prolapse or rectocele
- postnatal damage to pelvic floor

301
Q

What are the associated feature of constipation?

A
  • Lower abdominal pain/discomfort
  • Distention/bloating
  • Nausea or loss of appetite
  • Urinary retention
  • Overflow diarrhoea
  • Confusion/delirium or functional decline
302
Q

What is the management of constipation?

A

Lifestyle factors:
- high fibre diet
- adequate fluid intake
- regular exercise
- toileting routines (regular, unhurried, adequate privacy)
Laxatives: (stepped approach)
- bulk-forming: e.g. ispaghula(fybogel)
- osmotic: e.g. macrogol (laxido) or lactulose
- stimulant: e.g. bisacodyl or senna
- stool-softeners: e.g. docusate
* for opioid-induced: give osmotic/stimulant

303
Q

How is faecal loading and/or impaction managed?

A

Initial treatment:
- hard stool: high dose oral macrogol (osmotic)
- soft stool or ongoing hard stool: start/add oral stimulant
If no/low response:
- bisacodyl suppository (stimulant) for soft stool, glycerol (softener) +/- bisacodyl suppository for hard stool
- mini enema such as docusate (softer and weak stimulant) or sodium citrate (osmotic)
If response is still inadequate:
- sodium phosphate (osmotic) or arachis oil (softener) enema

304
Q

Describe appendicitis

A

Sudden inflammation of the appendix, usually due to obstruction of the lumen because of…
- faecolith (hard mass of faecal matter)
- lymphoid hyperplasia
- foreign body
- tumour
This leads to…
- increased mucus production
- bacterial overgrowth
- impaired lymphatic and venous drainage
- eventual ischemia and necrosis

305
Q

What are the signs/symptoms of appendicitis?

A
  • Pain: periumbilical, moving to right iliac fossa, aggravated by moving, coughing, breathing
  • Nausea, vomiting, anorexia
  • Constipation (sometimes diarrhoea)
  • Fever (low-grade)
  • Tachycardia
  • Abdominal distension
  • Guarding and rebound tenderness in RIF
  • McBurney’s point tenderness (2/3 along a line from the umbilicus to ASIS)
  • Rovsing’s sign (pain in LIF increases pain felt in RIF)
306
Q

What investigations are needed for appendicitis?

A
  • FBC: leucocytosis (neutrophil-predominant)
  • CRP: raised
  • Imaging: US, CT
  • Rule out: UTI and pregnancy (ectopic)
307
Q

What is the management of appendicitis?

A
  • Emergency hospital admission
  • IV fluids and antibiotics (treat conservatively in uncomplicated cases)
  • Appendicectomy (gold-standard)
308
Q

Define Parkinson’s disease?

A

A chronic and progressive neurodegenerative disorder, resulting from dopamine deficiency in the basal ganglia due to cell loss in the substantia nigra, which leads to a movement disorder with classical parkinsonian symptoms (bradykinesia + tremor/rigidity/postural instability)

309
Q

What are the signs/symptoms of Parkinson’s disease?

A

Bradykinesia: (slowness of initiation of voluntary movement, progressive reduction in speed/amplitude of repetitive actions)
- problems with fine finger movements (e.g. doing up buttons, writing)
- deteriorated walking (small steps, dragging one foot, reduced arm swing)
- reduced or flat facial expression
- onset is unilateral then progresses to bilateral
Tremor:
- at rest
- improves on moving, concentration, and during sleep
- commonly in thumb and index finger (‘pin-rolling’), wrist or leg
Rigidity:
- predominantly unilateral
- lead-pipe rigidity (resistance when limb is passively flexed)
- cogwheel rigidity (regular intermittent relaxation of tension when limb is passively flexed)
Postural instability:
- balance problems
- stooped posture

310
Q

What are the other causes of parkinsonism?

A
  • Drug-induced: antipsychotics, antiemetics, antidepressants, calcium channel blockers, and others
  • Medical conditions: cerebrovascular disease (repeated strokes), Lewy body or Alzheimer’s dementia, repeated head injuries, Wilson’s disease
311
Q

What are the investigations needed for Parkinson’s disease?

A
  • Diagnosis is clinical
  • CT/MRI: rule out other structural pathology
  • PET scan: localise dopamine deficiency
312
Q

What is the management for Parkinson’s disease?

A

For primary care:
- urgent referral to specialist (untreated)
- stop/reduce any drugs known to cause parkinsonism
Non-pharmacological:
- nurse specialists
- physio and OT
- SALT and dieticians
- nursing/care support
Pharmacological:
- levodopa (dopamine agonist)
- dopa-decarboxylase inhibitor (e.g. madopar)
- monoamine oxidase-B inhibitors (e.g. rasagiline)
- other dopamine agonists (e.g. pramipexole - oral, rotigotine - transdermal)
- catechol-O-methyltransferase inhibitors (e.g. entacapone)

313
Q

What are the red flags for back pain?

A

Cauda equina syndrome:
- sudden onset bilateral radicular leg pain
- severe/progressive neurological deficit (motor weakness)
- recent onset of urinary incontinence, difficulty initiating/impaired sensation of urinary flow
- recent onset of faecal incontinence, impaired sensation of rectal fullness
- perianal/perineal sensory loss (saddle anaesthesia)
Spinal fracture:
- sudden onset sever central spinal pain, relieved by lying down
- history of trauma (e.g. road traffic collision, fall), or strenuous lifting in osteoporosis)
- structural deformity of spine (e.g. step between vertebrae)
- point tenderness over vertebra
Cancer:
- age 50 or over, gradual onset or progressive pain
- severe, unremitting pain, aggravated by strain
- localised spinal tenderness
- unexplained weight loss
- claudication (leg pain/cramping when walking)
- past history of cancer
Infection: (discitis, osteomyelitis, spinal/epidural abscess)
- fever, systemically unwell
- recent infection
- diabetes mellitus
- history of IVDU
- immunocompromised/suppressed

314
Q

What is the management for lower back pain (without radiculopathy)?

A
  • Arrange hospital admission if red flag symptoms
  • Asses risk for chronicity (STarT Back score)
  • Self management strategies: keep active, local heat
  • Analgesia: NSAID +/- paracetamol (short-term codeine if NSAID is not tolerated/ineffective)
  • Non-pharmacological: group exercise programme, physio, CBT
315
Q

Define sciatica

A

Radiating leg pain caused by inflammation or compression of the lumbosacral nerve roots forming the sciatic nerve
Alternative name: lumbar radiculopathy

316
Q

What are the causes of sciatica?

A
  • Herniated intervertebral disc
  • Spondylolisthesis
  • Spinal stenosis
  • Infection
  • Cancer
317
Q

What are the signs/symptoms of sciatica?

A
  • Unilateral leg pain radiating to below the knee to the foot or toes
  • Lower back pain
  • Numbness/tingling (paraesthesia) in the distribution of a nerve root
  • Weakness or reflex changes
  • Pain reproduces by single leg raise
318
Q

Define osteoporosis

A

Low bone mass and structural deterioration of bone tissue, caused by an imbalance of the bone remodelling process by osteoclasts and osteoblasts, leading to an increase in bone fragility and susceptibility to fracture

319
Q

What are the risk factor for osteoporosis?

A
  • Increasing age
  • Female sex
  • Low body mass
  • Parental history of hip fracture
  • Past history of fragility fracture
  • Corticosteroid therapy
  • Cushing’s syndrome
  • Alcohol intake of more than 3 units/day
  • Smoking
  • Increased risk of falls (visual/cognitive impairment, sedative medication, lack of co-ordination/strength)
  • Secondary causes (inflammatory arthritis, CKD, IBD, hyperthyroid, hypogonadism, COPD, diabetes, premature menopause, immobility)
320
Q

What are the investigations for osteoporosis?

A
  • DEXA scan: calculates bone mineral density and T score (<-2.5 = osteoporosis, between -1 and -2.5 = osteopenia)
  • Bloods: FBC, CRP, U&E, LFTs, TFTs, calcium, vitamin D
  • Assessment of fracture risk (FRAX score)
321
Q

What is the management for osteoporosis?

A
  • Lifestyle advice: regular exercise (strength), balanced diet, stop smoking, avoid excessive alcohol
  • Calcium and vitamin D supplements
  • Oral bisphosphonates (1st line = alendronate, alternative = risedronate)
  • Denosumab (6m s/c injection)
  • Zoledronic acid (annual IV infusion, instead of oral bisphosphonates)
  • Parathyroid hormone peptides (daily s/c injections e.g. teriparatide)
322
Q

Describe the metabolism of vitamin D

A
  • Dietary and skin-derived vitamin D is converted in the liver to 25-hydroxyvitamin D, which is the main circulating form
  • This is then converted to 1,25-hydroxyvitmin D in the kidneys and other tissues, and this production is regulated by PTH
323
Q

What are the risk factors for vitamin D deficiency?

A
  • Aged 65 and over
  • Low/no exposure to sunlight (e.g. those who cover their skin, who are house bound/confined indoors)
  • Lack of dietary vitamin D (egg yolk, oily fish, red meat, fat, liver, kidney)
  • Darker skin pigmentation
  • Gastrointestinal or malabsorption disorders
  • Severe liver or kidney disease
  • Pregnant or breastfeeding
  • Obesity
  • Drugs (orlistat, antiepileptics, corticosteroids, antacids, calcium channel blockers, antiretroviral treatment)
324
Q

What investigations are needed for vitamin D deficiency?

A
  • Vitamin D
  • Bone profile (calcium, phosphate, alkaline phosphate)
  • PTH
  • Asses for underlying causes: FBC, U&E, LFTs, TFTs, coeliac serology
325
Q

Define otitis media

A

Inflammation in the middle ear, associated with an effusion, accompanied by the rapid onset of signs/symptoms of an ear infection

326
Q

What are the risk factors for otitis media?

A
  • Young age
  • Male sex
  • Smoking or passive smoking
  • Frequent contact with other children (increased exposer to viral illness)
  • Formula feeding
  • Craniofacial abnormalities (e.g. cleft palate)
  • Family history
  • Recurrent URTIs
  • GORD
  • Prematurity
  • Prolonged bottle feeding in supine position
  • Use of dummy
327
Q

What are the signs/symptoms of otitis media?

A
  • In older children/adults: earache
  • In younger children: holding/tugging/rubbing ear, non-specific fever, crying, restlessness, poor feeding, cough, rhinorrhoea
  • On examination: red, yellow, or cloudy tympanic membrane, moderate-severe bulging of tympanic membrane and air-fluid level (effusion), perforated tympanic membrane, or discharge
328
Q

What is the management of otitis media?

A
  • Regular doses of paracetamol and ibuprofen
  • Antibiotics (for those systemically unwell, with discharge, bilateral infection): 5-7 day course of amoxicillin (or clarithromycin0
329
Q

Define otitis externa

A

Inflammation of the skin and subdermis of the external ear canal, which may involve the pinna or tympanic membrane

330
Q

What are the risk factors for otitis externa?

A
  • Skin conditions (e.g. eczema, psoriasis)
  • Acute otitis media
  • Contact dermatitis (local irritant/allergen)
  • Trauma to ear canal
  • Foreign body in ear (e.g. hearing aids)
  • Water exposure
  • Ear canal obstruction (e.g. ear wax)
331
Q

What are the signs/symptoms of otitis externa?

A
  • Itch in the ear canal
  • Ear pain/tenderness of pinna/tragus
  • Discharge
  • Hearing loss (due to occlusion)
  • On examination: ear canal is red and oedematous, debris/discharge in ear canal, tympanic membrane erythema, regional lymphadenopathy
332
Q

What is the management of otitis externa?

A
  • Self care measures: avoid damage to ear canal, keep eyes clean and dry
  • Analgesia: paracetamol, ibuprofen
  • Cleaning of ear canal: swabs, irrigation
  • Topical antibiotics w/wo corticosteroid
  • Oral antibiotics (if severe infection)

Phase 3a (10 decks)

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