General Practice Flashcards
Define Acne Vulgaris (Acne)?
Chronic inflammation caused by a blockage of the follicle, with or without localised infection, in pockets within the skin known as the pilosebaceous unit
What is the Epidemiology of Acne?
- It is one of the most common dermatological conditions globally,
- Prevalence is highest in adolescents and young adults
- The psychological impact of acne can be significant, affecting self-esteem and overall quality of life.
What are some risk factors for Acne?
- Hormonal changes (e.g. during puberty, menstrual cycle, polycystic ovary syndrome)
- Increased sebum (oil) production
- Blockage of hair follicles and sebaceous glands by keratin and sebum
- Bacterial colonization (Propionibacterium acnes)
- Family history of acne
- Certain medications (e.g. corticosteroids, hormonal treatments)
What is the pathophysiology of Acne?
- Acne results from increased production of sebum, trapping of keratin (dead skin cells) and blockage of the pilosebaceous unit.
- This leads to swelling and inflammation in the pilosebaceous unit.
- Androgenic hormones increase the production of sebum, which is why acne is exacerbated by puberty and improves with anti-androgenic hormonal contraception.
- Swollen and inflamed units are called comedones.
- Closed Comedones: “White heads” as their contents are not exposed to the skin surface or oxygen
- Open Comedones: “Black heads” as when they open the contents are exposed and become oxidised turning black.
- Proprionbacterium acnes is a commensal organism that colonises the skin. When a comedone is open this species can invade and form an inflammatory papule (a solid raised lesion <0.5mm diameter) associated with erythema
- As more neutrophils accumulate in the papule this may progress to form an inflammatory Pustule ( Lesion <0.5mm diameter containing pus)
Define these words:
Macules:
Papules:
Pustules:
Comedomes:
Blackheads:
Whiteheads:
Ice Pick Scars:
Hypertrophic Scars:
Rolling Scars:
Macules are flat marks on the skin
Papules are small lumps on the skin
Pustules are small lumps containing yellow pus
Comedomes are skin coloured papules representing blocked pilosebaceous units
Blackheads are open comedones with black pigmentation in the centre
Ice pick scars are small indentations in the skin that remain after acne lesions heal
Hypertrophic scars are small lumps in the skin that remain after acne lesions heal
Rolling scars are irregular wave-like irregularities of the skin that remain after acne lesions heal
What are the different classifications of Acne?
- Non-inflammatory: Comedomes (blackheads and whiteheads)
- Inflammatory: inflammatory papules, pustules, and nodules (cysts.)
- Mild acne: predominantly non-inflammatory lesions.
- Moderate acne: predominantly inflammatory papules and pustules.
- Severe acne: nodules (cysts), scarring, acne fulminans, and acne conglobata.
What are the clinical features of Acne?
- Open/closed Comedones, inflammatory papules and pustules, nodules, and cysts may be present.
- The face is most often affected. The neck, chest and back may also be affected.
- Psychological dysfunction due to changes physical appearance
- Scarring: associated with inflammatory acne. Hypertrophic and keloid scars are more common in darker skin tones.
What is Acne Fulminans?
An uncommon but severe, serious acne presentation.
- Inflammatory nodules/cysts that are painful, ulcerating, and haemorrhagic appear
- Associated systemic upset (raised white cell count, joint pain, fever, fatigue.)
- These patients should be reviewed urgently within 24 hours. It usually affects teenage male patients.
What are the investigations for Acne?
Clinical diagnosis and investigations are usually not needed
- Swabs may be indicated if diagnosis is uncertain
- If an endocrinological cause is suspected them maybe carry out investigations
What is the management of Acne?
Non-pharmacological
- Dont over clean skin
- Avoid oil based skin products
- Avoid picking/scratching
Treatment is initiated in a stepwise fashion on severity of symptoms
- No treatment may be acceptable if mild.
- Topical Benzoyl peroxide (topical Antibiotic): Reduce inflammation, toxic to P.acnes
- Topical retinoids: Slow sebum production
- Topical antibiotics (Clindamycin): prescribed in combination with retinoids or benzoyl peroxide
- Oral antibiotics (Lymecycline): Contraindicated in pregnancy or planning pregnancy
- Oral contraceptive pill (Dianette): Slow sebum production
- Oral Retinoids (Isotretinoin): Effective last line but only prescribed by a specialist
What is a contraindication to using Oral isotretinoin to treat acne?
Very effective at clearing the skin however it is strongly teratogenic so contraindicated in pregnancy or people planning pregnancy
What are some side effects to Isotretinoin?
- Dry skin and lips
- Photosensitivity of the skin to sunlight
- Depression, anxiety, aggression and suicidal ideation. Patients should be screened for mental health issues prior to starting treatment.
- Highly Teratogenic
- Rarely Stevens-Johnson syndrome and toxic epidermal necrolysis
What is a major concern when using Co-cyprindiol (Dianette) as a treatment for Acne?
Has a high risk of thromboembolism so is not prescribed long term and is usually discontinued once acne is controlled
What are some complications of Acne?
- Post-inflammatory erythema
- Post-inflammatory hyper- and hypo- pigmentation
- Psycho/social/sexual dysfunction
- Scars (atrophic, hypertrophic, keloid)
What are Keloid scars and what are some risk factors for them?
Keloid scars: over-proliferating scar tissue/collagen extending beyond the boundaries of the lesion. Takes 3-4 weeks typically to develop after injury.
Risk Factors:
- Darker skin/Chinese/Hispanic origin
- Less than 30 years of age
- Previous Keloid Scarring
Define Acute Bronchitis?
Acute bronchitis is defined as a self-limiting lower respiratory tract infection.
Bronchitis refers specifically to infections causing inflammation in the bronchial airways, whereas pneumonia denotes infection in the lung parenchyma resulting in consolidation of the affected segment or lobe.
What are some Risk factors for Acute Bronchitis?
- Viral or atypical bacterial infection exposure
- Cigarette smoking
- Household pollution exposure
What is the Epidemiology of Acute Bronchitis?
- Very common condition
- Highest incidence in autumn and winter months
What is the aetiology of Acute Bronchitis?
- Most commonly caused by Viral infections:
- Coronavirus,
- Rhinovirus
- RSV
- Adenovirus
What are the clinical features of Acute Bronchitis?
Patients typically present with an acute onset of:
- cough: may or may not be productive
- sore throat
- rhinorrhoea
- wheeze
The majority of patients with have a normal chest examination, however, some patients may present with:
- Low-grade fever
- Wheeze
What are the investigations for Acute Bronchitis?
Primarily a clinical diagnosis
- May use Pulmonary Function Tests
- May use Chest X-ray
- May use CRP
What is the key differential for Acute Bronchitis?
How does the presentation differ?
Pneumonia:
Acute bronchitis typically only has a wheeze on examination.
No CXR changes, dullness to percussion, focal crackles, and less systemic symptoms
What is the management of Acute Bronchitis?
Supportive Treatments:
- Analgesia
- Good fluid intake
- Consider SABA in patients with asthma affected by wheeze
- If suspected bacterial cause then antibiotics (Doxycycline)
Define Acute Stress Reaction?
Acute Stress Reaction (ASR) is an immediate and intense psychological response following exposure to a traumatic event.
- Characterized by intrusive memories, dissociation, heightened arousal, avoidance behaviours, and negative mood alterations
- ASR unfolds rapidly, typically within the initial three days to four weeks post-trauma
- ASR symptoms lasting > one month is Post Traumatic Stress Disorder (PTSD)
What is the ICD-11 Criteria for Acute Stress Reaction?
- Exposure: Direct or indirect to a traumatic event, resulting in intense emotional distress.
- Symptoms: Include dissociation, intrusive memories, negative mood, arousal, or avoidance.
- Duration: Persists for a brief period, typically between 3 days to 4 weeks post-event.
What are the clinical factures of Acute Stress Reaction?
intrusive thoughts e.g. flashbacks, nightmares
dissociation e.g. ‘being in a daze’, time slowing
negative mood
avoidance
arousal e.g. hypervigilance, sleep disturbance
What are some differential diagnoses for Acute Stress Reaction?
Adjustment Disorder:
- Adjustment disorder involves diverse maladaptive responses to stressors, leading to disproportionate mood disturbances, impaired functioning, and cognitive alterations persisting for up to six months.
Post-Traumatic Stress Disorder (PTSD):
- PTSD is marked by persistent intrusion symptoms, avoidance behaviours, negative alterations in mood and cognition, and heightened arousal following exposure to a traumatic event, with symptom duration extending beyond one month.
What is the management of Acute Stress Reaction?
First Line: Trauma-focused CBT
- Occasionally medication may be used for symptomatic management such as sleep disturbance (benzodiazepines)
Define Allergy?
An umbrella term for hypersensitivity of the immune system to allergens. Allergens are proteins that the immune system recognises as foreign and potential harmful, leading to an allergic immune response.
Define Atopy?
A term used to describe a predisposition to having hypersensitivity reactions to allergens. It refers to the tendency to develop conditions such as eczema, asthma, hayfever, allergic rhinitis and food allergies.
Give some common conditions that are classed as Type 1 Hypersensitivity reactions?
- Asthma
- Atopic eczema
- Allergic rhinitis
- Hayfever
- Food allergies
- Animal allergies
What is a Type 1 Hypersensitivity Reaction?
IgE antibodies to a specific allergen trigger mast cells and basophils to release histamines and other cytokines. This causes an immediate reaction. Typical food allergy reactions, where exposure to the allergen leads to an acute reaction, range from itching, facial swelling and urticaria to anaphylaxis.
What is a Type 2 Hypersensitivity Reaction?
Cytotoxic Mediated Immune Reaction
IgG and IgM antibodies react to an allergen and activate the complement system, leading to direct damage to the local cells.
Examples are haemolytic disease of the newborn and transfusion reactions.
What is a Type 3 Hypersensitivity Reaction?
Immune complexes accumulate and cause damage to local tissues.
Examples are autoimmune conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis and Henoch-Schönlein purpura (HSP)
What is a Type 4 Hypersensitivity Reaction?
Cell mediated hypersensitivity reactions caused by T lymphocytes. T-cells are inappropriately activated, causing inflammation and damage to local tissues.
Examples are organ transplant rejection and contact dermatitis
What should be covered when taking a history for allergy?
- Timing after exposure to the allergen
- Previous and subsequent exposure and reaction to the allergen
- Symptoms of rash, swelling, breathing difficulty, wheeze and cough
- Previous personal and family history of atopic conditions and allergies
What are the investigations for diagnosis allergy?
There are three main ways to test for allergy:
- Skin prick testing
- RAST testing, which involves blood tests for total and specific immunoglobulin E (IgE)
- Food challenge testing
What is the management for allergies?
- Establishing the correct allergen is essential
- Avoidance of that allergen
- Avoiding foods that trigger reactions
- Regular hoovering and changing sheets and pillows in patients that are allergic to house dust mites
- Staying in doors when the pollen count is high
- Prophylactic antihistamines are useful when contact is inevitable, for example hayfever and allergic rhinitis
- Patients at risk of anaphylactic reactions should be given an adrenalin auto-injector
Following exposure to an allergen what is the management?
- Antihistamines (e.g. cetirizine)
- Steroids (e.g. oral prednisolone, topical hydrocortisone or IV hydrocortisone)
- Intramuscular adrenalin in anaphylaxis
Antihistamines and steroids work by dampening the immune response to allergens. Close monitoring is essential after an allergic reaction to ensure it does not progress to anaphylaxis.
Describe the inheritance pattern for Membranopathies
Autosomal dominant
Name two most common Membranopathies
Spherocytosis (horizontal deformity) - more severe, present neonatal jaundice and haemolysis
Elliptocytosis (vertical deformity)
Describe the pathophysiology of Membranopathies
Deficiency of red cell membrane proteins caused by genetic lesions leading to haemolytic anaemia.
What are the common clinical features of Membranopathies?
Jaundice
Anaemia
Splenomegaly
What is Hereditary Spherocytosis?
Deficiency in structural membrane protein Spectrin
Makes RBCs more spherical and rigid
Mistaken to be damaged and therefore prematurely destroyed by the spleen
Causes Splenomegaly
What are the symptoms of Hereditary Spherocytosis?
General Anaemia
Neonatal Jaundice
Splenomegaly
50% have Gallstones
What is the investigations of Hereditary Spherocytosis and Elliptocytosis?
Diagnostic test?
FBC and blood film:
Normocytic Normochromic
Increased Reticulocytes + Spherocytes
Diagnostic Test:
EMA (Eosin-5 Maleimide) Binding Test
What is the treatment for Hereditary Spherocytosis?
acute haemolytic crisis:
- treatment is generally supportive
- transfusion if necessary
longer term treatment:
- folate replacement
- splenectomy
Name a common Enzymopathy.
Glucose-6-Phosphate Dehydrogenase deficiency
What is G6PD Deficiency?
X linked recessive enzymopathy causing 1/2 RBC lifespan and RBC degradation
Why does a deficiency in glucose-6-phosphate dehydrogenase lead to shortened red cell lifespan?
G6PD is required for glutathione synthesis
Glutathione protects Red blood cells against oxidative damage
How does G6PD deficiency present?
Mostly asymptomatic unless precipitated by oxidative stressor causing an attack:
- neonatal jaundice is often seen
- intravascular haemolysis
- gallstones are common
- splenomegaly may be present
What is the diagnostic investigations for G6PD Deficiency?
G6PD Enzyme Assay (Reduced Levels)
FBC:
- anaemia and raised reticulocytes
Blood film:
- Normal in between attacks
- Increased reticulocytes
- HEINZ bodies and BITE cells
What is the treatment for GP6D Deficiency?
Avoid Precipitants - Oxidative drugs
Blood transfusions when attacks come on.
What precipitants can lead to attacks of GP6D Deficiency?
Naphthalene
Anti-malarials
Aspirin
FAVA beans
Nitrofurantoin
What is anaemia?
- Low level of haemoglobin in the blood
- It is the result of an underlying disease, and not a disease itself
What are the normal haemoglobin and mean cell volume ranges for men and women?
Men:
Haemoglobin - 120-165 g/L
MCV - 80-100 femtolitres
Women;
Haemoglobin - 130-180 g/L
MCV - 80-100 Femtolitres
What is Mean Cell (corpuscular) Volume?
Size of the red blood cells
What level is considered anaemic in men and women?
- <135 g/L for men
- <115 g/L for women
What are the 3 main categories of anaemia?
- Microcytic anaemia (low MCV indicating small RBCs)
- Normocytic anaemia (Normal MCV indicating normal sized RBCs)
- Macrocytic anaemia (Large MCV indicating large RBCs)
What are the general Symptoms of Anaemia?
Tiredness
Shortness of breath
Headaches
Dizziness
Palpitations
Worsening of other conditions such as angina, heart failure or peripheral vascular disease
What are the general signs of anaemia?
Pale skin
Conjunctival Pallor
Tachycardia
Raised Respiratory Rate
What is Anaemia of Chronic Disease?
Secondary anaemia due to underlying pathology.
Commonest anaemia in hospitals
Occurs in patients with inflammatory disease
What is Iron Deficiency Anaemia?
Iron is required for the synthesis of Haemoglobin.
Therefore in Iron deficiency there is impaired synthesis of haemoglobin leading to Microcytic anaemia.
What is the most common form of anaemia world wide?
Iron Deficiency anaemia
What are some reasons a person may become iron deficient/causes of iron deficiency anaemia?
Iron is being lost (BLEEDING)
Insufficient dietary iron
Iron requirements increase (for example in pregnancy)
Inadequate iron absorption
Where is Iron mainly absorbed?
Duodenum and Jejunum
How is Iron Transported and stored?
Transported - Transferrin
Stored - Ferritin and Haemosiderin
Why do medications that reduce stomach acid production lead to impaired absorption of iron?
Iron is kept in the soluble ferrous (Fe2+) form by the stomach acid.
When it enters the intestines and the acid drops, it changes to Insoluble ferric iron (Fe3+)
The ferric iron is required for absorption.
PPIs will increase insoluble ferric iron in the stomach that cannot be absorbed.
What conditions may reduce iron absorption?
GI tract Cancer
Oesophagitis and Gastritis - GI bleeding
IBD, Colitis and Coeliacs - Impaired absorption
What are the Signs and Symptoms of Iron deficiency anaemia?
General Anaemia Sx
PICA
Brittle hair and nails
Koilonychia
Angular Stomatitis, Cheilitis
Atrophic Glossitis
What are the diagnostic investigations for Iron Deficiency Anaemia?
FBC - MCV = Low (microcytic anaemia)
Blood Film - Hypochromic RBC, Target cells, Howell Jolly Bodies
Iron Studies - Low Ferritin (<15), Low transferrin Saturation (<15%), Increased Total Iron Binding Capacity (TIBC)
Endoscopy/Colonoscopy if >60 yrs to look for GI bleed
What is the treatment of Iron Deficiency Anaemia?
Oral Fe - Ferrous Sulphate (Ferrous Gluconate if poorly tolerated)
Blood Transfusion
What are some Side effects of Treating Iron deficiency anaemia with Ferrous sulphate?
Cause GI Upset
Nausea
Diarrhoea
Constipation
Black stools
What is Sideroblastic Anaemia?
A microcytic anaemia characterised by ineffective erythropoiesis due to having the inability to incorporate Iron into blood cells
What is the Pathogenesis of Sideroblastic anaemia?
Defective Hb synthesis within Mitochondria
Often X linked inheritance
A Functional Iron deficiency where there is increased Fe but it is not used in Hb Synthesis
What are the investigations for Sideroblastic anaemia?
FBC - Microcytic
Blood film - Ringed Siderobasts
What is the Treatment for Sideroblastic Anaemia?
- Mainly supportive
- Iron chelation (Desferrioxamine)
- Consider B6 (Pyridoxine) if hereditary
What is Pernicious Anaemia?
- Autoimmune condition in which atrophic gastritis leads to a lack of intrinsic factor secretion from the parietal cells in the stomach
- Dietary B12 remains unbound and cannot be absorbed at the terminal ileum
- Therefore B12 deficiency leads to impaired maturation of RBCs and anaemia
What is vitamin B12 deficiency anaemia?
- Macrocytic anaemia with peripheral neuropathy and neuropsych complaints
- It is a megaloblastic anaemia, as well as folate deficiency anaemia
What are the causes of B12 deficiency?
- Pernicious anaemia: most common cause
- post gastrectomy
- vegan diet or a poor diet
- disorders/surgery of terminal ileum (site of absorption)
- Crohn’s: either diease activity or following ileocaecal resection
- metformin (rare)
What is the cause of pernicious anaemia?
Autoimmune atrophic gastritis
What is B12 used for and how is it absorbed?
- DNA synthesis cofactor and the production of red blood cells
- required for cell division - Without it, cells remain large (megaloblast)
- It is normally present in meat, fish and dairy, and it absorbed in the terminal ileum combined with intrinsic factor
What is the normal physiology of Vitamin B12 absorption
B12 typically binds to Transcobalamin in the saliva (provides protection against stomach acid)
Parietal cells release Intrinsic factor (IF)
IF forms complexes with Vit B12 which is then absorbed in the ileum
B12 is then used for RBC production
What is the Pathophysiology of B12 deficiency and Pernicious anaemia?
- antibodies to intrinsic factor +/- gastric parietal cells
- intrinsic factor antibodies → bind to intrinsic factor blocking the vitamin B12 binding site
- gastric parietal cell antibodies → reduced acid production and atrophic gastritis. Reduced intrinsic factor production → reduced vitamin B12 absorption
- vitamin B12 is important in both the production of blood cells and the myelination of nerves → megaloblastic anaemia and neuropathy
What are the signs and symptoms of Pernicious anaemia?
General Anaemia Sx
Signs:
Lemon Yellow Skin
Angular Stomatitis and glossitis
Neurological SX - B12 def causes suactue combined degeneration of the Spinal chord.
presents as loss of DCML, distal paraesthesia and neuropsych symptoms (mood disturbances)
What neurological symptoms may be seen in Pernicious anaemia?
Subacute Combined Degeneration of the Spinal Cord
Impairment of the dorsal columns, lateral corticospinal tracts and spinocerebellar tracts.
dorsal column involvement
- distal tingling/burning/sensory
- loss is symmetrical and tends to affect the legs more than the arms
- impaired proprioception and vibration sense
lateral corticospinal tract involvement
- muscle weakness, hyperreflexia, and spasticity
- upper motor neuron signs typically develop in the legs first
- brisk knee reflexes
- absent ankle jerks
- extensor plantars
spinocerebellar tract involvement
- sensory ataxia → gait abnormalities
- positive Romberg’s sign
What are the diagnostic investigations of B12 Deficiency and Pernicious Anaemia?
MCV Increased - macrocytic anaemia
Blood film - Megaloblasts + Oval Macrocytes
Low serum B12 levels
Anti-IF antibodies and Anti-parietal Abs
What is the treatment of Pernicious anaemia?
Vitamin B12 replacement
- usually given intramuscularly
- no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections
- Neurological features require more frequent injections
Folic Acid Supplementation
What is Folate Deficiency Anaemia?
- A type of MACROcytic anaemia with absence of neurological signs
- Folate is required for cell division and DNA synthesis.
Without it maturing RBCs wont divide - Megalobastic
How long does B12 deficiency and pernicious anaemia take to develop?
Years
How long does Folate deficiency anaemia take to develop?
Months
What are the causes of folate deficiency anaemia?
- Poor diet (poverty, alcohol, elderly)
- Increased demand (Pregnancy, renal disease)
- Malabsorption (Coeliac)
- Drugs, alcohol and methotrexate
What is the hallmark symptom of megalobastic anaemia?
Headache
Loss of appetite and weight
What are the signs and symptoms of folate-deficiency anaemia?
General Anaemia Sx
Angular Stomatitis and Glossitis
No Neurological Sx - distinguish between B12 Def.
What is the diagnostic test for Folate deficiency Anaemia?
FBC and Blood film - Macrocytic and Megaloblasts
Decreased serum folate
What is the treatment for Folate deficiency anaemia?
Dietary advice - leafy greens and brown rice
Folate supplements
If pancytopenic then give packed RBC Transfusion
What is Autoimmune Haemolytic Anaemia?
Autoimmune Abs against RBCs causing intra and extravascular haemolysis
What are the hereditary causes of haemolytic anaemia?
- Enzyme defects (G6P dehydrogenase deficiency)
- Membrane defects (Spherocytosis, elliptocytosis)
- Haemoglobinopathies (Abnormal Hb production) (Sickle cell, thalassaemia)
What are the types of Autoimmune haemolytic anaemia?
Warm AIHA
- IgG mediated
- Commonly causes extravascular haemolysis (splee)
Cold AIHA
- IgM Mediated
- Causes haemolysis at 4 degrees
- Commonly causes intravascular haemolysis
What is the specific test to Diagnose Autoimmune Haemolytic Anaemia?
Direct Coombs Test - Agglutination of RBCs with Coombs reagent
What are the signs and symptoms of haemolytic Anaemia?
- Anaemia symptoms (Pallor, fatigue, dyspnoea)
- Jaundice (Increase in bilirubin)
- Splenomegaly (increased haemolysis)
- Dark urine (PNH)
What are the investigations for haemolytic anaemia?
Low Hb
FBC - Normocytic Anaemia
Blood film - Shistocytes, increased reticulocytes’
Jaundice features: Inc bilirubin, Inc urinary urobilin, High faecal stercobilin
Direct coombs Test - positive for autoimmune
What is the treatment of Coombs +ve haemolytic anaemia?
Treatment of any underlying disorder
- Steroids (+/- rituximab) are generally used first-line
Severe Cases
- RBC transfusion and folic acid
- Splenectomy
How does CKD cause anaemia?
Decreased EPO causes reduced erythropoiesis
Normocytic and Normochromic anaemia
What is Aplastic Anaemia?
A Pancytopenia where Bone Marrow fails and stops making haematopoietic stem cells from pluripotent cells..
What is Haemolytic Anaemia?
Anaemia caused by haemolysis - early breakdown of RBCs
What are the different Mean Corpuscular Volumes in the different types of anaemia?
Microcytic - CMV <80
Normocytic - CMV 80-95
Macrocytic - CMV >95
What is a Megaloblastic Anaemia?
An anaemia characterised by large (macrocytic) non-condensed chromatin due to impaired DNA synthesis.
B12 deficiency
Folate Deficiency
What are the main causes of splenomegaly?
Infection
Liver disease
Autoimmune disease - SLE/RA
Cancers (often haematological)
What can be reasons for Low blood count/anaemia?
Increased Loss:
BLEEDING
Haemolysis
Decreased Production:
Iron deficiency
B12 deficiency
Folate deficiency
BM failure
What is a hypochromic cell?
Pale cells due to less haemoglobin
What are the causes of anaemia of chronic disease?
Crohn’s
RA
TB
SLE
Malignant disease
CKD
What is the pathology of anaemia of chronic disease?
- Increased Hepcidin → Decreased iron absorption and release → Functional iron deficiency.
- Inflammatory cytokines (IL-6, TNF-α, IFN-γ) → Reduced erythropoiesis and blunted response to erythropoietin.
- Shortened RBC lifespan → Increased destruction of red blood cells.
- Iron sequestration in macrophages → Impaired hemoglobin synthesis.
What are the investigations of anaemia of chronic disease?
FBC and blood film
Normocytic/microcytic and hypochromic (pale)
Low serum iron and low total iron-binding capacity (TIBC)
Increased or normal serum ferritin
What is the treatment for anaemia of chronic disease?
Treat underlying cause
Recombinant erythropoietin
What is the pathology of G6PD Deficiency?
G6PD vital in hexose monophosphate shunt which maintains glutathione in reduce state. Glutathione protects the RBC from oxidative crisis
Therefore in deficiency the RBCs are easily damaged by oxidative stress.
What are some differential Diagnoses for Iron deficiency anaemia?
Thalassaemia
Anaemia of chronic disease
What would you not treat B12 deficiency anaemia with?
Folic acid supplements
Whilst this would treat the anaemia, this could mask the neurological symptoms predisposing you to an irreversible neurological deficit
What are some complications of Pernicious anaemia?
Heart failure
Angina
Neuropathy
How can you tell the difference between B12 and folate deficiency anaemia?
Both macrocytic megaloblastic anaemias
B12 presents with anaemia Sx and Neurological deficits.
Folate has no neurological deficits.
Where does haemolysis occur?
Intravascular - within blood vessels
Extravascular - within reticuloendothelial system (most common)
By macrophages in spleen (mainly), liver and bone marrow
What are the acquired causes of haemolytic anaemia
Autoimmune haemolytic anaemia
Infections - malaria
Secondary to systemic disease
What is the treatment of autoimmune haemolytic anaemia?
Folate and iron supplementation
Immunosuppressives - prednisolone/ciclosporin
Splenectomy
What are the causes of aplastic anaemia?
What is the mnemonic to remember them?
A – Autoimmune conditions (e.g., lupus)
P – Parvovirus B19 and other viral infections (like hepatitis, HIV, EBV)
L – Lithium (or other drugs/medications like chemotherapy, antibiotics)
A – Alcohol or Toxins (like benzene)
S – Stem cell disorders (e.g., Fanconi anemia)
T – Treatments with radiation or chemotherapy
I – Idiopathic (unknown cause)
C – Congenital causes (e.g., dyskeratosis congenita, Shwachman-Diamond syndrome)
What are the signs and symptoms of aplastic anaemia?
Anaemia
Increased susceptibility to infection
Increased bruising
Increased bleeding (especially from nose and gums)
What are the investigations for aplastic anaemia?
FBC – would show pancytopenia (low levels of all blood cells i.e. RBCs, WBCS etc.)
Reticulocyte count – low or absent
BM biopsy – hypocellular marrow with increased fat spaces
What is the treatment for aplastic anaemia?
Remove causative agent
Blood/platelet transfusion
BM transplant
Immunosuppressive therapy – anti-thymocyte globulin (ATG) and ciclosporin
Define Anal Fissure?
Linear tears or cracks in the mucosa of the distal anal canal, often causing severe pain and bleeding during or after bowel movements.
What is the Aetiology of Anal Fissures?
- Constipation: Hard stools can cause tearing in the distal anal canal.
- Pregnancy: Increased risk during the third trimester and post-delivery.
What are the clinical features of Anal Fissures?
- Severe anal pain or a tearing sensation during bowel movements, lasting for hours afterward.
- Anal spasms reported by about 70% of patients.
- Bright red PR bleeding typically noticed on the stool or the toilet paper.
What are the differential diagnoses for anal fissures?
- Hemorrhoids: Painful, swollen veins in the lower portion of the rectum or anus. Signs include painless bleeding during bowel movements, itching or irritation in the anal region, discomfort, swelling around the anus, and a lump near the anus.
- Anal abscess or fistula: Symptoms include anal pain, rectal discharge, bleeding, irritation, and fever.
- Anal cancer: Symptoms can include anal bleeding, anal itching, a lump or mass at the anal opening, pain or feeling of fullness in the anal area.
- Inflammatory bowel disease (Crohn’s disease or ulcerative colitis): Symptoms include diarrhea, rectal bleeding, abdominal cramps and pain, an urgent need to move the bowels, and weight loss.
What are the investigations for Anal fissures?
Clinical physical examination
What is the management for anal fissures?
Management of an acute anal fissure (< 1 week)
- soften stool is the aim
- Dietary advice: high-fibre diet with high fluid intake
- Bulk-forming laxatives are first-line - if not tolerated then lactulose should be tried
- Lubricants such as petroleum jelly may be tried before defecation
- Topical analgesia/anaesthetics - Lidocain ointment
Management of Chronic Anal Fissure
- Continue above management
- Topical GTN Ointment is first line
Patients with atypical anal fissures or symptoms/signs suggestive of Crohn’s disease should be referred to a gastroenterologist.
Define Asthma
Asthma is a chronic inflammatory airway disease leading to reversible airway obstruction. The smooth muscle in the airways is hypersensitive and responds to stimuli by constricting and causing airflow obstruction.
What is the Pathophysiology of Asthma?
Environmental trigger against specific allergens leads to sensitisation reaction where IgE Abs against antigen bind to mast cells.
Secondary exposure leads to an immune system activation and activation of Th2 cells.
Th2 cells produce cytokines such as IL3, 4, 5, 13.
IL-4 leads to IgE Crosslinking and degranulation of mast cells releasing histamine and leukotrienes.
IL-5 leads to eosinophil activation and release of proteins
This leads to a Hypersensitivity Rxn which causes Smooth muscle bronchospasm and increased mucus production leading to narrow airways and airway obstruction.
What happens to the airways in chronic asthma?
Initially asthma and inflammation of the airways is reversible.
Over chronic asthma the inflammation in the airways causes irreversible damage such as scarring and fibrosis causing thickening of the epithelial BM causing permanent narrowing of the airways.
What pathological changes are responsible for airway narrowing in Asthma?
- Increased number of and hypertrophy of smooth muscle
- Constriction of smooth muscle cells (bronchoconstriction)
- Increased mucous production
- Swelling and inflammation (of mucosa)
- Thickened basement membrane
- Airway hyperreactivity, cellular infiltration
What is Occupational Asthma?
Asthma caused by environmental triggers within the workplace
What are some risk factors for asthma?
- Family history
- Personal history of atopy
- Maternal smoking
- Viral infections
- Lower socioeconomic status
- Occupational settings: Dusts, moulds, sands
What are some typical triggers for Asthma?
- Infection
- Night time or early morning
- Exercise
- Animals
- Cold, damp or dusty air
- Strong emotions
- NSAIDs and Beta blockers
What are the clinical features of Asthma?
Symptoms:
- Wheeze
- Dyspnoea
- Cough (may be nocturnal)
- Chest tightness
- Diurnal variation (symptoms worse in the morning)
Note: symptoms may worsen following exercise, weather changes or following the use of nonsteroidal anti-inflammatory drugs (NSAIDs)/beta blockers.
Signs:
- Tachypnoea
- Hyperinflated chest
- Hyper-resonance on chest percussion
- Decreased air entry
- Wheeze on auscultation
What are the investigations for Asthma?
Peak Flow Diary:
- Due to diurnal variation theres readings will be lower in the morning
- Twice daily readings over 2-4 weeks
- Variability of 20% is positive and supports diagnosis
Spirometry with Reversibility Testing:
- FEV1/FVC < 0.7 is suggestive of obstructive airway disease
- Bronchodilator reversibility testing should increase FEV1/FVC by > 12% and 200ml
Fractional Exhaled Nitric Oxide (FeNO):
- NO is a marker of airway inflammation
- >40 ppb in adults or >35 ppb in children is a positive result and supports diagnosis
What are the NICE guidelines for diagnosing suspected asthma?
NICE 2020 Guidelines
Initial Investigations:
- FeNO
- Spirometry + Bronchodilator Reversibility
Where there is diagnostic uncertainty:
- Peak Flow Variability is the next step
Still Uncertainty:
- Direct bronchial challenge test with histamine or methacholine
What is the Non-pharmacological management for Asthma?
- Smoking cessation
- Avoidance of precipitating factors (eg. known allergens)
- Review inhaler technique
- Regular exercise
- Vaccinations/yearly flu jab
What is the Pharmacological Management for Asthma in Adults?
- Start a short-acting beta 2 agonist inhaler (e.g. salbutamol) as required
- Add a regular low dose corticosteroid inhaler
Assess Inhaler Technique
- Consider offering a leukotriene receptor antagonist (LTRA) in addition to the low dose ICS. Review the response to treatment in 4 to 8 weeks.
- Add a long-acting beta-2 agonist inhaler (e.g. salmeterol). Continue salmeterol only if the patient has a good response. (Consider stopping LRTA)
- If asthma uncontrolled, offer to change the person’s ICS and LABA maintenance therapy to a maintenance and reliever therapy (MART) regimen with a low maintenance ICS dose.
- Titrate the inhaled corticosteroid up to a moderate dose.
- If asthma is uncontrolled on a moderate maintenance ICS dose with a LABA (either as MART or a fixed-dose regimen), with or without an LTRA, consider a trial of an additional drug (Theophylline). Alternatively change ICS to high dose
What are some conditions classed as Asthma Mimics?
- Acid Reflux/GORD
- Churg-Strauss Syndrome (EGPA)
- Allergic Bronchopulmonary Aspergillosis (ABPA)
What is an Acute exacerbation of Asthma?
An acute exacerbation of asthma involves a rapid deterioration in symptoms.
What are the presenting features of an acute asthma exacerbation?
- Progressively shortness of breath
- Use of accessory muscles
- Raised respiratory rate (tachypnoea)
- Symmetrical expiratory wheeze on auscultation
- The chest can sound “tight” on auscultation, with reduced air entry throughout
What are the different severities of an acute asthma exacerbation?
Moderate: PEF > 50% predicted
Severe: PEF < 50% predicted
Life threatening: PEF < 33% predicted
What are the features of a Moderate acute asthma exacerbation?
PEF > 50% predicted
Normal speech
What are the features of a Severe acute asthma exacerbation?
- PEF 33-50% predicted
- O2 saturations < 92%
- Incomplete sentences
- Signs of respiratory distress
Respiratory rate: >25
Heart rate: >110 bpm
What are the features of a Life threatening asthma exacerbation?
33, 92, CCHEST:
- PEF < 33% predicted
- <92% - Oxygen Stats
- Cyanosis
- Confusion/Consciousness/AMS
- Hypotension
- Exhaustion and poor respiratory effort
- Silent Chest/no wheeze
- Tachycardia
What are the investigations for an Acute Asthma Exacerbation?
- Routine blood tests
- Chest X-ray to rule out pneumothorax or consolidation
- ABG as respiratory alkalosis is likely
What is the management for an Acute Asthma Exacerbation?
Maintain oxygen saturations between 94-98% with high flow oxygen if necessary.
All patients should receive steroids (Oral Prednisolone or IV hydrocortisone) given IV only if the patient is unable to take the dose orally
- Administer inhaled salbutamol via spacer: 10 puffs every 2 hours
- Proceed to nebulised salbutamol if necessary
- Add nebulised ipratropium bromide
- If O2 saturations remain <92%, add magnesium sulphate
- Add intravenous salbutamol if no response to inhaled therapy
- If severe or life-threatening acute asthma is not responsive to inhaled therapy, add IV aminophylline
If the patient is not responding to salbutamol or ipratropium, consult with a senior clinician
Define Primary Angle-closure Glaucoma/ acute angle-closure glaucoma (PACG/AACG)?
A type of glaucoma characterized by the blockage or narrowing of the drainage angle formed by the cornea and the iris, resulting in a sudden increase in intraocular pressure.
What is the epidemiology of PACG?
- Predominantly affects older individuals >40 years
What are some risk factors for PACG?
- Increasing age
- Family history
- Female (four times more likely than males)
- Chinese and East Asian ethnic origin
- Shallow anterior chamber
- Hyperopia (long-sightedness) and short axial length of the eyeball
What medications can precipitate PACG?
- Adrenergic medications (e.g., noradrenaline)
- Anticholinergic medications (e.g., oxybutynin and solifenacin)
- Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects
What is the pathophysiology of PACG?
- Occurs when the iris bulges forward and seals off the trabecular meshwork from the anterior chamber
- This prevents aqueous humour from draining and leading to a continual increase in intraocular pressure.
- The pressure builds in the posterior chamber, pushing the iris forward and exacerbating the angle closure.
It is an ophthalmological emergency requiring rapid treatment to prevent permanent vision loss.
What is the presentation of PACG?
Symptoms
- Severely Painful Red Eye: an extremely painful eye that develops rapidly, with pain spreading throughout the orbit
- Blurred vision: Can progress to vision loss
- Halos: patients will often describe coloured haloes around lights
- Systemically unwell: nausea and vomiting are very common presenting symptoms
Signs
- Red eye: ciliary flush with a hazy cornea
- Mid-dilated or fixed pupil
- Hazy Cornea
- Closed iridocorneal angles on gonioscopy
- Corneal oedema
Hard Eyeball due to Raised IOP (defined as >21 mmHg)
What are some differential diagnoses of PACG?
- Open-angle glaucoma: Gradual loss of peripheral vision, usually in both eyes, and tunnel vision in the advanced stages.
- Acute anterior uveitis: Red, painful eye, blurred vision, photophobia, and a small, irregular pupil.
- Retinal detachment: Sudden appearance of floaters, flashes of light in the periphery, and a shadow or curtain over a portion of the visual field.
What are the investigations for PACG?
Gonioscopy - assessing angle between iris and cornea
Tonometry - measurement of intraocular pressure
Ophthalmological examination
What is the immediate initial management of Acute angle closure glaucoma (PACG) in the community?
Acute angle-closure glaucoma requires immediate admission and urgent referral to ophthalmology. Measures while waiting for an ambulance are:
- Lying the patient on their back without a pillow
- A Parasympathetomimetic (Pilocarpine) eye drops (2% for blue and 4% for brown eyes)
- Acetazolamide 500 mg orally
- Analgesia and an antiemetic, if required
How does Pilocarpine work?
Pilocarpine acts on the muscarinic receptors in the sphincter muscles in the iris and causes pupil constriction (it is a miotic agent). It also causes ciliary muscle contraction.
These two effects open up the pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular meshwork.
How does Acetazolamide work?
Acetazolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour.
What is the definitive management of PACG?
Surgical management o reduce the Intra-ocular pressure
Peripheral/laser iridotomy: makes a hold in the iris allowing aqueous humour to flow from the posterior chamber to the anterior chamber to relieve the pressure
Define Blepharitis?
Blepharitis refers to inflammation of the eyelid margins.
One of the most common reaons for eye related primary care visits
What is the aetiology of Blepharitis?
It may due to either:
- meibomian gland dysfunction (common, posterior blepharitis)
- Seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis).
- Also can be caused by HSV/VZV infection
- Blepharitis is more common in patietns with rosacea
What are the symptoms of Blepharitis?
What are the signs?
The symptoms of blepharitis include:
- Painful, gritty, itchy eyes
- Eyelids sticking together upon waking
- Dry eye symptoms (due to reduced meibomian gland oils)
- Symptoms associated with the causative condition (e.g., seborrhoeic dermatitis, acne rosacea)
The signs of blepharitis include:
- Erythema of the eyelid margins
- Crusting or scaling at the eyelid margin
- Visibly blocked Meibomian gland orifices
What is the management of Blepharitis?
Blepharitis is a chronic condition for which there is no cure, but it can be well controlled and is rarely sight-threatening. The main management strategies include:
- Softening of the lid margin using hot compresses twice a day
-
‘lid hygiene’ - mechanical removal of the debris from lid margins:
- cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used
- an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has recently been boiled
- artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film
Define a Stye?
Acute infection of a gland at the edge of the eyelid or under the eyelid causing a small painful lump
External hordeolum
- Infection of an Eyelash follicle
- It is an infection of the glands of Zeis or Glands of Moll
Internal Hordeolum: is an abscess of the meibomian gland
What is a Chalazion?
A chalazion (Meibomian cyst) is a retention cyst of the Meibomian gland.
It presents as a firm painless lump in the eyelid.
The majority of cases resolve spontaneously but some require surgical drainage
What is the presentation of a stye?
Presents as a painful, red hot lump on the eyelid that points outwards, causing localized inflammation.
What is the presentation of a Chalazion?
Not usually painful, but evolves into a non-tender swelling that points inwards.
What are some differential diagnoses to a Stye/Chalazion?
- Blepharitis: Chronic inflammation of the eyelid, symptoms include red, swollen eyelids, crusting of the eyelashes, and a gritty sensation in the eye.
- Dacryocystitis: Infection of the tear sac, symptoms include pain, redness, and swelling in the inner corner of the eye.
- Cellulitis: Infection of the skin, symptoms include redness, swelling, warmth, and pain.
What is the management of a Stye/chalazion?
Stye
- Warm compresses to promote drainage.
- Topical antibiotics if infected.
- Incision and drainage in cases of large or persistent styes.
Chalazion
- Warm compresses to encourage the gland to drain.
- Steroid injections or surgical removal if it does not resolve after several weeks.
- Antibiotics are not typically needed unless there is secondary infection.
Define Entropion?
- Entropion refers to when the eyelid turns inwards with the lashes pressed against the eye.
- Causes pain and can result in corneal damage and ulceration
- Management is taping down the eyelid to prevent it turning inwards + regular lubrication to prevent the eye drying out.
- Definitive management is Surgical
Define Ectropion?
- Ectropion refers to when the eyelid turns outwards, exposing the inner aspect.
- Usually affects the bottom lid resulting in exposure keratopathy due to poor lubrication and protection of the eye ball
- Management is to regularly lubricate the eye
Define Trichiasis?
- Trichiasis refers to inward growth of the eyelashes. It results in pain and can cause corneal damage and ulceration.
- Management involves removing the affected eyelashes.
- Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent them from regrowing.
Define Benign Prostatic Hyperplasia (BPH)?
Benign prostatic hyperplasia (BPH) is a very common condition affecting men in older age (usually over 50 years). It is caused by hyperplasia of the stromal and epithelial cells of the prostate. It usually presents with lower urinary tract symptoms.
What is the pathophysiology of BPH?
- Benign proliferation of the transitional zone of the prostate (in contrast to peripheral layer expansion seen in prostate carcinoma)
- After 30, men produce ~1% less testosterone each year but 5a-reductase increases with age 🡪 increased dihydrotestosterone levels
- Prostate cells respond by living longer and growing 🡪 hypertrophy
- As the prostate gets bigger, it may squeeze or partly block:
- The bladder 🡪 urine retention 🡪 bladder dilation and hypertrophy 🡪 urine stasis 🡪 bacterial growth 🡪 UTIs
- The urethra 🡪 urination problems
What is Responsible for the growth of the Prostate in BPH?
Dihydrotestosterone is responsible for prostatic growth
What is the presentation of BPH?
Lower Urinary Tract Symptoms:
Storage:
- Frequency
- Urgency
- Nocturia
- Incontinence
Voiding:
- Straining/ Stream Poor
- Hesitancy
- Incomplete Emptying
- Terminal Dribbling
What scoring system is used to assess the severity of LUTS in men?
international Prostate Symptom Score (IPSS)
What investigations are done initially to asses men who present with LUTS?
Digital rectal examination
Abdominal examination
Urinary frequency volume chart, recording 3 days of fluid intake and output
Urine dipstick to assess for infection, haematuria
Prostate-specific antigen (PSA) for prostate cancer, depending on the patient preference
What are some diagnostic investigations for BPH?
Trans-rectal Ultrasound Scan
Biopsy to rule out prostate cancer
What are some causes that can lead to a raised PSA?
- Prostate cancer
- Benign prostatic hyperplasia
- Prostatitis
- Urinary tract infections
- Vigorous exercise (notably cycling)
- Recent ejaculation or prostate stimulation
What is the management of BPH?
If Symptoms are minimal: Watch and Wait
Lifestyle advice:
- Reduce caffeine
- Relax when voiding
Medication: if symptoms are not controlled or if experience complications of BOO
- 1st Line - alpha blocker - Tamsulosin (act immediately)
- 2nd Line - 5-alpha Reductase inhibitors - Finasteride (take 6-12 months)
Surgery (last resort)
- Transurethral resection of prostate (TURP)
What is the mechanism of action of Tamsulosin?
Alpha blocker that will relax the bladder neck increasing urinary flow rate and improving obstructive Symptoms of BPH
What is a side effect of Tamsulosin?
Dizziness, postural hypotension, dry mouth, depression, drowsiness
Retrograde ejaculation – bladder neck relaxes so sperm travels back into bladder
What is the mechanism of action of Finasteride?
5-alpha reductase inhibitor that will block conversion of testosterone to dihydrotestosterone to reduce prostatic growth
What are the Side Effects of Finasteride?
- Fatigue, lethargy
- Erectile Dysfunction
- libido loss
What is are the complications of transurethral resection of prostate surgery?
- Bleeding
- Infection
- Impotence
- Urinary incontinence
- Erectile dysfunction
- Retrograde ejaculation
- Urethral strictures
- Failure to resolve symptoms
What are some possible complications of BPH?
- Auria - no urination
- Retention
- Hydronephrosis
- UTI
- Renal Stones
Define Olecranon Bursitis?
Inflammation and swelling of the olecranon bursa over the elbow.
The olecranon is the bony lump at the elbow, which is part of the ulna bone.
What are Bursae?
- Bursae are sacs created by synovial membrane filled with a small amount of synovial fluid.
- They are found at bony prominences (e.g., at the greater trochanter, knee, shoulder and elbow).
- They act to reduce the friction between the bones and soft tissues during movement.
Define Bursitis?
Bursitis is inflammation of a bursa. This causes thickening of the synovial membrane and increased fluid production, causing swelling.
What is the aetiology of Olecranon Bursitis?
- Friction from repetitive movements or leaning on the elbow (common in students, drivers, plumbers etc)
- Trauma
- Inflammatory conditions (e.g., rheumatoid arthritis or gout)
- Infection – referred to as septic bursitis
What is the presentation of Olecranon Bursitis?
The typical presentation is a young/middle-aged man with an elbow that is:
- Swollen
- Warm
- Tender
- Fluctuant (fluid-filled)
What may be some addition features of Olecranon bursitis when it is caused by infection?
- Hot to touch
- More tender
- Erythema spreading to the surrounding skin
- Fever
- Features of sepsis (e.g., tachycardia, hypotension and confusion
What is the management of Olecranon Bursitis?
Management:
- Rest
- Ice
- Compression bandaging if tolerated
- Elevation to reduce swelling
- Analgesia (e.g., paracetamol or NSAIDs)
- Protecting the elbow from pressure or trauma
- Aspiration of fluid may be used to relieve pressure
- Steroid injections may be used in problematic cases where infection has been excluded
When infection is suspected or cannot be excluded, management involves:
- Aspiration of the fluid for microscopy and culture: rule out crystal arthropathy and septic arthritis
- Antibiotics
Define Trochanteric Bursitis?
Trochanteric bursitis refers to inflammation of a bursa over the greater trochanter on the outer hip (femur).
It produces pain localised at the outer hip, referred to as greater trochanteric pain syndrome.
What is the aetiology of Trochanteric Bursitis?
- Friction from repetitive movements
- Trauma
- Inflammatory conditions (e.g., rheumatoid arthritis)
- Infection – referred to as septic bursitis
What is the clinical presentation of Trochanteric Bursitis (Greater Trochanteric Pain Syndrome)?
- middle-aged patient with gradual-onset lateral hip pain (over the greater trochanter) that may radiate down the outer thigh.
- Aching or burning pain
- Worse with activity, standing/sitting for long periods/lying on affected side
- May disrupt sleep
- Tenderness on examination over the greater trochanter
- Positive Trendelenburg gait
- Not usually any swelling compared to bursitis in other areas
What are some differential diagnoses for Trochanteric Bursitis?
- Hip osteoarthritis: Characterised by chronic pain in the hip, morning stiffness, reduced range of motion, and pain that worsens with activity.
- Iliotibial band syndrome: Presents with lateral knee pain, tenderness, and often a snapping or popping sensation on the outer knee.
- Hip fracture: Acute, severe pain following trauma, inability to weight-bear, and physical examination may reveal shortening and external rotation of the leg.
- Lumbar radiculopathy: Characterised by pain radiating from the lower back to the lower limb, often accompanied by numbness or weakness in the affected limb.
What are the investigations for Trochanteric Bursitis?
What movements will cause pain?
Generally a clinical diagnosis
- Examination and palpation of the greater trochanter
- Trendelenburg Test
- Resisted, abduction, internal and external rotation of the hip (Pain on these resisted movements supports the diagnosis)
What is the management of Trochanteric Bursitis?
Usually Self limiting
- Reduce compressive forces: Weight loss, avoidance of excessive hip adduction
- Rest
- Ice
- Analgesia (e.g., ibuprofen or naproxen)
- Physiotherapy
- Steroid injections in some cases to reduce inflammation
Define Chronic Kidney Disease (CKD)?
Chronic kidney disease (CKD) describes a chronic reduction in kidney function where the GFR <60ml/min sustained over three months. It tends to be permanent and progressive.
What is the Epidemiology of CKD?
CKD has an estimated prevalence of 9–13% worldwide.
What are the stages of CKD?
KDIGO Criteria gives a G score based on eGFR (ml/min/1.73m^) and A score (Albumin:creatinine ratio mg/mmol):
Stage 1 (G1):
- eGFR >90
- A1: <3 mg/mmol
Stage 2 (G2):
- eGFR 60-89
- A2: 3-30 mg/mmol
Stage 3a (G3A):
- eGFR 45-59
- A3: >30 mg/mmol
Stage 3b (G3b): eGFR 30-44
Stage 4 (G4): eGFR 15-29
Stage 5( G5/End stage): eGFR <15
Patients are typically asymptomatic until stage 4 or 5 CKD
What are some risk factors for CKD?
Kidney function naturally declines with age
- diabetic nephropathy
- chronic glomerulonephritis
- chronic pyelonephritis
- hypertension
- adult polycystic kidney disease
What are the clinical features of CKD?
Most patients with CKD are Asymptomatic until stage 4/5
- Fatigue
- Pallor (due to anaemia)
- Foamy urine (proteinuria)
- Nausea
- Loss of appetite
- Pruritus (itching)
- Oedema
- Hypertension
- Peripheral neuropathy
CRF HEALS
What are the complications of CKD?
Cardiovascular disease
Renal osteodystrophy
Fluid (oedema)
Hypertension
Electrolyte disturbance (hyperkalaemia, acidosis)
Anaemia
Leg restlessness (uraemia)
Sensory neuropathy (uraemia)
What is the most common cause of death in CKD?
Cardiovascular disease
What are the investigations for CKD?
CKD staging is based on the eGFR and Urine Albumin:Creatinine Ratio (ACR)
- FBC: Anaemia (normocytic)
- U&Es: Raised creatinine and urea, Low eGFR (ACR > 3 is significant)
- Urine Dipstick: Proteinuria and Haematuria
- Renal Ultrasound: Bilaterally small kidneys in CKD
Others:
- Blood pressure (for hypertension)
- HbA1c (for diabetes)
- Lipid Profile (for hypercholesterolaemia)
- ECG: for hyperkalaemia
What are the management targets of CKD?
Focuses on preserving kidney function, managing complications of CKD and preparing for RRT
Lifestyle Interventions:
- Maintaining health weight
- Health diet
- Exercise
- Smoking cessation
Hypertension:
- Blood pressure <140/90 mmHg in patients with CKD and ACR <70 mg/mmol
- Blood pressure <130/80 mmHg in patients under 80 with CKD and ACR >70 mg/mmol
Diabetes: Individualised targets but generally:
- HbA1c <53 mmol/mol
What is the Pharmacological Management of CKD?
Slow disease progression
- ACE inhibitors
- SGLT2 inhibitors (Dapagliflozin)
Reduce risk of complications:
- Exercise, maintain healthy weight and smoking cessation
- Atorvastatin 20mg for primary prevention of CVD
Management of Complications:
- Oral sodium bicarbonate: for metabolic acidosis
- Iron and erythropoietin replacement: to treat anaemia
- Vitamin D, Low phosphate diet for Renal Bone Disease
End-stage Renal Disease:
- Special dietary advice
- Dialysis
- Renal Transplant
What are the options for Dialysis in End stage renal disease?
Haemodialysis:
Peritoneal Dialysis:
Haemofiltration:
What is the pathophysiology of Anaemia as a complication of CKD?
- Healthy kidneys produce erythropoietin, a hormone that stimulates the production of red blood cells.
Reduced Erythropoietin Levels:
- CKD results in lower erythropoietin and a drop in red blood cell production.
Reduced Iron Absorption
- Inflammation and reduced renal clearance of Hepcidin
- Decreased iron absorption from the gut
- Reduced iron stores for erythropoiesis
What is the management of Anaemia due to CKD?
- Iron deficiency if present is treated first (IV iron)
- EPO stimulating agents such as recombinant EPO
What is the pathophysiology of Renal Bone Disease as a complication of CKD?
Basic problems in chronic kidney disease (CKD):
- 1-alpha hydroxylation normally occurs in the kidneys → CKD leads to low vitamin D
- The kidneys normally excrete phosphate → CKD leads to high phosphate
This, in turn, causes other problems:
- The high phosphate level ‘drags’ calcium from the bones, resulting in osteomalacia
- Low calcium: due to lack of vitamin D, high phosphate
- Secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D
What is the management of Renal bone disease due to CKD?
- Low phosphate diet
- Phosphate binders
- Active forms of vitamin D (alfacalcidol and calcitriol)
- Ensuring adequate calcium intake
- Parathyroidectomy in certain cases
What is Vaginal Candidiasis?
Also known as Thrush/yeast infection
Vaginal infection with a Yeast of the Candida family most commonly Candida albicans
How many presentations of Vaginal Candidiasis is required for it to be classified as recurrent?
Recurrent vaginal candidiasis is defined as 4 or more symptomatic episodes within 1 year
What are the risk factors for Vaginal Candidiasis?
- Increased oestrogen (higher in pregnancy, lower pre-puberty and post-menopause)
- Poorly controlled diabetes
- Using SGLT2 inhibitors
- Pregnancy
- Immunosuppression (e.g. using corticosteroids)
- Broad-spectrum antibiotics
What is the main causative organism of Vaginal candidiasis?
Candida albicans - 85-90% of the cases.
Transmission is typically non-sexual
What are the clinical features of Candidiasis?
Symptoms:
- Itching
- Cottage cheese non-offensive discharge
- typically does not smell but may have sour milk odour
- dysuria
- superficial dyspareunia
- tenderness,
- Burning sensation.
Examination findings:
- Redness
- Satellite lesions
- fissuring,
- swelling,
- intertrigo,
- thick white discharge.
What are some differential diagnoses for Vaginal Candidiasis?
- Bacterial vaginosis: Characterised by greyish-white discharge, fishy odour, and absence of significant inflammation.
- Trichomoniasis: Presents with yellow-green, frothy discharge, dysuria, and itching.
- Chlamydia or Gonorrhoea: These sexually transmitted infections can cause similar symptoms such as discharge, but often also present with pelvic pain or bleeding.
- Genital herpes: Characterised by painful blisters or open sores in the genital area.
What are the investigations for Vaginal Candidiasis?
Clinical Diagnosis and Routine investigations usually not required
- Testing Vaginal pH with a swab can help differentiate between Bacterial Vaginosis, Trichomonas (pH > 4.5) and candidiasis (pH < 4.5)
- Charcoal wab + microscopy can confirm the diagnosis
What is the management of Vaginal Candidiasis?
Antifungal Treatment:
- First Line: Oral Antifungal Tablets (Fluconazole, Itraconazole): 150mg capsule as a single dose
- Second Line: Antifungal pessary (Clotrimazole): 500mg as a single dose
- Antifungal Cream (Clotrimazole): 10% 5g as a single dose if vuvlal symptoms
if pregnant then only local treatments (e.g. cream or pessaries) may be used - oral treatments are contraindicated
What is Oral Candidiasis?
Oral candidiasis is also called oral thrush. It refers to an overgrowth of candida, a type of fungus, in the mouth.
This results in white spots or patches that coat the surface of the tongue and palate.
What are some risk factors for Oral Candidiasis?
- Inhaled corticosteroids (particularly with poor technique, not using a spacer and not rinsing with water afterwards)
- Antibiotics (disrupt the normal bacterial flora giving candida a chance to thrive)
- Diabetes
- Immunodeficiency (consider HIV)
- Smoking
What is the management of Oral Candidiasis?
- Miconazole gel
- Nystatin suspension
- Fluconazole tablets (in severe or recurrent cases)
Define Conjunctivitis?
Conjunctivitis (Pink Eye) is inflammation of the conjunctiva. The conjunctiva is a thin layer of tissue that covers the inside of the eyelids and the sclera.
- Conjunctivitis may be Infectious (bacterial, viral) or Non-infectious (allergic/irritant)
- It may be unilateral or bilateral.
What is the Aetiology of Conjunctivitis?
Allergic Conjunctivitis:
- Type 1 hypersensitivity reaction
- common triggers include pollen, dust mites, pet dander
Viral Conjunctivitis:
- Most commonly caused by Adenoviruses
- May be caused by Herpes Simplex Virus
- Highly Contagious
- Often associated with URTIs or Colds
Bacterial Conjunctivitis:
- S. aureus, S. pneumoniae, H. influenzae, M. catarrhalis
- May be caused by STIs such as Gonorrhoea or Chlamydia
What are the clinical features of Conjunctivitis?
General Presentation:
- Non-painful eye
- Red bloodshot eye
- Itchy or Gritty sensation
- Irritation
- Excessive tearing
- Discharge
Viral Presentation:
- Clear discharge
- Associated with dry cough, sore throat and blocked nose
Bacterial Presentation:
- Purulent discharge
- Complaints of eyelids being stuck together (often in morning)
What are some causes of an Acute painful red eye?
- Acute angle-closure glaucoma
- Anterior uveitis
- Scleritis
- Corneal abrasions or ulceration
- Keratitis
- Foreign body
- Traumatic or chemical injury
What are some causes of an Acute painless red eye?
- Conjunctivitis
- Episcleritis
- Subconjunctival haemorrhage
What is the management of Conjunctivitis?
Typically resolves in 1-2 weeks without needing treatment
- Hygiene measures to reduce the spread
- Clean the eyes with cooled boiled water and cotton wool to help clear the discharge
- Antihistamines (oral/topical) if allergic conjunctivitis
- Chloramphenicol or Fusidic acid eye drops for bacterial conjunctivitis if necessary
Define Contact Dermatitis?
Contact dermatitis is a skin condition marked by inflammation of the skin, resulting from direct contact with substances that irritate the skin (irritant contact dermatitis) or provoke an allergic response (allergic contact dermatitis).
What are the risk factors for Contact Dermatitis?
- Exposure to irritants or allergens in the environment or workplace
- Personal or family history of atopic dermatitis or other allergic conditions
- Occupation involving frequent exposure to potential irritants or allergens
- Use of certain skincare products or cosmetics containing allergenic ingredients
- Previous episodes of contact dermatitis increase the risk of future occurrences
What is the pathophysiology of Irritant Contact Dermatitis?
Non-allergic reaction:
Occurs when the skin’s natural barrier is disrupted by exposure to irritating substances, such as harsh chemicals, detergents, or solvents (weak acids/alkalis). This results in direct damage to the skin’s cells and inflammation.
What is the pathophysiology of Allergic Contact Dermatitis?
This is a delayed type IV hypersensitivity reaction. Exposure to an allergen (often a low-molecular-weight chemical) sensitizes the immune system over time. Upon re-exposure (e.g. after repeated hair dyes), an immune response is triggered, leading to inflammation and the characteristic skin rash.
What is the presentation of Irritant Contact Dermatitis?
- Eczema due to contact with an irritant.
- There may be burning, pain, and stinging.
- Erythematous
- Eczematous rash appears localised to the direct area of contact
What is the presentation of Allergic Contact Dermatitis?
- Presents as an itchy, eczematous rash (vesicles, fissures, erythema), typically 24-48 hours after exposure.
- The rash may extend beyond the boundaries of immediate contact
What are some typical allergens that cause allergic Contact Dermatitis?
- Nickle found in jewellery, watches, metal buttons on clothing
- Acrylates found in nail cosmetics
- Fragrances
- Rubber/plastics
- Hair dye
- Henna
What are the investigations for Contact Dermatitis?
Contact dermatitis is a clinical diagnosis and investigations aren’t always needed. However, investigations may include:
- Patch Testing: used to identify allergens responsible for allergic contact dermatitis.
- Skin Biopsy: rarely necessary, but it can help confirm the diagnosis or rule out other conditions.
What is the management of Contact Dermatitis?
- Avoidance of the irritant/allergen: 8-12 weeks avoidance may be needed before improvements are seen
- liberal emollient and soap substitutes
- Topical steroids (depends on severity of dermatitis)
- Antihistamines for pruritis relief
Define Chronic Obstructive Pulmonary Disease (COPD)?
Chronic obstructive pulmonary disease (COPD) is characterised by irreversible, progressive obstruction of the airways caused by long term damage to lung tissue.
It comprises both:
- Chronic bronchitis – involves hypertrophy and hyperplasia of the mucus glands in the bronchi
- Emphysema – involves enlargement of the air spaces and destruction of alveolar walls
What is the Epidemiology of COPD?
- Approximately 1.2 million people, or about 2% of the UK population, are living with diagnosed COPD.
- Each year, COPD accounts for approximately 30,000 deaths or 26% of all lung disease-related deaths.
- Majority of patients have a history of tobacco smoking
What are some risk factors for COPD?
- Tobacco smoking (active or passive)
- Occupational exposure to dust
- Air pollution
- Alpha-1 antitrypsin deficiency
Prognosis is worsened by:
- Advancing age
- Ongoing smoking
- Reduced body weight
- Low FEV1
Define Chronic Bronchitis?
A inflammatory lung condition that develops over time in which the bronchi and bronchioles become inflamed and scarred
Chronic Bronchitis is a clinical term relating to a chronic productive cough for at least 3 months over 2 consecutive years.
Alternative explanations for the cough should also be excluded.
What is Emphysema as a pathological Definition?
Refers to abnormal air space enlargement distal to terminal bronchioles with evidence of alveoli destruction and no obvious fibrosis. Damage to the alveolar sacs and alveoli decreases the gas exchange surface
What is the pathophysiology of Chronic Bronchitis?
- Chronic exposure to noxious particles such as smoking or air pollutants causes hypersecretion of mucus in the large and small bronchi.
- Airway inflammation and fibrotic changes result in narrowing of the airways and subsequently chronic airway obstruction.
- Cigarette smoke interferes with the action of cilia in removing noxious particles.
- Cigarette smoke also dampens the ability of leukocytes in eliminating the bacteria in the airways.
What is the pathophysiology of Emphysema?
- Abnormal irreversible enlargement of the airspaces distal to the terminal bronchioles, due to destruction of their walls.
- This reduces the alveolar surface area thus impeding efficient gaseous exchange.
- Cigarette smoke stimulates accumulation of neutrophils and macrophages which produce neutrophil elastase that destroys alveolar walls.
- In a normal lung, α1-antitrypsin is responsible for inhibiting excessive activity of neutrophil elastase. However, in emphysema, the normal balance of proteases and antiproteases is lost.
- The stimulated neutrophils release free radicals that inhibit the activity of α1-antitrypsin.
- This results in loss of elastic recoil and subsequently airway collapse during expiration and air trapping.
What are the different types of Emphysema?
Centriacinar:
- The proximal part of the airways such as the respiratory bronchioles, mainly the upper lobes.
- Caused by cigarette smoking
Panacinar:
- The entire acini from respiratory bronchioles to alveolar duct and alveoli, mainly the lower lobes.
- Caused by alpha1-antitrypsin deficiency
Distal/Paraseptal Acinar:
- The distal part of the airways, mainly the paraseptal region
- Caused by Fibrosis, atelectasis
What are the clinical symptoms of COPD?
- Productive cough
- Recurrent respiratory infections (especially in winter)
- Wheeze
- Dyspnoea (shortness of breath)
- Reduced exercise tolerance
- Weight loss
What are the clinical signs of COPD?
- Accessory muscle use for respiration
- Prolonged expiratory phase
- Pursed lip breathing (Common in Emphysema)
- Tachypnoea
- Cachexia
- Hyperinflation – reduction of the cricosternal distance (barrel chest)
- Reduced chest expansion
- Hyper-resonant percussion
- Decreased/quiet breath sounds
- Wheeze
- Cyanosis (Common in Chronic bronchitis)
- Cor pulmonale (signs of right heart failure)
What clinical features are NOT seen in COPD and thus suggest and alternative diagnosis?
- Clubbing
- Haemoptysis
- Chest Pain
What is the MRC Dyspnoea Scale?
Grade 1: Breathless on strenuous exercise
Grade 2: Breathless on walking uphill
Grade 3: Breathlessness that slows walking on the flat
Grade 4: Breathlessness stops them from walking more than 100 meters on the flat
Grade 5: Unable to leave the house due to breathlessness
What are the investigations for COPD?
Clinical Diagnosis with Spirometry
Spirometry:
- FEV1/FVC <0.7
- Little to no response with Bronchodilator reversibility testing
Other Investigations:
Bloods: FBC for polycythaemia, anaemia, infection
ABG: Reduced PaO2 +/- Raised PaCO2
ECG: to assess for heart failure or Cor pulmonale
Chest X-ray: To exclude other pathology such as cancer
Sputum Culture: To assess for Chronic infections such as pseudomonas
Serum a1AT: Look for alpha1-antitrypsin deficiency
What may be seen on an ECG in COPD?
- P-pulmonale showing Right Atrial Hypertrophy due to increased pulmonary pressures
- Right ventricular Hypertrophy if there is Cor pulmonale
What may be seen on Chest X-ray in COPD?
- Hyperinflated chest (>6 anterior ribs)
- Bullae
- Decreased peripheral vascular markings
- Flattened hemidiaphragms
How is the Severity of COPD Assessed?
Post Bronchodilator when FEV1/FVC ratio < 70%
Stage 1: Mild - FEV1 >80% of predicted
Stage 2: Moderate - FEV1 50-79% of predicted
Stage 3: Severe - FEV1 30-49% of predicted
Stage 4: Very Severe - FEV1 <30% of predicted
What are some differential diagnoses for COPD?
- Asthma: Characterised by reversible airway obstruction, episodic symptoms and response to bronchodilators.
- Bronchiectasis: Persistent productive cough, recurrent respiratory infections and abnormal bronchial dilatation on CT chest.
- Heart Failure: Shortness of breath, orthopnea, paroxysmal nocturnal dyspnoea, and signs of fluid overload such as peripheral oedema and elevated jugular venous pressure.
- Pulmonary Fibrosis: Progressive dyspnoea, non-productive cough, and inspiratory crackles on auscultation.
What is the Non-pharmacological management of COPD?
- Smoking cessation (significantly worsens lung function and prognosis)
- Nutritional support
- Flu and pneumococcal vaccinations
- Pulmonary rehabilitation
What is the Pharmacological Management for COPD?
Initial Medical Treatment: Short Acting Bronchodilators:
- SABA: Salbutamol
- SAMA: Ipratropium Bromide
Second Step when symptoms or exacerbations are problematic and is determined based on asthmatic/steroid responsive features:
No Steroid Responsive Features:
- Offer LABA (Salmeterol) PLUS LAMA (Tiotropium).
- Anoro Ellipta, Ultibro Breezhaler, DuaKlir Genuair
- If no improvement then consider 3 month trial of LABA Plus LAMA Plus ICS (to change back to LABA + LAMA in 3 months if not worked)
Has Steroid Response Features:
- Offer LABA Plus ICS
- Fostair, Symbicort, Seretide
- If day-day symptoms continue or pt has 1 severe/2 moderate exacerbations then offer LABA Plus LAMA Plus ICS
LABA + LAMA + ICS:
- Trimbow, Trelegy Ellipta, Trixeo Aerosphere
What are the steroid responsive features that may guide COPD management?
- Raised blood eosinophil count
- Previous diagnosis of asthma or atopy
- Variation in FEV1 of more than 400mls
- Diurnal variability in peak flow of more than 20%
What are some other management options in Severe cases (Guided by Specialists?)
- Nebulisers (e.g., salbutamol or ipratropium)
- Oral theophylline
- Oral mucolytic therapy to break down sputum (e.g., carbocisteine)
- Prophylactic antibiotics (e.g., azithromycin)
- Oral corticosteroids (e.g., prednisolone)
- Oral phosphodiesterase-4 inhibitors (e.g., roflumilast)
- Long-term oxygen therapy at home
- Lung volume reduction surgery (removing damaged lung tissue to improve the function of healthier tissue)
- Palliative care (opiates and other drugs may be used to help breathlessness)
What are the indications for Long Term Oxygen Therapy (LTOT)?
Used in Severe COPD where there is:
- Chronic Hypoxia (Sats <92%)
- polycythaemia
- Cyanosis
- Core pulmonale
Smoking is a contraindication due to the fire risk
What is an Acute Exacerbation of COPD?
An acute COPD exacerbation presents rapidly worsening symptoms, such as cough, shortness of breath, sputum production and wheezing. Viral or bacterial infection often triggers it.
(Often caused by haemophilus influenzae)
What are the investigations for an Acute Exacerbation of COPD?
ABG: Showing Respiratory failure and Respiratory Acidosis
Others:
- Chest X-ray: Look for pneumonia or other pathology
- ECG: Look for arrhythmias or evidence of heart strain
- FBC: Look for infection (raised WCC)
- U&Es: Check Electrolytes
- Sputum or blood cultures
What is the management of an Acute Exacerbation of COPD?
Ensure Patent Airway:
Ensure Oxygen Saturations of 88-92% (if pt has a history of CO2 retention)
First-line medical treatment of an acute exacerbation of COPD involves:
- Regular nebulisers (e.g., salbutamol and ipratropium)
- Steroids (e.g., prednisolone 30 mg once daily for 5 days)
- Antibiotics if there is evidence of infection
Respiratory physiotherapy can be used to help clear sputum.
Additional options in severe cases include:
- IV aminophylline
- Non-invasive ventilation (NIV)
- Intubation and ventilation with admission to intensive care
What is a common complications of COPD exacerbations?
respiratory Failure: COPD patients are chronic retainers of CO2 and therefore their kidneys adapt to produce extra HCO3 to compensate the acidotic state. In acute exacerbations the kidneys cannot produce enough HCO3 quickly leading to respiratory failure
- Low pH indicates acidosis
- Low pO2 indicates hypoxia and respiratory failure
- Raised pCO2 indicates CO2 retention (hypercapnia)
- Raised bicarbonate indicates chronic retention of CO2
What are some complications of COPD?
- Cor pulmonale
- Recurrent Respiratory Tract Infections: S. pneumoniae/H. influenzae
- Respiratory failure
- Pneumothorax: rupture of bullous disease (in Emphysema)
- Polycythaemia or anaemia
- Depression
What is Cor Pulmonale?
Cor pulmonale refers to right-sided heart failure caused by respiratory disease.
- The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) limits the right ventricle pumping blood into the pulmonary arteries.
- This causes back-pressure into the right atrium, vena cava and systemic venous system.
What are the causes of Cor Pulmonale?
- COPD (the most common cause)
- Pulmonary embolism
- Interstitial lung disease
- Cystic fibrosis
- Primary pulmonary hypertension
What are the clinical symptoms of Cor pulmonale?
early Cor pulmonale is asymptomatic
- Shortness of breath
- Peripheral oedema
- Breathlessness of exertion
- Syncope (dizziness and fainting)
- Chest pain
What are the clinical signs of Cor pulmonale?
- Hypoxia
- Cyanosis
- Raised JVP (due to a back-log of blood in the jugular veins)
- Peripheral oedema
- Parasternal heave
- Loud second heart sound
- Murmurs (e.g., pan-systolic in tricuspid regurgitation)
- Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
What is the Management of Cor pulmonale?
Symptom management and treating the underlying cause:
Diuretics: For oedema and fluid overload
LTOT is often used
Define Tinea?
Also known as Ringworm
A superficial fungal infection of the skin caused by dermatophytes, a group of fungi that invade and grow in dead keratin.
The most common type of fungus that grows is Trichophyton
What is the Epidemiology of Tinea?
- Can affect anyone
- Related to poor hygiene
What are the different types of Tinea?
Tinea capitis refers to ringworm affecting the scalp (caput meaning head)
Tinea pedis refers to ringworm affecting the feet, also known as athletes foot (pedis meaning foot)
Tinea cruris refers to ringworm of the groin (cruris meaning leg)
Tinea corporis refers to ringworm on the body (corporis meaning body)
Onychomycosis refers to a fungal nail infection
Tinea manuum refers to ringworm on the hand
What are some risk factors for Tinea?
- Fungal infection in another part of their body
- Poor Hygiene
- Close contact with infected individuals or animas
- Immunocompromised nature
What are the clinical features of Tinea?
- Itchy erythematous scaly rash that is well demarcated.
- The rash has a central clearing giving it the appearance of a ring.
What are some differential diagnoses for Tinea?
- Psoriasis: Characterised by silver-scaled plaques in typical locations such as elbows, knees, and scalp.
- Eczema (dermatitis): Generally causes dry, itchy, and inflamed skin.
- Pityriasis rosea: Features a herald patch followed by a ‘Christmas tree’ pattern of rash.
- Lyme disease: Erythema migrans, the initial sign, is a red, expanding rash that sometimes presents with a bull’s eye appearance.
What are the investigations for Tinea?
Clinical Diagnosis supported by good response to anti-fungal medications
- Green flourescence under Woods Lamp
- May be supported with culture of skin/scalp scrapings
What is the management of Tinea?
General Hygiene Advice
Anti-fungal medications:
- Anti-fungal creams such as clotrimazole and miconazole
- Anti-fungal shampoo such as ketoconazole for tinea capitis
- Oral anti-fungal medications such as fluconazole, griseofulvin and itraconazole
- Fungal Nail infections are treated with amorolfine nail lacquer for 6-12 months
- In resistance cases oral terbinafine may be required but this needs LFT monitoring before and after.
What advice should you give to patients with Tinea to prevent it reoccurring?
- Wear loose breathable clothing
- Keep the affected area clean and dry
- Avoid sharing towels, clothes and bedding
- Use a separate towel for the feet with tinea pedis
- Avoid scratching and spreading to other areas
- Wear clean dry socks every day
What is Intertrigo?
An inflammatory condition of the skin folds, resulting from skin-on-skin friction, often exacerbated by heat, moisture, maceration, and lack of air circulation. It is frequently complicated by secondary bacterial or fungal infections.
What is the epidemiology of Intertrigo?
- Obese patients
- Hyperhydrosis
- Diabetes mellitus
- Infants, due to short necks, relative chubbiness, and flexed posture. Intertrigo in infants may be exacerbated by drooling.
- Individuals who frequently wear closed-toe or tight-fitting shoes, which can induce toe web intertrigo. This commonly affects those participating in athletic, occupational, or recreational activities.
- Those with other predisposing factors, including urinary and faecal incontinence, hyperhidrosis, diabetes, poor hygiene, and malnutrition.
What is the Aetiology of Intertrigo?
The moist, damaged skin associated with intertrigo provides a fertile environment for the proliferation of various pathogens, leading to frequent secondary cutaneous infections:
- Bacterial infection: Staphylococcus aureus, group A beta-haemolytic streptococcus, and various gram-negative organisms may occur alone or in combination. Proliferation may lead to keratinocytic necrosis.
- Fungal infection: Candida is the fungus most commonly associated with intertrigo. In the toe webs, gram-negative bacteria often coexist.
What are the clinical features of Intritrigo?
- Itching, Burning and Pain in the affected areas
- Distribution: The condition is most prevalent in the groin, axillae, and inframammary folds. It may also affect antecubital fossae; umbilical, perineal, or interdigital areas; neck creases; and folds of the eyelids.
- Morphology: The condition is characterised by erythematous patches, often symmetrical. Erythema may progress to more severe inflammation with erosions, fissures, exudation, crusting, and maceration.
What are some differential diagnoses for Intritrigo?
- Seborrhoeic eczema: Can present similarly but often has scalp involvement and lacks the typical satellite lesions of Candidal intertrigo.
- Psoriasis: May appear similar, but psoriasis is often associated with nail changes and glistening, well-demarcated, symmetrical flexural lesions.
- Tinea cruris: Lesions are often annular or polycyclic, and tend to have a leading erythematous scaly edge.
- Erythrasma, atopic eczema, irritant contact dermatitis, allergic contact dermatitis, and scabies can all involve skin folds and therefore be mistaken for intertrigo.
- Hailey-Hailey disease and pemphigus vegetans are less common conditions that can be mistaken for intertrigo.
What are the investigations for Intritrigo?
Clinical diagnosis based on examination and response to treatment:
May require:
- Fungal culture to rule out fungal infection
- Bacterial culture to identify secondary bacterial infection
- Skin biopsy for histopathological examination in unclear or refractory cases
What is the Management of Intritrigo?
Minimise moisture and friction: Loose-fitting clothing, weight loss if necessary, and the use of barrier creams can all reduce skin-on-skin friction and moisture.
Promote skin hygiene: Regular cleaning of the affected areas with mild soap and water.
Patient Education: On the chronic and recurrent nature of the disease and importance of preventive measures
Topical agents:
- Zinc oxide ointment (reduces friction)
- Application of topical antifungal, antibacterial, or corticosteroid agents, depending on the causative organisms and severity of inflammation.
- Clotrimazole
What are the Crystal Arthropathies?
- Gout
- Pseudogout
What are the types of crystals formed in Crystal arthritis?
Gout:
- Needle Shaped monosodium Urate Crystals
- Negatively Birefringent in polarised light
Pseudogout:
- Rhomboid Brick shaped Pyrophosphate crystals
- Positively Birefringent in Polarised Light
Define Gout?
Gout is a form of Crystal arthritis caused by the deposition of monosodium urate crystals in and around the joints leading to an acute inflammatory response
What are some risk factors for Gout?
Nonmodifiable
- Male sex
- Age over 50 years
- Family history of gout
- Inherited syndrome with uric acid overproduction (eg. Lesch–Nyhan syndrome)
Modifiable
- Obesity
- High purine diet such as meats and alcohol
- Hypertension
- Chronic kidney disease
- Diabetes
- Metabolic syndrome
- Medications (eg. thiazide diuretics, ACE inhibitors and aspirin)
What factors can impair the excretion/removal of uric acid?
CKD
Diuretics, ACEis
Pyrazinamide
Lead Toxicity
What are some triggers of Gout?
- Seafood/protein binges – eating lots of high-protein foods raises levels of uric acid
- Chemotherapy – increases cell breakdown
- Trauma and surgery – increases cell breakdown
- Alcohol excess
- Intercurrent illness
- Medications that interfere with the handling of uric acid (eg. allopurinol)
What is the pathogenesis of Gout?
High purine intake (food/alcohol)
Is oxidised to Uric acid by Xanthine oxidase.
Normally uric acid is then excreted by the kidneys
But in hyperuricaemia this cannot occur fast enough and this can lead to kidney damage
The Uric acid is converted to monosodium urate crystals that trigger intracellular inflammation.
These deposit in joints and cause an inflammatory arthritis
What substances can be anti-gout?
Dairy
What are the clinical features of Gout?
- Excruciating, sudden, burning pain in the affected joint
- Swelling, redness, warmth and stiffness in the affected joint
- Asymmetric joint distribution
- Gouty Tophi: Nodular masses of urate acid crystals subcutaneously commonly seen on the hands, elbows and ears
- Mild fever
- Tachycardia as a transient sympathetic response to the pain of an acute attack
What are the most commonly affected joints in Gout?
- Base of the Big Toe (Metatarsophalangeal joint/MTP Joint)
- Base of the Thumb (Carpometacarpal join/ CMC Joint)
- Wrist
What are some differential diagnoses for Gout?
- Pseudogout: Typically affects the larger joints such as the ankle, knee, hips, wrist and shoulder
- Septic Arthritis: Vital to rule this out so any suspicion of an acute onset arthritis should have this checked
What are the investigations for Gout?
Joint Aspiration:
- Negatively birefringent needle shaped Monosodium Urate Crystals
Serum Uric Acid Level:
- Useful for long term management
- Should be obtained at least 2 weeks after the attack as during this they may be falsely low or normal (Since all the uric acid is in the joint space)
X-ray of affected joints:
What may be seen on X-ray in Gout?
- Maintained joint space (no loss of joint space)
- Lytic lesions in the bone
- Punched out erosions
- Erosions can have sclerotic borders with overhanding edges
What is the Management of an Acute Gout Flare?
First Line: NSAIDs
- Naproxen 500mg BD
- Co prescribed with a PPI for gastric protection
- Avoid if renal impaired, cardiac failure and IHD
Second Line: Colchicine
- Colchicine 500ug BD
- Use with cation in liver or renal disease and can cause diarrhoea
Third Line: Oral Corticosteroids
- Prednisolone, 30mg OD for 5-7 days
- Intra-articular corticosteroids is also an option
What is the Prevention Management for Gout?
Lifestyle Changes:
- Reduce alcohol consumption
- Reduce purine based food consumption - Meat and seafood
- Increase Dairy consumption and hydration
- Regular Exercise and weight loss
Review Medications that may cause hyperuricaemia
Urate Lowering Therapies: Xanthine Oxidase Inhibitors
- Allopurinol or Febuxostat
- Should not be started until weeks after first acute attack. Once started then continued during further acute attacks
Define Pseudogout?
Pseudogout is a crystal arthropathy caused by calcium pyrophosphate crystals collecting in the joints.
It is formally known as calcium pyrophosphate deposition disease (CPPD). It may also be called chondrocalcinosis.
What are some risk factors for Pseudogout?
- Advanced age
- Female Gender
- Osteoarthritis
- Injury or previous joint surgery
- Metabolic Diseases: Hyperparathyroidism, Haemochromatosis, Hypophosphataemia, Diabetes
- Hypomagnesaemia
- Acute attacks may be precipitated by intercurrent infection
What are some triggers of a Pseudogout attack?
4 H’s
H – Hyperparathyroidism (high calcium levels and surgery)
H – Hemochromatosis (iron overload)
H – Hypothyroidism (underactive thyroid and T4 replacement)
H – Hydration issues (dehydration, illness, IV fluids, blood transfusions)
What are the clinical features of Pseudogout?
Often Asymptomatic
- Acute Monoarthritic pain: Shoulder, Wrist and Knee most common
- Affected joints are acutely inflamed, swollen, effusive, warm and tender
- Patients may display acute systemic illness with fever and general malaise
What are the investigations for Pseudogout?
Joint Aspiration:
- Positively birefringent rhomboid shaped Calcium Pyrophosphate Crystals
X-ray of affected joints:
- Chondrocalcinosis
- X-ray changes similar to Osteoarthritis (LOSS:)
- Loss of joint space
- Osteophytes (bone spurs)
- Subarticular sclerosis (increased density of the bone along the joint line)
- Subchondral cysts (fluid-filled holes in the bone)
Bloods:
It is important to consider secondary causes of pseudogout, particularly in younger patients:
- Ferritin
- Iron-binding studies
- Bone profile
- Alkaline phosphatase
What is the management of Pseudogout?
symptomatic treatment only - No disease modifying drugs:
First Line: NSAIDs
- Naproxen 500mg BD
- Co prescribed with a PPI for gastric protection
- Avoid if renal impaired, cardiac failure and IHD
Second Line: Colchicine
- Colchicine 500ug BD
- Use with cation in liver or renal disease and can cause diarrhoea
Third Line: Oral Corticosteroids
- Prednisolone, 30mg OD for 5-7 days
What is Verrucae Vulgaris?
Common warts are elevated, round, hyperkeratotic skin papules with a rough greyish-white or light brown surface Caused by HPV
What is the Epidemiology of Verrucae Vulgaris?
- Very common
- More common in children then adults
- Clearance rates in children are related to time of diagnosis
What are some risk factors for Verrucae Vulgaris?
- Water immersion
- Occupations involving the handling of meat and fish
- Nail biting
- Age < 35 years
- Immunocompromised
What is the Aetiology of Verrucae Vulgaris?
Common warts are caused by the Human Papillomavirus (HPV) infection of keratinocytes.
Various strains of the HPV virus are responsible such as HPV 1, 2, 4, 27, 57, 63
What are the clinical features of Verrucae Vulgaris?
- Rough papule on the hand, finger, periungual, or other skin area
- Filiform papule on the skin of the body or face
- Flat pink, slightly scaly papule on the face or digits.
What are the investigations for Verrucae Vulgaris?
Clinical Diagnosis based on appearance
May consider:
- Skin Biopsy
- Immunoperoxidase stain
- Skin culture
What are some differential diagnoses to Verrucae Vulgaris?
- Seborrhoeic keratosis
- Lichen planus
- Melanoma
- Squamous Cell Carcinoma
What is the Management of Verrucae Vulgaris?
Often Spontaneous regression of warts will occur
- Salicylic Acid and Debridement
- Cryotherapy: using a liquid nitrogen spray to freeze the wart off
Define Diverticular Disease?
A term used to describe conditions related to the presence of diverticula, which are small, bulging pouches of mucosa that can form in the lining of the digestive system that leads to the patient experiencing symptoms
Define Diverticulosis?
Refers to the presence of diverticula, without inflammation or infection where the patient is asymptomatic
Define Diverticulum?
is a pouch or pocket of mucosa in the bowel wall, usually ranging in size from 0.5 – 1cm that form from the lining of the bowel.
What is the most common part of the GI tract affected in Diverticular Disease?
Lower part of the colon (Sigmoid Colon)
Define Diverticulitis?
A subset of diverticular disease, occurs when these diverticula become inflamed or infected.
This condition is typically characterized by severe abdominal pain, fever, and nausea.
What is the Epidemiology of Diverticular Disease?
- Common in individuals over the age of 50
- Common in those who consume a western diet (Low Fibre)
What are some Risk Factors for Diverticular Disease?
High Pressures in the Colon:
- Age > 50
- Low Fibre Diet
- Obesity/Sedentary Lifestyle
- Smoking
- Constipation
- Connective Tissue Disorders
- NSAIDs and Opiates
What is the pathophysiology of Diverticular Disease?
- Wall of large intestine has a layer of circular muscle.
- The points where arteries enter are areas of weakness.
- Increased pressure over time can cause the mucosa to herniate through the muscle layer and pouch causing a diverticulum.
- If faecal matter of bacteria gather –> this can lead to inflammation and rupture of the vessels causing GI bleeding
What are the clinical features of Diverticular Disease?
- Pain and tenderness in the left iliac fossa / lower left abdomen
- Fever
- Diarrhoea
- Nausea and vomiting
- Rectal bleeding
- Palpable abdominal mass (if an abscess has formed)
- Raised inflammatory markers (e.g., CRP) and white blood cells
What are the clinical features of Acute Diverticulitis?
- Pain and tenderness in the left iliac fossa / lower left abdomen
- Fever
- Diarrhoea
- Nausea and vomiting
- Rectal bleeding
- Palpable abdominal mass (if an abscess has formed)
- Raised inflammatory markers (e.g., CRP) and white blood cells
What are the investigations for Diverticular Disease?
First line
Gold standard
Blood Tests:
- FBC: inflammatory picture
- U&Es: Urea increased
- CRP/ESR: Elevated
- WCC: raised leukocytes
Abdominal Imaging:
- CT abdo/Pelvis with contrast (Gold Standard for Diverticular Disease)
- Colonoscopy/Endoscopy if acute bleeding
What is the Management of Diverticulosis?
No treatment is required
What is the Management of Diverticular Disease?
- Patients advised to increase dietary fibre intake and hydration
- Bulk forming Laxatives (Ispaghula Husk)
- If evidence of Diverticulitis then patients are initially managed with oral antibiotics
- Analgesia
What is the Management of Uncomplicated Diverticulitis?
- Oral Co-amoxiclav (5 days)
- Analgesia (avoid opiates and NSAIDs)
- Only taking clear liquids (avoid solid food) until symptoms improve
- Follow-up within 2 days to review symptoms
What is the management of Complicated Diverticulitis?
Patients with severe pain, complications or resistant to antibiotics should be admitted to hospital
- Nil by mouth or clear fluids only
- IV Antibiotics
- IV Fluids
- Analgesia
- Urgent Investigations (CT scan)
- Urgent Surgery may be required for complications
What are some complications of Acute Diverticulitis?
Short-term complications include:
- Abscess formation: Initially managed with bowel rest, broad-spectrum antibiotics ± CT-guided percutaneous drainage. Surgical management is considered if medical management fails.
- Perforation: A surgical emergency suspected in cases of generalised peritonitis. Free air on the abdominal x-ray and high clinical suspicion necessitate urgent exploratory laparotomy.
- Large Haemorrhage requiring blood transfusions
Long-term complications include:
- Fistula formation: Most commonly colovesical fistulas, presenting with pneumaturia, faecaluria, and recurrent UTIs. Diagnosed with cystoscopy or cystography and require surgical repair. Colovaginal, coloenteric, colouterine, and colourethral fistulas may also occur.
- Fibrosis: Secondary to inflammation, resulting in strictures and large bowel obstruction.
Define Fibromyalgia?
A chronic, complex, and widespread pain syndrome. Patients experience body pain that occurs at specific tend anatomical sites over at least three months.
What is the Epidemiology of Fibromyalgia?
- More common in females
- Presents between the ages of 20-40
- Has a familial predisposition
What is the aetiology of Fibromyalgia?
Unknown but likely multifactorial
What are some risk factors for Fibromyalgia?
- Females: Middle aged 30-60 yrs
- Family history of Fibromyalgia
- Depression
- Stress
- Poverty
- IBS
What are the clinical features of Fibromyalgia?
Pain features:
- Chronic widespread muscle pain > 3 months
- Pain found at specific tender points: 11/18 (9 pairs of points)
- Pain worse with stress and cold weather
- Morning stiffness <1hr
Other features:
- Fatigue: and waking up fatigued despite sufficient sleep
- Non-restorative sleep
- Cognitive disturbances: Problems with focus and memory
- Mood disorder: depression and anxiety
- Sleep Disturbances: insomnia
What are the specific tender points associated with Fibromyalgia?
Specific tender points throughout body: (9 pairs)
- Occiput
- Low cervical region
- Trapezius
- Supraspinatus
- Second rib
- Lateral epicondyle
- Gluteal region
- Greater trochanter
- Knees
What are some differential diagnoses for Fibromyalgia?
- Rheumatoid arthritis: Characterized by joint pain, swelling, and redness
- Chronic fatigue syndrome: Marked by severe, unexplained fatigue
- Lupus: Presents with rash, joint pain, and kidney problems
- Hypothyroidism: Accompanied by weight gain, constipation, and cold sensitivity
What are the investigations for Fibromyalgia?
Primarily clinical diagnosis after exclusion of other causes
- Widespread pain and tenderness for at least 3 months at 11 of 18 tender points
- Other investigations reveal no acute findings
What is the management of Fibromyalgia?
Conservative Management:
- Lifestyle modifications: Regular Exercise, stress management, relaxation techniques
- Patient education of condition
- Cognitive Behavioural Therapy
Medical Management:
- Simple analgesia
- Antidepressant medications
Define Folliculitis?
Folliculitis refers to the inflammation of a hair follicle that results in the formation of papules or pustules, commonly known as ‘pimples’.
What is the aetiology of Folliculitis?
Bacterial Infection of hair follicles
- Primarily Staphylococcus aureus
What are the clinical features of Folliculitis?
- Papules and pustules that can appear anywhere on the body specifically around hair growth regions.
- Not found on palms of hands and soles of feet (no hair follicles here)
What are some differential diagnoses for Folliculitis?
- Acne Vulgaris: Presents with comedones, papules, pustules, nodules and possible scarring. Mainly seen on face, chest, and back.
- Impetigo: Characterised by honey-colored crusty sores, often beginning as small red papules.
- Contact Dermatitis: Symptoms include erythema, pruritus, and vesicles. Occurs in areas of skin exposure to irritants or allergens.
- Herpes Simplex: Characterised by grouped vesicles on an erythematous base, often with a history of recurrence and previous similar episodes.
- Rosacea: Presents with erythema, telangiectasia, and inflammatory papules and pustules, predominantly on the face.
What are then investigations for Folliculitis?
Clinical diagnosis based on physical examination
What is the Management of Folliculitis?
Application of topical antibiotics, with a suggested addition of antibacterial soaps (e.g. chlorhexidine-containing solutions like Hibiscrub).
- Oral antibiotics may also be required in more severe cases or cases that don’t respond to topical treatments.
- Specific variants may require tailored antibiotic approaches
Define Gastro-Oesophageal Reflux Disease (GORD)?
A clinical diagnosis based on the presence of typical symptoms (dyspepsia, ““heartburn”” or ““acid reflux””) resulting from the reflux of gastric contents into the oesophagus caused by a defective lower oesophageal sphincter.
What are the risk factors for GORD?
- Obesity
- Hiatus Hernia
- Smoking
- Alcohol use
What is the Aetiology of GORD?
Defective lower oesophageal sphincter which enables the reflux of gastric contents into the lower oesophagus causing irritation
What are some triggers of GORD?
- Greasy and spicy foods
- Coffee and tea
- Alcohol
- Non-steroidal anti-inflammatory drugs
- Stress
- Smoking
- Obesity
- Hiatus hernia
What are the clinical features of GORD?
- Dyspepsia (Heart burn)
- Acid regurgitation
- epigastric or chest pain
- Bloating and Belching
- Nocturnal Cough
- Tooth Erosion
What are the ALARMS symptoms of Gastroenterology?
Anaemia
Loss of weight
Anorexia
Recent onset of progressive symptoms
Massess/Melena - or bleeding from any part of GIT
Swallowing Difficulties (Dysphagia)
+55yrs
What are the gastro Red Flag features that warrant a two week wait referral?
- Dysphagia (at any age gets an immediate TWW referral)
-
Aged over 55 years with Unintentional weight loss plus
- Upper abdominal pain
- Reflux
- Treatment resistant dyspepsia
- rectal bleeding with bowel habbit change for 3/52 over the age of 40
What are some differential diagnoses for GORD?
- Gastric ulcers: These may present with epigastric pain, nausea, vomiting, and weight loss.
- Oesophageal cancer: This may present with dysphagia, weight loss, and potentially haematemesis.
- Zollinger-Ellison Syndrome: This may present with severe dyspepsia, diarrhoea and peptic ulcers
- Functional dyspepsia: This condition may present with similar gastrointestinal symptoms without a clear organic cause.
What are the investigations for GORD?
8 week therapeutic trial of Proton Pump Inhibitor
If symptoms don’t improve or patient has alarm symptoms then
- Oesophagealgastroduodenoscopy (OGD): Usually normal in GORD
- 24-hr oesophageal pH monitoring (the gold standard test for diagnosis)
- Oesophageal Manometry
What is the Management of GORD?
Lifestyle interventions
- Weight loss
- Dietary changes
- Elevation of the head of the bed at night
- Avoidance of late-night eating.
Proton pump inhibitor therapy.
- Omeprazole/Lansoprazole
- For patients <40 years old who present with typical symptoms and no red flags, commence treatment with a standard-dose PPI for 8 weeks in combination with lifestyle changes.
Antacids for symptomatic relief: Gaviscon, Rennie
H2 Receptor Antagonists: Famotidine
Anti-reflux surgery for refractory cases: Laparoscopic fundoplication
What lifestyle changes should be advised in a patient with GORD?
- Reduce tea, coffee and alcohol
- Weight loss
- Avoid smoking
- Smaller, lighter meals
- Avoid heavy meals before bedtime
- Stay upright after meals rather than lying flat
What are some potential complications of GORD?
- oesophagitis
- ulcers
- anaemia
- benign strictures
- Barrett’s oesophagus
- oesophageal carcinoma
Describe h.pylori.
A gram negative bacilli with a flagellum that is present in 50% of the populations gastric mucosa
How does helicobacter pylori infection cause gastric damage?
- secretes urease → urea converted to NH3 → alkalinization of acidic environment → increased bacterial survival
Pathogenesis mechanism:
- Helicobacter pylori releases bacterial cytotoxins (e.g. CagA toxin) → disruption of gastric mucosa
What conditions can arise as a result of H.pylori infection?
Peptic Ulcer Disease (PUD)
Gastritis
Gastric carcinomas
What is the diagnostic test to investigate H.pylori infection?
Urea Breath Test:First Line
Stool Antigen Test:
Rapid urease test: Performed during endoscopy (CLO Test)
What is the treatment of H.pylori infection?
Triple-therapy: For 7 days
- Proton Pump Inhibitor - Omeprazole
- Clarithromycin
- Amoxicillin (metronidazole if CI)
What is Barrett’s Oesophagus?
The constant reflux of acid into the lower oesophagus causes a change in the epithelium called metaplasia.
This is a change from the stratified squamous epithelium to the columnar epithelium from the stomach in the lower 3rd of the oesophagus.
Barrett’s Oesophagus is considered premalignant.
What does Barrett’s Oesophagus predispose a patient to?
Considered premalignant: predisposing the patient to adenocarcinoma.
What is the treatment of Barrett’s Oesophagus?
- Endoscopic Monitoring: For progression to adenocarcinoma
- Proton Pump Inhibitors: Omeprazole
- Endoscopic Ablation: Can destroy abnormal cells which are then replaced with normal squamous epithelial cells. Only used in treating high grade dysplasia to reduce cancer risk
Define Zollinger-Ellison Syndrome?
Defined as a pathophysiological condition characterised by the development of multiple ulcerations in the stomach and duodenum.
This is the result of an uncontrolled release of gastrin from a gastrinoma, a type of neuroendocrine tumour that commonly presents in the pancreas or the duodenum.
What is the Aetiology of Zollinger-Ellison Syndrome?
Associated with Multiple Endocrine Neoplasia Type I (MEN-1)
What is the mnemonic to remember the tumours associated with the different types of Multiple Endocrine Neoplasia?
MEN 1: 3 P’s
- Pituitary Adenoma
- Parathyroid
- Pancreatic tumours (Insulinoma, Gastrinoma (Zollinger-Ellison))
MEN 2a 2 P’s +1 M
- Parathyroid
- Medullary Thyroid
- Phaeochromocytoma
MEN 2B 1 P + 2 M’s
- Phaeochromocytoma
- Mucosal neuromas
- Marfanoid habitus
What are the clinical features of Zollinger-Ellison Syndrome?
- Abdominal pain, particularly in the epigastric region
- Diarrhoea
- Ulceration of the duodenum, which can often lead to gastrointestinal bleeding
- Non-responsiveness to simple Proton Pump Inhibitors (PPIs)
What are the investigations for Zollinger-Ellison Syndrome?
Fasting Gastrin Levels: Best Screening test
Secretin Stimulation Test an unusually large increase in gastric occurs following secretin administration confirms the diagnosis
Somatostatin Receptor Scintigraphy for imaging of the Tumour
Endoscopy to identify duodenal ulcerations
What is the Management of Zollinger-Ellison Syndrome?
Surgical resection of Gastrinoma
- Chemotherapy if Metastatic disease
Medical Management:
- Proton Pump Inhibitors
- Somatostatin analogues
What is Diabetes Mellitus?
A disorder of carbohydrate metabolism characterised by hyperglycaemia
What are some different types of Diabetes Mellitus?
- Type 1 DM - Insulin dependent
- Type 2 DM - Insulin Independent - Maybe be gestational or medication induced)
- MODY (Maturity Onset Diabetes of Youth)
- Pancreatic diabetes
- Endocrine diabetes - Acromegaly, Cushing’s
- Malnutrition related diabetes
What are some signs of osteoarthritis in the hands?
- Heberden’s nodes (in the DIP joints)
- Bouchard’s nodes (in the PIP joints)
- Squaring at the base of the thumb (CMC joint)
- Weak grip
- Reduced range of motion
What are the X-Ray changes seen in Osteoarthritis?
LOSS:
- L – Loss of joint space
- O – Osteophytes (bone spurs)
- S – Subarticular sclerosis (increased density of the bone along the joint line)
- S – Subchondral cysts (fluid-filled holes in the bone)
What is the difference between a vasovagal episode and a seizure?
