General Practice/ Primary Care (Joe) 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, affecting individuals of all ethnicities and ages.
- Prevalence is highest in adolescents and young adults, with up to 80% of individuals experiencing some degree of acne during their lifetime.
- While most common in adolescents, adult-onset acne can occur, affecting people well into their 30s and beyond.
- Acne affects both males and females, but the prevalence and severity may vary between genders.
- 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: 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, with 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?
Reduce symptoms, Reduce Scarring, Minimise psychosocial impact
Treatment is initiated in a stepwise fashion on severity of symptoms
- No treatment may be acceptable if mild.
- Topical Benzoyl peroxide: 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.
- 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?
Pneumonia:
- History: Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia.
- Examination: No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze. Moreover, systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.
What is the management of Acute Bronchitis?
Supportive Treatments:
- Analgesia
- Good fluid intake
- Consider SABA in patients severely affected by wheeze
- If a bacterial cause then antibiotics
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?
- Rapid onset of intense psychological distress post-trauma.
- Symptoms: Intrusive memories, dissociation, heightened arousal, avoidance, and negative mood alterations.
- Emotional reactions: Overwhelming anxiety, sense of unreality.
- Physiological manifestations: Palpitations, hypervigilance.
- Behavioural responses: Efforts to escape reminders.
- Duration: Typically three days to four weeks.
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 (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?
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?
Direct Coombs Negative (positive = Autoimmune Haemolytic Anaemia)
FBC and blood film:
Normocytic Normochromic
Increased Reticulocytes + Spherocytes
What is the treatment for Hereditary Spherocytosis?
Splenectomy
Folic Acid
Neonatal Jaundice - Phototheraphy
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:
Back pain
Chronic haemolytic anaemia
Acute haemolysis
Rapid anaemia - pallor, fatigue, SOB,
Jaundice + Dark urine
Caused by
Ingestion of fava beans
Common drugs – quinine, sulphonamides, quinolones and nitrofurantoin
What is the diagnostic investigations for G6PD Deficiency?
Reduced G6PD levels
FBC - anaemia and raised reticulocytes
Blood film:
Normal in between attacks
Attack - increased reticulocytes and 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 too much Iron
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?
Low dietary intake - vegans
Atrophic gastritis
Gastrectomy
Crohn’s disease
Coeliac disease = malabsorption
Drugs (Metformin, PPI, H2 antagonists)
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?
Autoimmune destruction of Parietal cells
Therefore reduced intrinsic factor produced
Therefore poor absorption of B12
B12 cannot be used to produced RBCs
Anaemia
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 demyelination
What neurological symptoms may be seen in Pernicious anaemia?
Symmetrical paraesthesia
Muscle Weakness
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?
Dietary advice (Salmon and eggs)
B12 Supplements
PO Hydroxocobalamin
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?
- Divided into two subtypes depending on temperature:
- WARM type - IgG mediated - occurs at normal or warm temperatures (Idiopathic)
- COLD type - IgM mediated - also called cold agglutinin disease
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?
- Treat underlying condition
- RBC transfusion and folic acid
- Prednisolone
- Rituximab
- 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?
Inflammation releases ferritin which reduces the stores of usable iron.
Iron in the blood is used up by bacteraemia
High levels of hepcidin expression – inhibits duodenal iron absorption and macrophage release of iron
CKD can reduce EPO leading to less RBC synthesis
All these factors will cause Anaemia of chronic disease
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
Can cause fulminant neurological Deficits
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?
Congenital
Acquired e.g. aplastic anaemia
Chemotherapeutic drugs
Infections – EBV, HIV, TB, Hepatitis
Pregnancy
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?
First Line:
- Treatment of constipation with the use of laxatives and dietary fibre.
- Use of topical analgesics, such as lidocaine cream or jelly.
Second-line:
- Topical calcium channel blockers (diltiazem), or oral nifedipine / diltiazem.
Patients with atypical anal fissures or symptoms/signs suggestive of Crohn’s disease should be referred to a gastroenterologist.
Define Tachycardia?
A heart rate >100 BPM
Define Bradycardia?
A heart rate <60 bpm
How can tachycardias be classified?
Narrow Complex Tachycardias (QRS <120ms)
Broad Complex Tachycardias (QRS >120ms)
What are the narrow complex tachycardias?
Often occur Above the ventricles (supra ventricular)
In Atria:
Sinus Tachycardia
Atrial Fibrillation (Irregular Irregular Rhythm)
Atrial Flutter (Regular Irregular Rhythm)
Focal Atrial Tachycardia
In Atrioventricular Node:
AV Re-entry Tachycardia (AVRT)
AV nodal Re-entry Tachycardia (AVNRT)
What are the broad complex tachycardias?
Ventricular Tachycardia (Regular Irregular Rhythm)
Ventricular Fibrillation (Irregular Irregular Rhythm)
What are the types of Bradycardia?
SAN Dysfunction (followed by QRS):
Sinus Bradycardia
1st Degree heart Block
AVN Dysfunction (not followed by QRS):
2nd Degree Heart Block (Mobitz Type I and II)
3rd Degree Heart Block
What is Sinus Tachycardia?
> 100 bpm + Sinus Rhythm
What is the Aetiology of Sinus Tachycardia?
Physiological response to exercise and excitement
Anaemia, Infection, Fever, HF, Thyrotoxicosis, Acute PE, Hypovolemia, Atropine
What is the ECG in Sinus Tachycardia?
P waves piggyback onto the T waves = camel hump T waves
What is the treatment of Sinus Tachycardia?
Correct the cause
Beta Blockers to slow sinus rate e.g., atenolol
What is a supraventricular Tachycardia?
Any tachycardia that arises from the atrium or atrioventricular junction
What are the 4 Main types of SVT?
Atrial fibrillation
Atrial flutter
Atrioventricular nodal re-entry tachycardia (AVNRT)
Atrioventricular reciprocating tachycardia (AVRT)
What is the 1st Line management in SVT?
Vagal Manoeuvres (Valsalva Manoeuvre + Carotid Sinus Massage)
Adenosine if doesnt work
What is the most common arrhythmia?
Atrial Fibrillation
What is the pathology of AF?
Atrial activity is chaotic and mechanically ineffective (atrial activation 300-600/min)
AVN conducts only a proportion of atrial impulses, with an irregular ventricular response
HR 120-180bpm
Blood pools in atria leading to increased risk of clotting and Thrombo-embolic events
What is the Aetiology of AF?
SMITH:
Sepsis
Mitral Valve Pathology (stenosis or regurgitation)
Ischemic Heart Disease
Thyrotoxicosis
Hypertension
What are the types of AF?
First detected episode
Recurrent – 2 or more episodes of AF
- Paroxysmal – terminate spontaneously (usually <24 hours)
- Persistent – not self-terminating (usually last >7 days)
Permanent – continuous AF which cannot be cardioverted or cardioversion deemed inappropriate
What is the presentation of AF?
Symptoms:
Palpitations, SOB, Syncope
Signs:
Irregularly irregular pulse
What are the complications of AF?
Emboli - Due to the pooling of blood in the atria which can lead to thrombus formation.
What are the investigations of AF?
ECG:
Irregularly irregular rhythm
Absent P waves
Narrow QRS
Bloods – Cardiac enzymes, TFTs
Echo
What is the Treatment of Acute AF?
Cardioversion (electrical/amiodarone) – usually 1st line
Correct electrolyte imbalances + Rate control + Anti-coagulate
What is the treatment of Chronic AF?
Rate control
1st Line: Beta blockers (atenolol) or rate limiting CCB (diltiazem)
If Sedentary Lifestyle then Digoxin
If this doesnt work then Combine any two.
Then assess Stroke Risk with CHA2DS2VASc and ORBIT
If risk then Add anticoagulation (DOAC 1st or Warfarin with metal valve)
How does amiodarone work?
Amiodarone works by increasing the duration of ventricular and atrial muscle action by inhibiting Na,K-activated myocardial ATPase – which means nerve impulses take longer to initiate contraction – it is an anti-arrhythmic mediation.
What is first line control of AF and when is it not used?
Rate Control:
- BB (1st), CCB (Diltiazem)
- If Sedentary then Digoxin
Used Unless: RANCH:
Reversible cause of AF
Ablation for atrial flutter
New onset <48 hours
Clinical Judgement
Heart Failure secondary to AF
When is Rhythm Control used in AF?
If Rate Control is not working (ie. Rate still bad or still have Sx)
OR RANCH (reversible, Aflu, New onset, Clin Judge, Heart Failure)
AF < 48 hrs or Severely Haemodynamically unstable
Immediate DC Cardioversion: (electrical first then Amiodarone)
AF > 48 hrs and they are stable:
Delayed Cardioversion: after 3 weeks of anti-coagulation
If all medical management has failed or is CI:
Then ABLATION
What are the options for Cardioversion?
Pharmacological:
Flecainide - pill in pocket
Amiodarone (drug of choice in patients with structural heart disease)
Electrical: defibrillator
What are the Class I, II, III, IV anti arrhythmic Drugs?
Class I: Sodium channel Blockers (Flecainide, quinidine, Lidocaine)
Class II: Beta Blockers
Class III: Amiodarone
Class IV: CCB (Verapamil or Diltiazem)
What score is used to calculate risk of stroke in AF?
CHA2DS2VASc Score:
Congestive HF
Hypertension (>140/90)
Age >75 (+2)
Diabetes Mellitus
Stroke or TIA prior (+2)
Vascular Disease
Age 65-74
Sex (Female Gender)
0 = No anticoagulation
1 = Consider anticoagulation in males (not females)
2 = Oral Anticoagulation (DOAC (1st Line) then Warfarin)
What score is used to assess Bleeding risk in AF?
ORBIT:
Older age (>74)
Reduced haemoglobin (anaemia)
Bleeding history
Insufficient Kidney Function
Treatment with antiplatelet
> 4 = High Risk
What is the target INR on warfarin?
2-3 (2.5)
What is Atrial Flutter?
Regular Irregular heart rhythm
What is the pathology of Atrial Flutter?
Type of SVT caused by a re-entrant circuit within the right atrium
Ventricular rate determined by the AV conduction ratio: 2:1 (commonest), 3:1, 4:1, variable rate
So the atria only contract to the ventricles every 2nd turn due to AVN delay
What is the ECG in Atrial Flutter?
‘Sawtooth’ pattern (F wave)
Regular atrial rate
What is the treatment of Atrial Flutter?
Rate control (beta-blockers), Rhythm control (DC cardioversion) and Anticoagulation (warfarin)
Radiofrequency catheter ablation – curative for most patients
What is the pathology of an AVNRT?
AV nodal re-entry tachycardia (AVNRT):
Circuits from within the AVN (‘ring’ of conduction tissue)
ECG: Absent P waves (or seen immediately before QRS)
What is the pathology of an AVRT?
AV reciprocating tachycardia (AVRT):
Accessory pathway connecting the atria and ventricles
Wolff-Parkinson-White syndrome (WPW) – bundle of kent
What is the acute treatment of an AVNRT/AVRT?
Stable:
Vagal Manoeuvres (Valsalva + Carotid Sinus Massage)
If doesnt work then adenosine
Unstable
Electrical Cardioversion
What is the Long Term treatment of an AVNRT/AVRT?
Beta Blockers
Radio-frequency Ablation
What is the ECG of Wolf Parkinson White Syndrome (WPW)?
Short PR interval (due to early depolarization of ventricle)
Wide QRS complex
Slurred start to the QRS (delta wave)
ST changes
What are some associations with WPW?
HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD
What is the management of WPW?
Definitive: Radiofrequency Ablation
Medical Therapy: Sotalol, Amiodarone, Flecainide
Why do you get the delta wave in WPW?
Bundle of kent accessory pathway allows the transfer of conduction to the ventricles slightly faster than AVN and therefore the delta wave is the early contraction of the ventricles
What are broad complex tachycardias associated with?
Prolonged QT syndrome
What is Ventricular Tachycardia?
Ventricle does not fully depolarize through the Purkinje fibres leading to rapid electrical conduction around the ventricles
Due to re-entrant circuit due to scarring from past ischemia/infarction OR triggered by long QT or digoxin toxicity
What is the ECG in V-Tach?
broad complex tachycardia with wide QRS complex
What is the treatment of V-Tach?
Stable - Amiodarone
Unstable Electrical DC and IV Amiodarone
What is Ventricular Fibrillation?
No pattern of ECG due to the fibrillation of the ventricles.
They do not contract and no blood is ejected meaning this is a life threatening situation
What is the Treatment of V-Fib?
Defibrillation + IV amiodarone
What are the causes of Sinus Bradycardia?
Athlete
Extrinsic:
- Vasovagal attacks
- Drugs (BB, Digoxin, Amiodarone
- Hypothermia
- Hypothyroidism
- Raised ICP
Intrinsic:
- Acute ischaemia
- Infarction of SAN
What is the treatment for Sinus Bradycardia?
Extrinsic: Treat Underlying cause
Intrinsic - Atropine
Define 1st Degree heart Block?
PR interval is prolonged (over 0.20s)
Define 2nd Degree Heart Block?
Mobitz type I: Progressive PR interval prolongation, until a P wave fails to conduct and a QRS is dropped
Mobitz type II: PR interval is constant, but QRS complexes are regular missed
Define 3rd Degree Heart Block?
Complete Heart Block
Ventricular contraction completely independent of atria contractions
What are the features of complete Heart Block?
Syncope
Heart failure
Regular bradycardia (30-50 bpm)
Wide pulse pressure
JVP: cannon waves in neck
Variable intensity of S1
What is the treatment of heart Block?
Stable: Observe
Unstable / Risk of Asystole ( Type II Mobitz, 3rd degree):
- IV Atropine 500mcg
- Permanent implantable pacemaker
What are the causes of LBBB?
myocardial infarction
hypertension
aortic stenosis
cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
What is the ECG of LBBB?
WiLLiaM
Slurred S wave in V1
R wave in V6
What are the causes of RBBB?
Normal
PE
IHD
ASD
VSD
Cor pulmonale
What is the ECG of RBBB?
MaRRoW:
R wave in V1
Slurred S wave in V6
What is Long QT Syndrome?
Inherited condition associated with delayed repolarization of the ventricles
May lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/ sudden death
What are the causes of Long QT?
Romano Ward Syndrome
Amiodarone
TCA/SSRIs
Hypocalcaemia, Hypokalaemia, Hypomagnesaemia
MI
What is the management of long QT?
Avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)
Beta-blockers (sotalol may exacerbate)
Implantable cardioverter defibrillators – high risk cases
What is Torsades De Pointes (Twisting of the Tips)
Form of polymorphic ventricular tachycardia associated with a long QT interval
where the QRS will twist around the base line
Either terminate spontaneously (revert back to sinus rhythm) or progress into ventricular tachycardia (cardiac arrest)
What is the management of Torsades De Pointes?
Correct the Cause (EG. Electrolyte Disturbances)
Magnesium Infusion
Defibrillation if V-Tach occurs
What are the Cardiac Arrest Rhythms? Which are shockable?
Shockable:
Ventricular Tachycardia
Ventricular Fibrillation
Non-Shockable:
Pulseless Electrical Activity
Asystole
What are the indications for a pacemaker?
Symptomatic bradycardias
Mobitz Type 2 AV block
Third degree heart block
Severe heart failure (biventricular pacemakers)
Hypertrophic obstructive cardiomyopathy (ICDs)
What Thromboprophylaxis is best for patients with arrhythmias and a metallic heart valve?
Warfarin is preferred.
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 closed angle glaucoma (PACG)?
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. Measures while waiting for an ambulance are:
- Lying the patient on their back without a pillow
- 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?
Blepharitis is commonly caused by Staphylococcus infection, HSV or VZV infection,
- Meibomian gland dysfunction,
- seborrheic dermatitis
- rosacea
What are the symptoms of Blepharitis?
The symptoms of blepharitis include:
- Painful, gritty, itchy eyes
- Eyelids sticking together upon waking
- Dry eye symptoms
- 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:
- Lid hygiene – at least twice a day
- Avoidance of contact lens use during flare-ups
Define a Stye?
External hordeolum is an abscess at an eyelash follicle commonly caused by staphylococcus
It is an infection of the glands of Zeis or Glands f Moll
Internal Hordeolum: is an abscess of the meibomian gland which can lead to a chalazion if the gland becomes blocked
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?
Initially 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?
- Warm compresses applied several times a day can help to relieve symptoms and promote drainage.
- Over-the-counter pain relievers can be used to manage pain.
- Topical antibiotic ointments may be used to treat bacterial infections.
- In persistent cases, surgical intervention may be required to drain the abscess or remove the chalazion.
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
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 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 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 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)
