GENERAL PRACTICE 1 - Misc, Pysch, Endo, Gastro, Cardio Flashcards
What causes acne?
caused by chronic inflammation, in pockets in the skin that contain hair follicles and sebaceous glands.
It results from increased production of Sebum that traps keratin and blocks the pilosebaceous unit.
Androgenic hormones increase the production of sebum
This leads to units that are swollen and inflamed, which are known as comedones
Bacteria that colonize the skin can excessively grow and exacerbate acne.
What bacteria causes acne?
Propionibacterium acnes. Excessive growth of this bacteria can exacerbate acne
What are the different lesions that can occur in acne?
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 (whiteheads, I think)
Blackheads are open comedones with black pigmentation in the centre
What are the topical treatments for acne?
Topical benzoyl peroxide reduces inflammation, helps unblock the skin and is toxic to the P. acnes bacteria
Topical retinoids (chemicals related to vitamin A) slow the production of sebum (women of childbearing age need effective contraception)
Topical antibiotics such as clindamycin (prescribed with benzoyl peroxide to reduce bacterial resistance)
What are the oral treatments for severe acne?
Oral antibiotics such as lymecycline
Oral contraceptives -Co-cyprindiol (Dianette)
Oral isotretinoin (Roaccutane)
What are some side effects of Roaccutane?
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
. This needs careful follow-up and monitoring and reliable contraception in females. Retinoids are highly teratogenic.
Outline what acute bronchitis is. What is seen in it?
Self limiting lower respiratory tract infection
Bronchitis = infections causing inflammation in bronchial airways
Typically cough worse at night/with exercise
Lasts > 2 wks in 1/2 patients, 4 wks in 1/4 patients
May be associated w/ bronchospasm ± mucus production
What are the main causes of acute bronchitis?
Most cases viral infection, same as causes of URTIs:
Coronavirus
Rhinovirus
Respiratory syncytial virus (RSV)
Adenovirus
What are some investigations you could do in acute bronchits?
Mostly clinical diagnosis
Pulmonary function testing (to evaluate for asthma, result: mild/moderate bronchial obstruction)
CXR (rule out pneumonia)
CRP
?procalcitonin (emerging test for diagnosis of bacterial infections - tends to be higher in severe bacterial infections and low in viral infections)
What are some reasons why you may perscribe antibtioics in acute bronchitis?
Reasons to prescribe antibiotics immediatelyN Investigate further and/or
give antibiotics (e.g. amoxicillin 500mg tds) if:
- Systemically very unwell
- Symptoms/signs of serious illness or complications, e.g. pneumonia
- At high risk of serious complications because of pre-existing
co-morbidity, e.g. significant heart, lung, renal, liver, or neuromuscular
disease, immunosuppression, CF, or young children born prematurely - Aged >65y with acute cough and ≥2 or more of the following, or aged >80y with acute cough and ≥1 of the following:
- Hospitalization in the previous year
- Type 1 or type 2 DM
- History of CCF
- Current use of oral steroids
Define what an acute stress reaction is
Acute stress disorder is an intense, unpleasant, and dysfunctional reaction beginning shortly after an overwhelming traumatic event and lasting less than a month
If symptoms persist longer than a month, people are diagnosed as having posttraumatic stress disorder.
Define Anaemia
Anaemia is a decrease in haemoglobin below reference range due to a reduction in cell mass or increased plasma volume
What can anaemia be subdivided into? What are the names of the categories?
Anaemia can be classified based on the Mean Corpuscular Volume (MCV).
It is based on the size of the red blood cell (the MCV)
- Microcytic anaemia(low MCV indicating small RBCs)
- Normocytic anaemia(normal MCV indicating normal sized RBCs)
- Macrocytic anaemia(large MCV indicating large RBCs)
Nearly all types of anaemia present with the same symptoms and signs - What are the general symptoms for anaemia?
Symptoms:
* Fatigue
* Lethargy
* Dyspnoea – difficulty or laboured breathing
* Palpitations
* Headache
What are the main causes of Microcytic anaemia?
TAILS
Thalassaemias
Anaemia of chronic disease
Iron deficiency
Lead poinsoing
Sideroblastic anaemia
Anaemia caused by iron deficiency is the most common cause of anaemia worldwide. - What are some causes of it?
- Vegetarian/ vegan diet -
- H.pylori infection causes gastric ulcers and bleeding, and takes iron for itself
- Pregnancy
- Young children and adolescents
- Inflammatory bowel disease/Coeliac impairs iron absorption
- Certain drugs e.g. PPIs inhibit gastric acid, so non haem cannot be absorbed as it is not converted into haem iron
Heavy menstruation
What happens to RBC production as a result of iron deficiency?
Leads to impaired haemoglobin production.
Since there’s not enough haemoglobin for a normal sized RBC, the bone marrow starts pumping out microcytic RBCs. - these have less Haemoglobin so are called hypochromic, as appear pale
Microcytic RBCs can’t carry enough oxygen to the tissues - hypoxia.
Hypoxia signals the bone marrow to increase RBC production.
The bone marrow goes into overdrive and pumps out incompletely formed RBCs.
What are some signs of iron deficiency anaemia?
○ Pallor
○ Conjunctival pallor
○ Glossitis inflammation of the tongue
○ Koilonychia (spoon-shaped nails)
○ Angular stomatitis sored on the corners of the mouth
What are some symptoms of iron deficiency anaemia?
- Symptoms
○ Fatigue
○ Dyspnoea
○ Dizziness
○ Headache
○ Nausea
○ Bowel disturbance
○ Hairloss
○ Pica (abnormal cravings)
○ Possible exacerbation of cardiovascular co-morbidities causing angina, palpitations, and intermittent claudication.
What would someone with iron deficiency anaemia’s iron studies (serum iron, serum ferritin, total iron binding capacity, and transferrin saturation) look like?
What confirms a test of iron deficiency anaemia
○ Serum iron - low
○ Serum ferritin: low in anaemia
○ Total iron binding capacity: can be used as a marker for how much transferrin is in the blood. Increased in anaemia
○ Transferrin saturation: gives a good indication of the total iron in the body. Decreased in anaemia
Note - ferritin is an acute phase protein, so can also increase with inflammation (i.e. due to infection/malignancy)
Ferritin is a test that shows the relative total body iron stores. A serum ferritin level below 30 micrograms/L confirms a diagnosis of iron deficiency anaemia (IDA)
What are the management options of iron deficiency anaemia?
- Treat the underlying cause
- Oral iron supplements: ferrous sulphate or ferrous fumarate
○ Side effects: constipation and black coloured stools, diarrhoea, nausea and dyspepsia/epigastric discomfort. - Iron infusion e.g. cosmofer
- Blood transfusions may be needed in severe cases
What are some chronic disease that can lead to anaemia?
What type of anaemia?
Microcytic anaemia
Causes:
Crohn’s
Rheumatoid arthritis
TB
Systemic lupus erythematosus
Malignant disease
CKD
What is
a) Alpha Thalassaemia?
b) Beta Thalassaemia?
What is it’s genetic pattern, autosomal or sex linked, dominant or recessive?
Alpha Thalassaemia - genetic disorder where there’s a deficiency in production of the alpha globin chains of haemoglobin
Beta thalassaemia - is a genetic disorder where there’s a deficiency in the production of the β-globin chains of haemoglobin.
BOTH AUTOSOMAL RECESSIVE
What are some signs of alpha thalassaemia?
Patients with alpha thalassaemia trait are usually asymptomatic. Clinical features of HbH disease are highly variable and generally develop in the first years of life
- Signs
- Pallor: due to anaemia
- Jaundice: due to unconjugated bilirubin
- Chipmunk facies: compensatory extramedullary hematopoiesis in the skull causes marrow expansion
- Hepatosplenomegaly
- Failure to thrive
What are some symptoms of alpha thalassaemia?
- Shortness of breath: due to anaemia
- Palpitations: due to anaemia
- Fatigue: due to anaemia
- Swollen abdomen: due to hepatosplenomegaly
Beta Thalassaemia - what is seen in Thalassaemia intermeida - what would a patient with this experience?
Patients with beta thalassaemia intermedia have two abnormal copies of the beta-globin gene. This can be either two defective genes or one defective gene and one deletion gene.
Thalassaemia intermedica causes a more significant microcytic anaemia
Beta Thalassaemia - what is seen in Thalassaemia major - what would a patient with this experience?
Patients with beta thalassaemia major are homozygous for the deletion genes. They have no functioning beta-globin genes at all. This is the most severe form and usually presents with severe anaemia and failure to thrive in early childhood.
Thalassaemia major causes:
Severe microcytic anaemia
Splenomegaly
Bone deformities
What are the investigations for suspected Alpha and Beta Thalassaemia?
Blood film – will show hypochromic and microcytic anaemia, target cells visible on film Irregular and pale RBCs
FBC - Increased reticulocytes and nucleated RBCs in peripheral circulation - known as reticulocytosis
Lab work may also show high serum iron, high ferritin, and a high transferrin saturation level.
Hb electrophoresis –
Skull XR – hair on end sign, enlarged maxilla
What is the management for thalassaemia?
Depends on severity of the symptoms!!
- Regular blood transfusions: may be required and will be guided by the Hb level.
- Iron chelation:desferrioxamine acts as an iron chelator and can be given to treat or prevent iron overload in patients with regular transfusions
- Folate supplementation:haemolysis leads to increased cell turnover and a state of folate deficiency
- Splenectomy:
- Stem cell transplantation:the onlycurativeoption recommended in those with severe disease
What happens in Sideroblastic anaemia?
Sideroblastic anaemia, , is a form of anaemia in which the bone marrow produces ringed sideroblasts rather than healthy red blood cells (erythrocytes), so body can’t carry enough O2.
This is because it cannot incorporate iron into the haemoglobin
due to vitamin B6 deficiency
What are the two types of Normocytic anaemia diseases?
Haemolytic and Non Haemolytic
Haemolytic anaemia occurs when RBCs are destroyed before 120 days (lifespan dependent on cause of haemolysis)
Define what sickle cell anaemia is
Sickle cell anaemia is an autosomal recessive mutation in the beta chain of haemoglobin, resulting in sickling of red blood cells (RBCs) and haemolysis.
Outline the pathophysiology behind sickle cell anaemia - what leads to the change in structure to one of the beta chains?
Sickle cell disease is caused by defective haemoglobin.
The β-globin chains end up misshapen due to a point mutation in the beta globin gene, or HBB gene.
This point mutation leads to hydrophilic glutamic acid being substituted for a hydrophobic valine changing the structure of the beta chain.
Outline the pathophysiology behind sickle cell anaemia - name some of the characteristics of HbS
- HbS is prone tosicklingand haemolysis.
- HbS carries oxygen well
But when deoxygenated, HbS changes its shape, and clumps with other HbS proteins, causing the RBC to turn into a crescent shape
In order to counteract anaemia, in sickle cell disease, what does the bone marrow do?
To counteract the anaemia of sickle cell disease, the bone marrow makes increased numbers of reticulocytes. This can cause the bones to enlarge.
Extramedullary hematopoiesis can also happen - leading to splenomegaly.
What is more likely to happen with Sickled blood cells compared to normal? What will this lead to?
Sickled RBCs can get stuck in capillaries, known as vaso-occlusion.
This can lead to vaso-occlusive crisis causing symptoms e.g. dactylitis (inflammation in finger or toe), priapism (long lasting painful erection), acute chest syndrome, stroke, depending on where the occlusion is.
Name some triggers that will cause sickling in Sickle disease/trait
Triggers that will cause sickling in Sickle cell disease/sickle trait
- Hypoxia
- Acidosis
- Infection
- Dehydration
HAID
sickle cell disease patients will sickle sooner than sickle cell trait patients!
HbAS(trait) patients sickle at PaO22.5 - 4 kPa, whilstHbSS(disease) patients at PaO25 - 6 kPa.
What are some chronic symptoms of sickle cell anaemia?
-
Chronic symptoms:
- Pain
- Related to anaemia: fatigue, dizziness, palpitations
- Related to haemolysis: jaundice, and gallstones
Sickle cell crisis - What are some of the crisis’ that can happen, that will lead to acute symptoms?
Splenic Sequestration crisis - affects Spleen
Aplastic crisis - affects bone
Vaso-occlusive crisis - can affect bone, lungs, CNS, genitalia
What can these sickle cell crisis be brought on by?
They can occur spontaneously or be triggered by stresses such as infection, dehydration, cold or significant life events.
Sickle Cell Vasoocclusive crisis - What happens in it, and what can it lead to?
In Bones, Lungs, CNS, Kidney, Genitalia
Painful, vaso-occlusive episodes occur as RBCs sickle in various organs - leading to Distal Ischaemia
In Bone - can lead to Dactylitis inflammation of digits, and Avascular Necrosis
In Lungs - can lead to Acute Chest syndrome - can see Chest pain, hypoxia, Pulmonary infiltrates on CxR
In CNS - can lead to stroke
Penis - Priapism
Kidney - Renal papillary necrosis
Sickle Cell Crisis - what is seen in a Aplastic crisis? What commonly causes the infection?
Severely reduced production of red blood cells due to bone marrow failure.
temporary loss of the creation of new blood cells. This is most commonly triggered by infection with parvovirus B19, effecting the Bone marrow
Sickle Cell Crisis - What is seen in a Splenic sequestrain crisis?
Splenic sequestration crisis is caused by red blood cells blocking blood flow within the spleen. This causes an acutely enlarged and painful spleen.
Leads to pooling of blood in the spleen, can lead to severe anaemia and hypovolaemia
What is the basic management seen in sickle cell crisis?
There is no specific treatment for sickle cell crises and they are managed supportively:
Have a low threshold for admission to hospital
Treat any infection
Keep warm
Keep well hydrated (IV fluids may be required)
Simple analgesia such as paracetamol and ibuprofen
Penile aspiration in priapism
Blood transfusion in anaemic cases
NIV/Breathing assistance in Acute Chest syndrome
Splenectomy in Splenic Sequestration Crisis
NSAIDs such as ibuprofen should be avoided where there is renal impairment.
What are the primary investigations to do for suspected sickle cell anaemia?
What confirms a diagnosis of sickle cell disease?
Screen neonates – blood/heel prick test
FBC: Low Hb, High reticulocyte count
Blood film – sickled erythrocytes
Hb electrophoresis for differential diagnosis – Hb SS present and absent Hb A confirms diagnosis of sickle cell disease
What is some of the ongoing management for sickle cell anaemia?
Supportive
Folic acid
Aggressive analgesia i.e. opiates
Treat underlying cause e.g. antibiotics
Fluids
Disease modifying
Hydroxycarbamide/hydroxyurea – increases HbF concentrations if frequent crises
Transfusion
Stem cell transplant
What is Hereditary Spherocytosis?
What is formed as a result, instead of normal RBCs?
Hereditary spherocytosis (HS) is an inherited haemolytic anaemia and is autosomal dominant in the majority of cases (75%), but can also be autosomal recessive.
Leads to the formation of spherocytes, - round mishaped RBCs
What is the diagnostic criteria for diagnosing hereditary spherocytosis?
No further tests are needed for diagnosis, if:
- Family history of HSand
- Typical clinical featuresand
- Positive laboratory investigations (spherocytes, raised MCHC, increase in reticulocytes)
What does MCV stand for?
MCV stands for Mean Corpuscular Volume, which is a measure of the average size of red blood cells.
What does MCHC stand for?
MCHC stands for Mean Corpuscular Hemoglobin Concentration, which is a measure of the average amount of hemoglobin in a red blood cell.
What are some investigations to consider in spherocytosis?
-
FBC:normocytic anaemia with an increased reticulocyte count and raised MCHC
- MCHC is increased as spherical RBCs lead to water diffusing out of the cell
- Blood film:spherocytosis
- LFTs:increased (unconjugated) bilirubin due to haemolysis
- Coombs test:negativein hereditary spherocytosis. (it is Positive in Autoimmune haemolytic anaemia)
What is the management for spherocytosis?
What should these patients be prescribed and why?
- Blood transfusion:patients should be managed with transfusions for symptomatic anaemia until splenectomy is possible or deemed appropriate
- Folic acid: all patients require daily folic acid supplementation until splenectomy
-
Splenectomy:removing the spleen reduces haemolysis
- Patients must bevaccinatedagainst encapsulated bacteria and be prescribed lifelongphenoxymethylpenicillin
How can Glucose-6-Phosphate Dehydrogenase Deficiency lead to anaemia? What type of anaemia?
A normocytic, Haemolytic Anaemia, where there is a genetic defect in teh G6PD protein
What are some triggers that lead to deficit G6PD causing anaemia?
Periods of increased stress, with a higher production of ROS, can lead to acute haemolytic anaemia.
e.g. infections (viral hepatitis or pneumonia), metabolic acidosis, fava beans, soy products, red wine, certain medications
What investigations would you do for suspected G6PD deficiency anaemia? How can a diagnosis be made?
- FBC: low levels of RBC, high reticulocytes
-
Blood film: heinz bodies and bite cells
– Bilirubin: elevated - Haptoglobin: low
- Coomb’s test: negative (used to detect immune mediated anaemias)
What is the management of G6PD deficiency?
- Avoid trigger of haemolysis e.g. fava beans and certain medications
- In certain cases, transfusions may be needed
What happens in Autoimmune haemolytic anaemia?
red blood cells are attacked by either IgM or IgG antibodies
What are the 4 causes of normocytic anaemia
○ A – Acute blood loss
○ A – Aplastic Anaemia e.g. bone marrow suppression or chronic kidney disease (lack of EPO)
H – Haemolytic Anaemia
H - Hypothyroidism
What happens aplastic anaemia?
Is the reduction in the number of pluripotent stem cells causes a lack of haemopoiesis (production of blood cells and platelets). The reduced number of new RBCs produced to replace the old ones causes anaemia.
anaemia, leukopenia, and thrombocytopenia. - low levels of all blood cells!
Outline the pathophysiology behind aplastic anaemia
Alterations in the immunologic appearance of haematopoietic stem cells because of genetic disorders, or after exposure to environmental agents, like radiation or toxins, or autoimmune
- ## This means that the hematopoietic stem cells start expressing non-self antigens and the immune system subsequently targets them for destruction.
Why can B12 and folate deficiency’s be referred to as Megaloblastic? What does Megalobastic mean?
Megaloblastic anaemia is the result of impaired DNA synthesis preventing the cell from dividing normally. Rather than dividing it keeps growing into a larger, abnormal cell. This is caused by a vitamin deficiency. (hence the macrocytosis)
What pathophysiological manifestations will occur due to Folate (B9) deficiency?
- This means that folate deficiency can eventually lead to pancytopenia. In response to the anaemia, the bone marrow compensates by releasing megaloblasts into the blood - and the final result is macrocytic, megaloblastic anaemia.
- Other rapidly dividing cells, include mucosal epithelial cells of the tongue. These are affected, preventing healing. This leads to glossitis.
What is the pathophysiology behind Pernicious Anaemia?
Pernicious anaemia is an autoimmune condition in which the parietal cells are attacked 🡪 atrophic gastritis and loss of IF production 🡪 B12 malabsorption
What investigations would you carry out for suspected Pernicious Anaemia?
Investigations:
FBC
Blood film – would show macrocytic RBCs
Autoantibody screen – check for IF and parietal cell antibodies (present in 50% and 90% of cases respectively)
Serum B12 - low
How can hypothyroidism lead to anaemia
hypothyroidism leads to Less production of EPO, can lead to decreased production of RBCs
What do you correct first in someone a combined B12 and folate deficiency??
In a combined B12 and folate deficiency, you MUST replace B12 before replacing folate
B12 deficiency is sometimes misdiagnosed as a folate
deficiency so you always correct the B12 as it can cause neurological
complications left untreated.
What is an anal fissure?
What are causes of it?
Tear in lower anal canal (distal to dentate line), usually due to trauma
Constipation
Anal trauma
Rarely: crohns, TB
What are some signs and symptoms of an anal fissure?
Extreme pain on passing motion
Pain may continue for 1-2 hours, can be burning nature
Blood in stool / on wiping
What are the treatments for an anal fissure?
Fluids + eat more fibres, stool softeners
If Sx continue for longer term, glyceryl trinitrate (GTN) ointment - expands blood vessels in/around anus, increasing blood supply to fissure helping it to heal faster
Outline what Generalized anxiety disorder consists of. What is used to guage it?
Chronic, excessive worry for 6+ months, causing distress or impairment
Hard to control
At least 3/6 Sx required to make diagnosis of GAD
GAD-7 anxiety questionnaire can establish severity of diagnosis
What are some risk factors/causes of developing GAD?
Family Hx anxiety
Physical/emotional stress
Financial, bereavement etc
Hx physical/sexual/emotional trauma (in childhood)
Excessively pushy parents in childhood
Other anxiety disorder - coexisting depression
Chronic physical health condition
Worries about physical health
Female 2:1 Male
Environmental triggers/contributors: family relationships, friendships, bullies, school pressures, alcohol and drug use e.g. benzodiazepines
What are some questions/ideas that are included on the GAD-7 questionaire?
Over the last 2 weeks,
Feeling nervous, anxious, or on edge?
Not being able to stop or control worrying?
Worrying too much about different things?
Trouble relaxing?
Being so restless that it is hard to sit still?
Becoming easily annoyed or irritable?
Feeling afraid as if something awful might happen?
Scores of 5, 10, and 15 are taken as the cut-off points for mild, moderate and severe anxiety, respectively. When used as a screening tool, further evaluation is recommended when the score is 10 or greater.
What are some other conditions you would want to do to rule out other causes of symptoms seen in GAD?
depression and obsessive compulsive disorder
Hyperthyroidism - do TFTs
Pheochromocytoma
Lung disease - excessive salbutamol use
Congestive HF - heart meds -> anxiety
Hypoglycaemia
Do Bloods, and BP
What is the management of GAD?
Mild anxiety can be managed with watchful waiting and advice about self-help strategies (e.g. meditation), diet, exercise and avoiding alcohol, caffeine and drugs.
Moderate to severe anxiety can be referred to CAMHS services to initiate:
Counselling
Cognitive behavioural therapy
Medical management. Usually an SSRI such as sertraline is considered.
OCD - Define what is meant by Obsessions, and give some examples of some
Obsessions = unwanted/uncontrolled thoughts and intrusive images, pt finds difficult to ignore
aggressive impulses e.g. - images of hurting a child or parent
contamination e.g. – becoming contaminated by shaking hands with another person
need for order e.g. – intense distress when objects are disordered or asymmetric
religious e.g. – blasphemous thoughts, concerns about unknowingly sinning
repeated doubts e.g. – wonder if a door was left unlock
OCD - Define what is meant by Compulsions
Give some examples
repetitive actions pt feels they must do, generating anxiety if not done - often way to handle the obsessions
checking e .g. – repeatedly checking locks, alarms, appliances
cleaning e.g. – hand washing
hoarding e.g. – saving trash or unnecessary items
mental acts e.g. – praying, counting, repeating words silently
What are some causes/Risk factors for developing OCD?
Genetic predisposition (twins, especially monozygotic)
Developmental factors
Emotional/physical/sexual abuse
Neglect
Social isolation
Teasing, bullying
Parental over protection
Psychological factors
Over-inflated sense of responsibility
Intolerance of uncertainty
Belief in controllability of intrusive thoughts
Stressors
Pregnancy
Postnatal period
Family Hx
Stressful life events
Environmental factors
Rarely
In adults: neurological conditions e.g. brain tumour, Huntington’s chorea, frontotemporal dementia, complication of brain injury to frontal lobe/basal skull
What is the treatment for OCD?
Mild functional impairment Offer short CBT (<10h), including
exposure-response prevention (ERP) or group therapy
* Moderate functional impairment Offer more intensive CBT (>10h)
or drug therapy (SSRI, e.g. fluoxetine 20–40mg od)
* Severe functional impairment Offer psychological therapy + drug
treatment. If inadequate response at 12wk, offer a different SSRI or
clomipramine. Refer if symptoms persist
What are some causes/risk factors for developing phobias?
animals (spides, snakes, worms)
Blood/injection/injury
Situational (lifts, flying, enclosed space)
Natural environment (storms, heights, water)
Other: choking, vomiting, clowns
Amygdala, anterior cingulate cortex and insula hyperactivity involved in underlying mechanism of action
What are the 3 types of Phobias?
Simple phobia Inappropriate anxiety in the presence of ≥1 object/situation, e.g. flying, enclosed spaces, spiders
Social phobia Intense/persistent fear of being scrutinized or negatively
evaluated by others leads to fear and avoidance of social situations (e.g. using a telephone, speaking in front of a group).
Agoraphobia fear of fainting and/or loss of control are
experienced in crowds, away from home, or in situations from which escape is difficult. Avoidance results in patients remaining within their
homes where they know symptoms will not occur.
What are the general treatments for phobias?
For simple phobias - Treatment is only needed if symptoms are frequent, intrusive, or prevent necessary activities. Exposure therapy is effective.
For social and agoraphobia -
drug therapy SSRIs, and TCAs eg Clomipramine
Psychological therapies CBT (cognitive restructuring) +/- exposure
Define what a Supraventricular Tachycardia is. What are the 4 types? What is the most common?
Any tachycardia which arises from the atrium or AV junction
Atrial fibrillation
Atrial flutter
AV nodal re-entry tachycardia (AVNRT) MOST COMMON
AV reciprocating tachycardia (AVRT)
Supraventricular Tachycardias - What is atrial flutter? What things characterise it?
It is irregular ORGANSIED atrial firing, around 250 - 300BPM (conduction pathway typically from around opening of tricuspid valve
Often associated with AF
Atrial HR = 300 BPM
Ventricular rate = 150/100/75 BPM (due to AV node conducting every 2nd/3rd/4th beat “flutter beat” , so see at least 2 P waves for every QRS complex - but QRS complexes will be regular
ECG - see flutter waves, which are a saw-tooth pattern of atrial activation, most prominent in leads II, III, aVF, and V1
Supraventricular Tachycardias - Name some causes of atrial flutter
- Idiopathic (30%)
- Coronary heart disease
- Thyrotoxicosis
- COPD
- Pericarditis
- Acute excess alcohol intoxication
Supraventricular Tachycardias - Outline the pathophysiology behind atrial flutter.
It is caused by the electrical signal re-entering/ re-circulating back into the atrium, due to an extra electrical pathway
It goes round and round, without interruption, so Atrial contraction is at 300bpm
The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node, causing 150 bpm ventricular contraction.
Can be sudden and brief in episodes, or on going
Supraventricular Tachycardias - what would you see on an ECG that would indicate Atrial flutter?
ECG: regular sawtooth-like atrial flutter waves (F waves) with P-wave after P-wave
Supraventricular Tachycardias - what is the management of atrial flutter?
- Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
- Rate/rhythm controlwith beta blockers or cardioversion (*use of electric shock to put heart back into rhythm)
- Radiofrequency ablationof the re-entrant rhythm (Uses heat generated by radio waves to destroy tissue)
- Anticoagulationbased on CHA2DS2VASc score
Supraventricular Tachycardias - What characterises AV nodal re-entry tachycardia (AVNRT)?
Most common type of SVT - AV nodal re-entry tachycardia (AVNRT)
Twice as common in women than men
The electrical conduction of the atrium re enters back through the AV node, Due to the presence of a “ring” of conducting pathways in the AV node, of which the “limbs” have different conduction times and refractory periods
This allows a re-entry circuit and an impulse to produce a circus movement tachycardia
Supraventricular Tachycardias - what is the are the key presentations of someone with AV nodal re-entry tachycardia/AV reciprocating Tachycardia?
(What’s the slightly rogue one)
Presentation
Regular rapid palpitations – abrupt onset and sudden termination
Neck pulsation – JV pulsations
Polyuria – due to release of ANP in response to increased atrial pressure during tachycardia
Chest pain and SOB
Symptoms
Palpitations
Dizziness
Dyspnoea
Central chest pain
Syncope
Supraventricular Tachycardias - What is AV reciprocating tachycardia? What is the best known type of this?
The eletrcial signals goes back in the atria via an accessory pathway.
The best known type of this is Wolff-Parkinson-White Syndrome, there is an accessory pathway (bundle of kent) between atria and ventricles
Supraventricular Tachycardias - What would you see on an ECG of someone with AV Nodal re-entry tachycardia?
P waves are either not visible, or are seen immediately before or after the QRS complex (short PR interval)
QRS complex is a normal shape because the ventricles are activated in the normal way (down bundle of His)
Supraventricular Tachycardias - what would you see on an ECG for AV Nodal Reciprocating Tachycardia? (WPW syndrome)
The early depolarisation of part of the ventricle leads:
- shortened PR interval
- slurred start to the QRS (delta wave)
- QRS is narrow
Patients are also prone to atrial and occasionally ventricular fibrillation
Supraventricular Tachycardias - What is the initial management of AV Nodal re-entry tachycardia and AV Reciprocating tachycardia?
Breath-holding
Carotid massage - massage the carotid on one side gently with two fingers.
Valsalva manoeuvre - Pt blows hard into resistance
Supraventricular Tachycardias - if carotid massage and Valsalva manoeuvre are unsuccessful, what can you give to treat AVNRT and AVRT?
If manoeuvres unsuccessful, IV adenosine
Causes a complete heart block for a fraction of a second
Effective at terminating AVNRT and AVRT
Supraventricular Tachycardias - What is Atrial fibrilation?
Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregular. This is due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.
This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles.
What does atrial fibrillation lead to?
- Irregularly irregularventricular contractions
- Tachycardia
- Heart failuredue topoor fillingof the ventricles duringdiastole
- Risk ofstroke
What are some common causes of atrial fibrillation?
PE/COPD
IHD, Heart failure
Rheumatic heart disease, Valve abnormalities
Alcohol intake
Thyroid issues - Hyperthyroidism
Sleep Apnoea
Electrolyte disturbances - Hyper/Hypo Kalaemia, Hypo magnesia
PIRATE
The most common causes of atrial fibrillation can be remembered with the “SMITH” mnemonic:
S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension
Alcohol and caffeine are lifestyle causes worth remembering.
What are some signs and symptoms of AF?
- Irregular irregular pulse
- Hypotension:red flag; suggest haemodynamic instability
- Evidence of heart failure:red flag; such as pulmonary oedema
- Palpitations
- Dyspnoea
- Chest pain: red flag
- Syncope: red flag
Can also be asymptomatic!
What investigations would you carry out for AF
ECG
Tests to look for causes of AF:
Serum Electrolytes
Thyroid Function Tests
Cardiac biomarker - eg Troponin
Chest x-ray look for heart failure
Transthorasic Echo - look for functional heart disease
What is the management for someone who is haemodynamically unstable with AF? What signs could indicate that this is the case?
Emergency electrical synchronised DC cardioversion
- Shock: hypotension (systolic blood pressure <90 mm Hg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
- Syncope
- Myocardial ischaemia
- Heart failure:
What is the first line management for someone who is haemodynamically stable with AF? What signs could indicate that this is the case? What Rate control would you do?
Start by controlling either rate of rhythm
Rate control:
- First line: beta-blocker(e.g. bisoprolol) or arate-limiting calcium-channel blocker (e.g. verapamil)
- Digoxin: may be considered first-line in patients with AF and heart failure
OF HAEMODYNAICALLY STABLE, DO RATE CONTROL BEFORE RHYTHM CONTROL
What Further management might be necessary for persistent AF/ or AF that has not been treated with meds
Left atrial ablation - small burns/freezes to scar heart tissue to break up electrical signals that cause irregular heartbeats
Electrical DC cardioversion
Anticoagulants - DOACS - Apixaban to reduce risk of strokes, or Warafarin if DOACs are CI, (aka in Metal heart valves)
Anticoagulants are often given to patient with AF to reduced their likelihood of developing clots that can cause strokes.
What scoring system is used to calculate stroke risk in AF? What types of factors are included on it?
CHADS2VASc score used to calculate stroke risk in AF
0 = no anticoagulation
1 = consider oral anticoagulation or aspirin
2 = Anticoagulants - DOACS - Apixaban to reduce risk of strokes
Congestive Heart failure = 1
Hypertension = 1
Age > 75 = 2
Age 65-74 = 1
Diabetes Mellitus = 1
Stroke or TIA = 2
Vascular disease = 1
Female sex = 1
What would you see on an ECG for someone in AF?
Irregularly irregular
F (Fibrillatory) waves
No clear P waves
Rapid QRS complex
absence of [isoelectric]
baseline
variable ventricular rate
What Rhythm control would you do in AF?
Rhythm control: - either pharmacological or electrical cardioversion
- Pharmacological: - anti-arrhythmics
- Flecainide or amiodarone: if no evidence of structural/ischaemic heart disease
- Amiodarone: if structural/ischaemic heart disease is present
- Electrical cardioversion:rapidly shock the heart back into sinus rhythm
IF HAEMODYNAICALLY UNSTABLE, DO RHYTHM CONTROL BEFORE RATE CONTROL (aka Cardioveresion)
What is a Delta wave? Why does it occur?
“ A delta wave is slurring of the upstroke of the QRS complex.
Occurs because the action potential from the SA node is able to conduct to the ventricles very quickly through the accessory pathway
=> QRS occurs immediately after the P wave, making the delta wave.
What things in a presentation would make you think of an asthma?
- Episodic symptoms
- Diurnal variability - typically worse at night
- Dry cough with wheeze and shortness of breath
- Hx of other atopic conditions - eczema, hayfever, food allergies
- Family Hx
- Bilateral widespread ‘polyphonic’ wheeze heard on auscultation
What things in a presentation that would be indicative of an alternative diagnosis (not ASTHMA)
- Wheeze related to coughs/colds more suggestive of viral induced wheeze
- Isolated/productive cough
- Normal investigations
- No response to treatment
Unilateral wheeze - suggests focal lesion/infection
What pathophysiological changes to the bronchi is seen in asthma?
Smooth muscle spasm around bronchioles
Increased mucus secretion.
Airway wall oedema
There is also an increase in vascular permeability and recruitment of additional immune cells from the blood.
Initially these inflammatory changes are completely reversible but longer term leads to thickening of the epithelial basement membrane, which permanently reduces the airway diameter.
—> also in chronic asthma - see smooth muscle hypertrophy
What drugs can trigger asthma? How can they do this?
Beta blockers - (block adrenaline from binding) Blocking these receptors leads to smooth muscle contraction, narrowing airways and decreasing blood pressure.
Aspirin inhibits COX1/2
leads to increase USE of LPOX pathway.
Produces leukotrienes (LTB4, 5, 6)
These are proinflammatory
What are some primary investigations of asthma?
- Fractional exhaled nitric oxide (FeNO):>40 ppb is positive in adults
-
Spirometry:FEV1/FVC <70% suggests obstruction
if positive for obstruction, then carry out Bronchodilator reversibility (BDR) - Peak flow rate (PEFR):measured multiple times a day over 2-4 weeks. Variability of >20% is diagnostic
- Airway hyperreactivity testing: a histamine or methacholine direct bronchial challenge is performed if the investigations above are inconclusive
- Allergy testing: immunoassay for allergen-specific IgE or skin-prick testing
What is the bronchodilator reversibility test? What values in this would be indicative of asthma?
Looks to see if bronchodilators can improve FEV1
In asthma, use of bronchodilators should lead to
improvement of FEV1 by ≥12%andincrease ≥200ml in volume post-bronchodilator
An improvement of less than 12% is indicative of COPD
What PEFR would be considered an moderate, severe, life threatening/fatal asthma attack?
Moderate - PEFR 50-75% of predicted
Acute Severe - PEFR 33-50%, Resp rate >25, HR >110, can’t complete sentences
Lifethreatening PEFR <33%, Sats <92%, Becoming tired, No wheeze,
What is the general 1st and 2nd line management of chronic, non exacerbatory asthma?
1st line - SAB2A, eg Salbutamol, PRN
2nd line - SABA; e.g. salbutamol + low dose ICSe.g. beclomethasone.
What is the treatment for acute asthma attacks?
OSHITME:
O2 if oxygen sats are low
Saba (Salbutamol nebulised)
Hydrocortisone IV
Ipratropium bromide added to nebulizer remember, ipratropium is a SAMA
Theophyline IV - Bronchodilator
MgSO4 - Magnesium sulphate,
Escalate
What is the general 3rd and 4th line management for chronic asthma?
3a. Before adding more drugs assess inhaler technique and compliance
3b. SABA + ICS + Leukotriene Receptor Antagonist (LTRA = montelukast)
4th - SABA + ICS + LABA (Salmeterol) +/- LTRA
after SABA, ICS, LABA, and LTRA for asthma what do you switch to?
SABA and MART(maintenance and reliever therapy); this is combined fast-acting LABA and ICS for symptomatic relief and maintenance in a single inhaler.
Can increase ICS dose!!!
ICS increase transcription of B2-receptor gene = more expression of it on cell surface receptors —> ICS help Beta Agonists to work
How does Peak flow measurements differ at different times of the day?
Morning lower, evening higher. Diurnal variation
Outline the pathophysiology of Eczema.
- Filaggrin breaks down to form amino acid pool (used for skin barrier)
- Loss of function mutations in filaggrin gene predispose to breaks in epidermal barrier
So increased exposure and sensitisation to cutaneous antigens, increased eczema risk
Tiny gaps in the skin barrier provide an entrance for irritants, microbes and allergens that create an immune response, resulting in inflammation and the associated symptoms.
Outline the clinical features of eczema
itching (pruritus) is the main symptom, -> results in scratching and exacerbation of the rash
The excoriated areas become erythematous, weeping, and crusted.
Outline some of the treatment options for eczema
The key to maintenance is to create an artificial barrier over the skin to compensate for the defective skin barrier.
This is done using emollients that are as thick and greasy as tolerated, used as often as possible, particularly after washing and before bed.
Flares can be treated with thicker emollients, topical steroids, “wet wraps” (covering affected areas in a thick emollient and applying a wrap to keep moisture locked in overnight) and treating any complications such as bacterial or viral infections.
Give examples of the some of the topical treatments used in eczema
Thin creams:
E45
Diprobase cream
Thick, greasy emollients:
50:50 ointment (50% liquid paraffin)
Hydromol ointment
Diprobase ointment
Steriods
Give some examples of topcial steriods used in eczema
Steroids - Thicker the skin, stronger the steroid - avoid steroids around eyes face and genitals in children
Mild: Hydrocortisone 0.5%, 1% and 2.5%
Moderate: Eumovate (clobetasone butyrate 0.05%)
Potent: Betnovate (betamethasone 0.1%)
What are some side effects of heavy topical corticosteroid use in eczema?
Side effects of corticosteroids
Thinning of skin -> more prone to flares, bruising, tearing, stretch marks, enlarged BV under skin surface (telangiectasia)
Systemic absorption of steroid
Excessive hair growth
contact dermatitis
acne
What pathogens can cause skin infections in eczema?
Bacterial - staphylococcus aureus. Treat with flucloxacillin.
Viral - herpes simplex virus (HSV) or varicella zoster virus (VZV). - treat with aciclovir.
What is the presentation of Eczema Herpeticum? (a viral skin infection caused by the herpes simplex virus (HSV) or varicella zoster virus (VZV).
A typical presentation is a patient who suffers with eczema that has developed a widespread, painful, vesicular (sometimes itchy) rash with systemic symptoms such as fever, lethargy, irritability and reduced oral intake.
Pus vesicles can burst leaving punched out ulcers
There will usually be lymphadenopathy (swollen lymph nodes).
What is atrophic vaginitis?
Is the dryness and atrophy of the vaginal mucosa related to a lack of oestrogen
The epithelial lining of the vagina and urinary tract responds to oestrogen by becoming thicker, more elastic and producing secretions. As women enter the menopause, oestrogen levels fall, resulting in the mucosa becoming thinner, less elastic and more dry. The tissue is more prone to inflammation. There are also changes in the vaginal pH and microbial flora that can contribute to localised infections.
can also be referred to as genitourinary syndrome of menopause
What is the presentation of atrophic vaginitis? What other conditiosn should make you consider it?
Itching
Dryness
Dyspareunia (discomfort or pain during sex)
Bleeding due to localised inflammation
consider it in older women presenting with recurrent urinary tract infections, stress incontinence or pelvic organ prolapse.
Specifcially ask symptoms of vaginal dryness and discomfort!!
What is the management of atrophic vaginitis?
Vaginal lubricants can help symptoms of dryness. Examples include Sylk, Replens and YES.
Topical oestrogen
- Estriol Cream or pessaries
- Estradiol Tablets or a ring
Give some complicaitons of topical oestrogen and outline how its use should be used, in atrophic vaginitis.
Topical oestrogen shares many contraindications with systemic HRT, such as breast cancer, angina and venous thromboembolism.
Women should be monitored at least annually, with a view of stopping treatment whenever possible.
What is bacterial vaginosis?
- It refers to an overgrowth of bacteria in the vagina specifically anaerobic bacteria
- It is not Sexually transmitted
MOST COMMON CAUSE OF VAGINITIS IN YOUNG WOMEN
What causes BV?
Loss of lactobacilli which produce lactic acid and keep the vaginal pH low
Gardnerella vaginalis (most common)
Mycoplasma hominis
Prevotella species
What is the presentation of BV?
Fishy-smelling watery grey or white vaginal discharge. Half of women with BV are asymptomatic.
What cells are shown with BV?
Clue cells
Eye anatomy/physiology - what are the The lacrimal puncti and the Meibomian glands?
Meibomian glands are in the posterior aspect of the eyelid (Figure 1). They are modified sebaceous glands that produce the lipid outer layer of the tear film.
The lacrimal puncti are responsible for tear drainage and are on the medial aspect of each eyelid.
Common eye problems - what is Blepharitis, and how does it present?
Blepharitis is inflammation of the eyelid. It is the most common cause of dry eye disease.
Can also see inflammation and congestions of the meibomian glands
Patients typically present with bilateral symptoms of ocular irritation, foreign body sensation, burning, redness and crusting. There may be paradoxical watering of the eye due to reflex tear secretion.
How do you treat and prevent blepharitis
Lid hygiene is important for treating and preventing blepharitis.
Three steps to cleaning eyelids should be performed at least once a day:
Warm compression of the eyelids with a warm compress to loosen debris
Eyelid massage to empty glands of debris
Cleaning eyelids with cotton wool to remove debris
Topical antibiotic ointments (e.g. chloramphenicol)
Common eye problems - what is a Hordeolum, and how does it present?
An external hordeolum is caused by a staphylococcal infection of an eyelash follicle. External hordeolum tend to affect children and young adults and are also known as a stye
An internal hordeolum is an infection of a meibomian gland and is far less common.
External hordeola present as tender, red eyelash follicle swellings
How do you treat a stye/hordeolum?
Hordeola often resolve spontaneously. Patients should be encouraged to perform warm compression of the eyelid multiple times a day to reduce swelling.
Other treatment options include:
Removal of the eyelash associated with external hordeolum
Incision of the hordeolum with a fine sterile needle
Topical antibiotics (e.g. chloramphenicol) or oral antibiotics (e.g. co-amoxiclav) if the hordeolum is recurrent or severe
Common eye problems - what is a Chalazion, and how does it present?
A chalazion is a granulomatous inflammatory lesion that forms in an obstructed meibomian gland.
They are non infectious
Chalazia present as painless red eyelid cysts in the internal eyelid (Figure 5). If chalazia are infected, they become internal hordeolum.
chalazia are not painful or tender to touch. In contrast, an external hordeolum is associated with pain (i.e. ‘styes sting’).
What is the management of a chalazion?
Chalazia often resolve spontaneously. Patients should be encouraged to perform warm compression of the eyelid (to loosen meibomian gland content) and eyelid massage (to express meibomian gland content) twice a day.
Common eye problems - what is an Entropion, and what is an ectropion? What neuro condition is associated with an ectropion?
Entropion is inward turning of the eyelid. Inward-turning eyelashes may irritate the cornea causing ulceration and risking sight loss.
Ectropion is an outward turning of the eyelid - can be caused by Bells Palsy.
What is trichiasis?
What are most cases caused by?
Trichiasis is when eyelashes grow inwards due to damaged eyelash follicles. Inward-growing eyelashes may irritate the cornea causing corneal ulceration and risking sight loss.
Most cases of trichiasis are caused by eyelid inflammation (chronic blepharitis).
What are some causes/Known risk factors for Bells Palsy
Viral;
herpes simplex
herpes zoster
EBV
cytomegalovirus infections
rubella
Risk factors include diabetes, a recent upper respiratory tract infection, and pregnancy
HIV, sarcoidosis and Lyme disease (Borrelia Burgdoferi infection)
Obesity, Hypertension
What is the pathophysiology of Bell’s palsy?
the nerve that controls facial muscles passes through a narrow corridor of bone on its way to the face
in Bell’s palsy that nerve becomes inflamed and swollen - usually related to a viral infection
How and why does Bell’s Palsy differ to a Stroke?
Bell’s Palsy is a peripheral nerve effect whereas a ischemic stroke is a central process. The forehead receives motor innervation from both hemispheres of the cerebral cortex.
A stroke that compromised motor innervation of the face would therefore only result in paralysis of the lower half of the face - the forehead is still receiving innervation from the unaffected hemisphere (as its a UMN lesion)
A peripheral lesion, such as Bell’s Palsy, interrupts the innervation after the motor commands from both hemispheres have joined, so that the forehead is paralyzed. (its a LMN lesion)
What is the management for Bell’s palsy?
steroids - prednisolone
antivirals - acyclovir
eye-care - reduced eye closing can lead to dry eye and corneal damage
Outline the pathophysiology behind Benign prostatic hyperplasia - why does it occur with increasing age? Where in the prostate is most effected?
With age the levels of testosterone drop but the levels of DHT increase as 5α-reductase activity increases. The entire prostate gland enlarges uniformly and small hyperplastic nodules can form within it.
Typically, hyperplastic nodules will form in the inner portions of the gland, specifically around the prostatic urethra, called the periurethral zone.
How can BPH cause symptoms? What symptoms do you see?
These nodules will compress the urethra making it more difficult to pass urine ==> smooth muscles of the bladder will have to work harder leading to bladder hypertrophy
The stagnation of the urine in the bladder also promotes bacterial growth leading to UTIs
So see
Dribbling
Straining when urinating
Painful urination (Dysuria)
Trouble initiating urination (Hesitancy)
Incomplete urination and more urination at night (Nocturia)
What are the signs of BPH?
Digital rectal examination findings
- Smooth, enlarged, and non-tender
Lower abdominal tenderness and palpable bladder
- Indicates acute urinary retention
- Perform bladder scan
- Requires urgent catheterisation
On a DRE, what is the difference in findings for BPH vs Prostate Cancer?
In BPH, the enlargement feels smooth and firm while in prostate cancer, the gland may feel hard and lumpy - Enlarged in Both though
What are the investigations for BPH?
Prostate-specific antigen (PSA): predicts prostate volume, may suggest cancer if significantly raised but BPH can also raise it
International Prostate Symptom Score (I-PSS):a 7-symptom questionnaire with an additional bother score to predict progression and outcome
Transrectal ultrasound:can estimate prostate size and weight
What are the non-surgical treatments for BPH that has bothersome symptoms?
α-1 antagonists: Tamsulosin it is considered first-line. It inhibits the action of noradrenaline and relaxes the smooth muscle.
5-α reductase inhibitors e.g. finasteride. This will work to reduce the prostate size but can take up to 6 months to work.
What are some side effects of the BPH treatments - a-1 anatagonists and 5-a reductase inhibitors?
α-1 antagonists: eg tamulosin - Postural hypotension, dizziness, dry mouth and depression
5-α reductase inhibitors eg Finasteride - reduced libido, erectile dysfunction, and gynaecomastia
What are the the surgical options for BPH and when would they be used?
Prostate <30 g:
- Transurethral incision of the prostate (TUIP): one or two cuts in the small grooves of the bladder neck to open the urinary channel and allow urine to pass through more easily.
Prostate 30-80g:
- Transurethral resection of the prostate (TURP): accessing the prostate through the urethra and “shaving” off prostate tissue from inside using diathermy (heat)
What is the most common form of prostate cancer? Where in the prostate is it found
Prostate adenocarcinoma - ARISE IN THE PERIPHERAL ZONE
Name some risk factors for prostate cancer
- Increasing age:highest rates amongst men aged 75 to 79 years
- Family history: 5-10% have a strong family history
- Afro-Caribbean ethnicity
- Being tall
- Obesity and high-fat diet
- Use of anabolic steroids
-
Cadmium exposure:found in cigarettes, batteries and those working in the welding industry
Certain genes
What genes have been linked to prostate cancer, as a risk factor?
BRCA1 and BRCA2 have been linked to prostate cancer
Where does prostate cancer usually spread to if it becomes metastatic?
Spreads to the bines of the vertebrae and pelvis resulting in hip and in back pain
What scoring system is used in diagnosing prostate cancer?
Gleason score
From biopsy - assigned a score on a scale of 3 to 5 from 2 different locations. Cancer cells that look similar to healthy cells receive a low score. Cancer cells that look less like healthy cells or look more aggressive receive a higher score.
What is a key risk factor for a breast abscess/infection? What are some key signs and symptoms of it?
Smoking
The presentation of mastitis or breast abscesses is usually acute, meaning the onset is within a few days.
Mastitis with infection in the breast tissue presents with breast changes of:
Nipple changes
Purulent nipple discharge (pus from the nipple)
Localised pain
Tenderness
Warmth
Erythema (redness)
Hardening of the skin or breast tissue
Swelling
The key feature that suggests a breast abscess is a swollen, fluctuant, tender lump within the breast.
What is bronchiolitis? Who is it most common in?
This is a lower respiratory tract infection which leads to the blockage of small airway in the lungs
– It is most seen in children younger than 2 and cases spike in autumn and winter
What is bursitis?
Acute/chronic inflammation of a bursa
Bursa = sac containing small amount synovial fluid
Lies between tendon ± skin/bone to act as friction buffer & facilitate movement of adjacent structures
most common in the shoulders, hips, elbows or knees.
What are some signs and symptoms of bursitis, and why do they happen?
Inflammation of bursa -> ^ synovial fluid production -> enlargement of bursa -> ^ friction during movement -> Sx
Localised pain and tenderness over a bursa
Swelling if superficially sited
Decreased active range of motion
Acute bursitis - tenderness, pain during activation of muscles adjacent to inflamed bursa
Chronic bursitis - swelling with minimal pain
In which two ways can Chronic kidney disease be classified?
How many stages in each?
By GFR and by the degree of persistent Albuminuria
Goes G1-G5 and A1-A3
Outline the pathophysiology in the adaptations of nephrons that is seen in CKD. (1)
In CKD, The initial failing and scarring of some nephrons leads to an increased filtration on the remaining Functioning, (remnant) nephrons
These remnant nephrons experience hyperfiltration (increased flow per nephron as blood flow remains the same), ==> adapt with glomerular hypertrophy, and reduced arteriolar resistance
Outline the pathophysiology seen in CKD - what does hyperfiltration/glomerular hypertrophy lead to? How can this be detected?
Increased flow, increased pressure and increased shear stress causes a vicious cycle of raised intraglomerular capillary pressure and strain, which accelerates remnant nephron failure
This increased flow and strain may be detected as new/increasing proteinuria
What are some general symptoms of CKD?
Can be asymptomatic early on
- Nausea
- Anorexia
- Loss of appetite
-
Frothy urine
Malaise,
oliguria, - decreased urine output
haematuria,
nocturia
What are some signs of CKD?
- Hypertension
- Fluid overload
- Uraemic sallow: a yellow or pale brown colour of skin
- Uraemic frost: urea crystals can deposit in the skin
- Pallor: due to anaemia
- Evidence of underlying cause: e.g. butterfly rash in lupus
Bilaterally small kidneys on ultrasound
Postural hypotension
Peripheral oedema
Pleural effusions
What type of imaging is often done in investigation CKD? What can it show and what does it look for?
Renal ultrasound – excludes obstruction, gives assessment of kidney size (small kidneys favour CKD) and also looks for other abnormalities such as cysts and masses
Outline gfr stages 1-5 for CKD - what is a cool tool you can use to remeber
1 >90 Normal or increased GFR with other evidence of renal damage
2 60–89 Slight decrease GFR with other evidence of renal damage
3 A - 45–59, 3 B - 30–44 = Moderate decreased GFR with or without evidence of other renal damage
4 15–29 Severe decreased GFR with or without evidence of renal damage
5 <15 Established renal failure
GFR clock!!!
What are the conditions that are classed as COPD?
Chronic Bronchitis
Emphysema
What happens to the
FEV, FEV1, and FEV1/FVC, and TLC in Obstructive conditions like COPD and Asthma?
In COPD, the airways become obstructed and the lungs don’t empty properly which leaves air trapped inside the lungs.
- FVC (max air exhaled in one breath): lowered
- FEV1 (first second of air breathed out in a single breath): lowered, more than the FVC
- FEV1:FVC ratio: lowered
- TLC (total lung capacity): increased due to air trapping
What is the pathophysiology behind chronic bronchitis
Hypertrophy and hyperplasia of bronchial mucinous glands and goblet cells. Also ciliary destruction. (ie due to cigarette smoke as main cause
More mucous in lumen - causes narrowing and obstruction,
epithelial layer may become ulcerated and undergoes metaplasia
Also, smoking makes the cilia short and less mobile, making it harder to move mucus up and out of bronchioles. A cough is sometimes the only way to clear this mucus.
Pathophysiology of chronic bronchitis - why may patients with this go on to develop hypoxia and hypercapnia?
Mucus plugs block airflow, == high levels of CO2 and low levels of O2 in the lung
–> so less O2 moves into blood and less CO2 moves out of blood.
Blood vessels can then undergo vasoconstriction to shunt blood away from damaged tissue towards healthy lung tissue.
What is Emphysema, as a pathological Definition?
A lung disease characterised by dilatation and destruction of the lung tissue causing enlarged air spaces distal to the terminal bronchioles
Outline the pathophysiology behind emphysema.
Occurs in the ACINUS - (the respiratory bronchioles, alveolar ducts and alveolar sacs distal to a single terminal bronchiole)
Irritants/chemicals damage alvolar wall EG cigarette smoke
immune cell infiltration releasing Leukotriene B4, IL-8 and TNF-a, as well as Neutrophil Proteases (elastases and collagenases)
- Neutrophil proteases break down alveolar septa break down, REDUCES TOTAL SURFACE AREA -
Loss of elasticity in the airways means that the airways collapse upon exhalation causing air trapping distally.
What are some signs and symptoms of emphysema
- Breathing with pursed lips (pink puffers): prevents alveolar collapse by increasing the positive end expiratory pressure
- Barrel shaped chest: due to air trapping and hyperinflation
- Loss of cardiac dullness:due to hyperexpansion of lungs from emphysema
- Dyspnoea
- Cough: could be productive
- Weight loss: due to energy expenditure while breathing
- Signs of CO2retention
- Drowsy
- Asterixis
- Confusion
What other tests may be done to look for the cause of COPD? on top of spirometry?
CXR:
DLCO (diffusing capacity of CO across lung):
Low in COPD, Normal in Asthma
Genetic testing for A1AT Def.
ABG - may show T2RF
ECG - heart function
CXR - flattened diaphragm
Bloods - anaemia
What would you see on a xray for someone with COPD
Hyperexpanded, enlarged lungs, air pockets (bullae) or a flattened diaphragm, and saber sheath trachea
Barrel shaped chest
What are some risk factors for depression?
Prior depression
Family Hx depression
Female
Hx abuse
Drug and alcohol use
Low socioeconomic status
Recent bereavement, stress or medical illness, traumatic life event
Co-existing medical conditions (chronic disease)
Outline the Pathophysiology of Hasimoto’s Thyroiditis. What 2 things are specifically attacked?
It is caused by autoimmune inflammation of the thyroid gland.
It is associated with antithyroid peroxidase (anti-TPO) antibodies and antithyroglobulin antibodies
Initially it causes a goitre after which there is atrophy of the thyroid gland.
What are some key signs of Hypothyroidism/Hasimoto’s Thyroiditis?
Bradycardia
Unexplained weight gain
Slow reflexes, Ataxia
Round Puffy face
Immobile Ileus - temporary arrest of Intestinal peristalsis
ASCITES - fluid in abdomen
What are some symptoms a patient might experience if they have any form Hypothyroidism?
Hoarse voice
Goitre - lump or swelling on neck from thyroid gland
Weight gain
Constipation
Cold intolerance
Menorrhagia – heavy periods
Tiredness
Lethargy
Poor memory
Puffy eyes
Arthralgia/myalgia
Symptoms of anaemia
Normal Physiology: Outline the relationship between Hypothalamus, Anterior Pituitary and Thyroid gland, and how what they release influences each other.
HYPOTHALAMUS: Releases THYROTROPIN RELEASING HOROMONE
====> causes ANTERIOR PITUITARY GLAND TO RELEASE THYROID STIMULATING HOROMONE (THYOTROPIN)
The binding of TSH to thyroid gland promotes every aspect of T3 and T4 production - Iodine pumping, Thyroglobulin synthesis, releasing of thyroid hormone in the blood
T3 - NEGATVIE FEEDBAKC ON THE ANTERIOR PITIUARY TO STOP REALSING TSH
Thyroxine = T4 (4 iodine)
Triiodothronine = T3 (3 iodine)
What are some signs of Grave’s Disease?
- Tremor
- Tachycardia/AF
- Goitre
- Hair loss/thin hair
- Lid lag/retraction
- Hyperkinesia - increased muscle activity
- Exophthalmos – bulging of the eye out of the orbit
What are some symptoms a Patient might experience if they have Grave’s Disease?
** Weight loss
* Irritability
* Heat intolerance*
* Insomnia
* Diarrhoea
* Sweats
* Palpitations
Anxiety
Pretibial myxedema specific to Grave’s
Outline the pathophysiology that typically causes Type 1 diabetes.
- Autoimmune destruction of pancreatic β-cells leading to an insulin deficiency
- β cells express HLA antigens on MHC in response to an environmental event (potentially a virus)
- Activates a chronic cell mediated immune response leading to chronic insulitis
Up to 90% of people have autoantibodies
80-90% of beta cells need to be destroyed before symptoms usually appear for type 1 diabetes
What does the secretion of glucagon, adrenaline, cortisol, result in? (Type 1 diabetes)
How do they present?
Gluconeogenesis, Glycogenolysis and ketogenesis.
Patients as a result present with ketoacidosis and hyperglycaemia.
Define type 2 diabetes
A progressive disorder defined by deficits in insulin secretion and insulin resistance that lead to abnormal metabolism and related metabolic derangements
Outline the pathophysiology of Type 2 diabetes
Repeated exposure to high levels of Glucose and insulin makes the cells in the body come resistant to insulin.
Over time, the pancreas (specifically the beta cells) becomes fatigued and damaged by producing so much insulin and they start to produce less.
Fasting glucose levels increases
What is the second line treatment for someone with type 2 diabetes?
What does it do?
What is added if pts with T2DM have a QRISK above 10%?
Medical management: First line: metformin titrated from initially 500mg once daily as tolerated.
Metformin is a “biguanide”. It increases insulin sensitivity and decreases liver production of glucose. It is considered to be “weight neutral” and does not increase or decrease body weight.
NICE suggest considering adding an SGLT-2 inhibitor in patients with a QRISK score above 10%.
3rd line treatment for T2DM: What can SGLT2 inhibitors do, and what can they lead to, as side effects?
eg empagliflozin, canagliflozin, dapagliflozin
They block the reabsorption of glucose in the kidney, increase glucose excretion, and lower blood glucose levels
Make you pee lots of glucose out =UTI and Thrush
Peeing out glucose can make your body think you’re in a fasting state - leading lipid break down - KETOACIDOSIS euglycaemic ketoacidosis
What insulin medication pattern do you see in T2DM
Just once a day, (Basal) sometimes twice (BD)
What is the fifth line treatment for someone with T2DM?
Insulin. Start with Basal Dose
If you see any red flag symptoms in GORD, what investigation would you do? What complications of GORD are you looking for
Endoscopy
oesophagitis, Barrett’s oesophagus or an alternative diagnosis (i.e. oesophageal/gastric malignancy).
Oesophageal adenocarcinoma
What are Diverticula?
Outpouching of the colon wall, most frequently in the sigmoid colon.
Define Diverticulosis
Diverticulosis:the presence of diverticula (out-pouching) in an asymptomatic patient
Define Diverticulitis
Diverticulitis:where diverticula become inflamed and infected, typically causing severe lower abdominal pain, fever, general malaise, and occasionally rectal bleeding
How do Diverticula form, leading to diverticulosis?
Areas in the large intestine where the smooth muscle is penetrated by blood vessels are weaker than normal.
Increased pressure in the lumen causes a gap to form in this muscle, allowing the mucosa to herniate through.
It happens in areas that are not covered by teniae coli
When would you use a colonoscopy when investigating diverticulitis? Why do you need to be cautious using it?
Colonoscopy: should generally be avoided in acute diverticulitis due to the risk of perforation, and is used if the diagnosis is unclear or alternative pathology is suspected
What would you offer in symptomatic diverticular disease?
1ST LINE –
dietary and lifestyle modifications
CONSIDER –
analgesia - Paracetamol, avoid NSAIDs
CONSIDER –
antispasmodic - dicycloverine
What are some signs and symptoms of Irritable bowel syndrome?
- Signs
- General abdominal tenderness may be felt.
- Symptoms
- Fluctuating bowel habit
- Diarrhoea
- Constipation
- Urgency
- Mucus PR
- Abdominal pain
- Pain worse after eating
- Improved by opening bowels
- Bloating
image source - unknown
Pathophysiology behind Crohn’s what are immune cells seen in it? In what way are the ulcers arranged at what is this called?
What is the most commonly affected site in Crohns?
T helper cells release cytokines which attract cells such as macrophages which release substances like proteases, platelet activating factor and free radicals
Ulcers occurs in patches known as skip lesions
the ileum is the most commonly affected site of crohns
What are some cutaneous, muscoskeletal and eye features you may see in a patient with Ulcerative collitis?
Erythema Nodosum - inflamed subcutaneous fat (see picture)
Pyoderma gangrenosum - rapidly enlarging, very painful ulcer.
- Osteoporosis and arthritis
- Clubbing
- Uveitis - eye inflammation
- Conjunctivitis
taken from netters illustrated human pathology
What is the gold standard investigation for UC? What would you see on it?
Colonoscopy -
- Red and raw mucosa with widespreadshallow ulceration
- No inflammation beyond the submucosa, unless fulminant disease
- Pseudopolyps: mucosa adjacent to ulcers is preserved, which has the appearance of polyps - They are caused by mucosal repair after chronic inflammation.
- Crypt abscessesdue to neutrophil migration through gland walls
- Goblet cell depletion, withinfrequentgranulomas
picture taken from netters illustrated human pathology
State some histological features that will be seen in ulcerative colitis
Pseudopolyps
Crypt abscess
Goblet cell depletion,
Infrequent granulomas
Increased plasma cells in lamina propria
Hypertension medication - what is the first line treatment for someone who is NOT black, and under 55 years
ACE-Inhibitor e.g. Ramipril (or angiotensin receptor blocker e.g. candesartan if contraindicated e.g. due to cough)
Anyone with diagnosed hypertension, even if its under control, need an annual review!
Hypertension medication - what is the second line treatment for hypertension?
ACE-inhibitor + CCB
Or if afro Caribbean - CCB and ARB
Anyone with diagnosed hypertension, even if its under control, need an annual review!
Hypertension medication - what is the fourth line treatment for treatment of hypertension?
On top of ACEi/ARB, CCB and Thiazide like Diuretic add either a:
(depends on K+ levels)
<4.5 mmol/L = potassium-sparing diuretic, like Spironolactone
>4.5 mmol/L = beta blocker (e.g., atenolol)
Remember to check adherence. Specialist management is indicated for uncontrolled blood pressure at step 4.
What is the first line medication given to anyone with T2DM, regardless of age or race?
ACEi, eg Ramipril
Anyone with diagnosed hypertension, even if its under control, need an annual review!
What is a classic presentation for peripheral vascular disease?
Aching in calves - claudication - relieved by taking a break
Pain when legs are elevated, if bed bound - relieved when lowering
Claudication = think angina of the limbs
What things would you do in order to examine for peripheral vascular disease?
Outline the special test you can do
Pale and cold leg on elevation - (Beuger’s angle <20’) – the leg will go pale and cold upon raising it 20’ off the couch.
Increased vascular filling time– Upon lowering, the leg may become hot and red as reperfusion occurs.
Perfusion time tends to be increased (>15s)
Oedema is not usually present
Evidence of poor skin health eg ulcers, dry scaly skin, cool peripheries and reduced capillary refill time
Absent (posterior tibial and dorsals pedis) pulses represent an increased chance of peripheral vascular disease
What causes the formation of venous ulcers?
What causes the formation of arterial ulcers?
Arterial ulcers develop as the result of damage to the arteries due to lack of blood flow to tissue. Ischaemia
Venous ulcers develop from damage to the veins caused by an insufficient return of blood back to the heart. (Stagnation of blood under pressure)
Outline some features of arterial ulcers, that are comparable to venous ulcers
Arterial ulcers
Occur distally, affecting the toes or dorsum of the foot/lateral malleolus
Are smaller and deeper than venous ulcers
Well defined borders
Have a “punched-out” appearance
Are pale colour due to poor blood supply
Are less likely to bleed
Are painful
Have pain worse at night (when lying horizontally), and on elevating, and then improved by lowering the leg
Outline some features of venous ulcers, that are comparable to arterial ulcers
Occur in the gaiter area (between the top of the foot and bottom of the calf muscle), and medial malleolus
Are larger and more superficialthan arterial ulcers
Have irregular, gently sloping border
Are more likely to bleed
Are less painful than arterial ulcers
Have pain relieved by elevation and worse on lowering the leg
Medail aspect of leg
What is systolic heart failiure?
What are it’s main causes?
Now more commonly known as heart failure with reduced ejection fraction (or HFrEF)
Ejection fraction <40% (SV/EDV)
Caused by
IHD
MI
Hypertension
Cardiomyopathy
What is diastolic heart failure? What are its made causes?
Inability to relax and fill
There is reduced preload because there is abnormal filling of the LV
Ejection fraction >50%
Caused by
Constrictive pericarditis
Cardiac tamponade
Hypertension
What are the signs of left sided heart failure?
Signs:
Cardiomegaly (displaced apex beat)
Pulmonary Oedema
3rd and 4th heart sounds
Pleural effusion
Crepitations in lung bases
Tachycardia
Reduced BP
Cool peripheries
Heart murmur
What are the signs/symptoms of Right hand sided heart failure?
Raised JVP – JVP distension
Hepatomegaly/Splenomegaly
Pitting oedema – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed
Ascites
Weight gain (fluid)
blood backing up into the systemic veins in
a) Jugular vein
b) liver and spleen
c) peritoneum
d) interstitial soft tissue space - legs and sacrum
leads to what signs/symptoms in right sided heart failure?
Blood back up into jugular vein Raised JVP, – JVP distension -
b) leads to Hepatomegaly and Splenomegaly (Hepatosplenomegaly)- In extreme cases and lead to cirrhosis of liver, known as cardiac cirrhosis
c) Fluid build up in peritoneum leads to Ascites and weight gain
d) leads to Pitting oedema – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed
What could a chest Xray show for someone with heart failure
ABCDE
Recommended for all suspected HF patients
Alveolar oedema - seen in Bat wing shadowing
Kerley B Lines interstitial oedema
Cardiomegaly
Dilated upper lobe vessels of lungs (prominent upper lobe veins)
Effusions (pleural)
A normal CXR does not exclude the possibility of Heart Failure
Heart failure medication 1:What is the first medications you should give in patients with heart failure with reduced ejection fraction?
- an ACE inhibitor, like Ramipril, and Beta blockers, like Bisoprolol
Start low, progress slow! - monitor BP and heart rate
ABAL
(can consider giving an Angiotensin 2 receptor blocker eg Candesartan if intolerant of ACE-i)
Heart failure medication 3 - After ACE inhibitors and beta blockers , what other medications can you give?
K+ sparing diuretic, like Spironolactone - Aldosterone receptor antagonist
ABAL
Outline trendelebergs test
– with the patient lying down, lift the affected leg to drain the veins completely. Then apply a tourniquet to the thigh and stand the patient up. The tourniquet should prevent the varicose veins from reappearing if it is placed distally to the incompetent valve. If the varicose veins appear, the incompetent valve is below the level of the tourniquet
