GENERAL PRACTICE 1 - Misc, Pysch, Endo, Gastro, Cardio Flashcards

Question

What are some symptoms of alpha thalassaemia?

Answer 1

- **Shortness of breath:** due to anaemia - **Palpitations:** due to anaemia - **Fatigue:** due to anaemia - **Swollen abdomen:** due to hepatosplenomegaly

Answer 2

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**

Answer 3

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

Answer 4

***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

Answer 5

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 only **curative** option recommended in those with severe disease

Answer 6

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

Answer 7

Haemolytic and Non Haemolytic Haemolytic anaemia occurs when RBCs are destroyed before 120 days (lifespan dependent on cause of haemolysis)

Answer 8

Sickle cell anaemia is an **autosomal recessive mutation in the beta chain** of haemoglobin, resulting in sickling of red blood cells (RBCs) and haemolysis.

Answer 9

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.

Answer 10

- HbS is prone to sickling and 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***

Answer 11

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.

Answer 12

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.

Answer 13

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 PaO2 2.5 - 4 kPa, whilst HbSS (disease) patients at PaO2 5 - 6 kPa.

Answer 14

- **Chronic symptoms:** - Pain - Related to anaemia: fatigue, dizziness, palpitations - Related to haemolysis: **jaundice, and gallstones**

Answer 15

Splenic Sequestration crisis - affects Spleen Aplastic crisis - affects bone Vaso-occlusive crisis - can affect bone, lungs, CNS, genitalia

Answer 16

They can occur spontaneously or be triggered by stresses such as infection, dehydration, cold or significant life events.

Answer 17

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

Answer 18

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**

Answer 19

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**

Answer 20

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.

Answer 21

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**

Answer 22

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

Answer 23

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

Answer 24

No further tests are needed for diagnosis, if: - Family history of HS **and** - Typical clinical features **and** - Positive laboratory investigations (spherocytes, raised MCHC, increase in reticulocytes)

Answer 25

MCV stands for Mean Corpuscular Volume, which is a measure of the average size of red blood cells.

Answer 26

MCHC stands for Mean Corpuscular Hemoglobin Concentration, which is a measure of the average amount of hemoglobin in a red blood cell.

Answer 27

- **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:** **negative** in hereditary spherocytosis. *(it is Positive in Autoimmune haemolytic anaemia)*

Answer 28

- **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 be **vaccinated** against encapsulated bacteria and be prescribed lifelong **phenoxymethylpenicillin**

Answer 29

A normocytic, Haemolytic Anaemia, where there is a genetic defect in teh G6PD protein

Answer 30

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

Answer 31

- **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)

Answer 32

- **Avoid trigger of haemolysis** e.g. fava beans and certain medications - In certain cases, **transfusions** may be needed

Answer 33

red blood cells are attacked by either IgM or IgG antibodies

Answer 34

○ A – Acute blood loss ○ A – Aplastic Anaemia e.g. bone marrow suppression or chronic kidney disease (lack of EPO) H – Haemolytic Anaemia H - Hypothyroidism

Answer 35

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!***

Answer 36

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. -

Answer 37

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)

Answer 38

- 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.

Answer 39

Pernicious anaemia is an autoimmune condition in which the parietal cells are attacked 🡪 atrophic gastritis and loss of IF production 🡪 B12 malabsorption

Answer 40

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

Answer 41

hypothyroidism leads to **Less production of EPO**, can lead to decreased production of RBCs

Answer 42

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.*

Answer 43

Tear in lower anal canal (distal to dentate line), usually due to trauma Constipation Anal trauma Rarely: crohns, TB

Answer 44

Extreme pain on passing motion Pain may continue for 1-2 hours, can be burning nature Blood in stool / on wiping

Answer 45

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

Answer 46

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

Answer 47

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

Answer 48

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.

Answer 49

depression and obsessive compulsive disorder Hyperthyroidism - do TFTs Pheochromocytoma Lung disease - excessive salbutamol use Congestive HF - heart meds -> anxiety Hypoglycaemia Do Bloods, and BP

Answer 50

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.

Answer 51

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

Answer 52

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

Answer 53

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

Answer 54

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

Answer 55

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

Answer 56

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.

Answer 57

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

Answer 58

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)

Answer 59

**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

Answer 60

- Idiopathic (30%) - Coronary heart disease - Thyrotoxicosis - COPD - Pericarditis - Acute excess alcohol intoxication

Answer 61

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

Answer 62

ECG: regular sawtooth-like atrial flutter waves (F waves) with P-wave after P-wave

Answer 63

- **Treat the reversible underlying condition** (e.g. hypertension or thyrotoxicosis) - **Rate/rhythm control** with beta blockers or cardioversion (*use of electric shock to put heart back into rhythm) - **Radiofrequency ablation** of the re-entrant rhythm (*Uses heat generated by radio waves to destroy tissue*) - **Anticoagulation** based on CHA2DS2VASc score

Answer 64

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

Answer 65

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

Answer 66

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

Answer 67

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)

Answer 68

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

Answer 69

Breath-holding Carotid massage - *massage the carotid on one side gently with two fingers.* Valsalva manoeuvre - *Pt blows hard into resistance*

Answer 70

If manoeuvres unsuccessful, **IV adenosine** Causes a complete heart block for a fraction of a second Effective at terminating AVNRT and AVRT

Answer 71

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.

Answer 72

- **Irregularly irregular** ventricular contractions - **Tachycardia** - **Heart failure** due to **poor filling** of the ventricles during **diastole** - Risk of **stroke**

Answer 73

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.

Answer 74

- **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!

Answer 75

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*

Answer 76

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**:

Answer 77

Start by controlling either **rate of rhythm** Rate control: - **First line: beta-blocker** (e.g. bisoprolol) or a **rate-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***

Answer 78

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)

Answer 79

**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

Answer 80

Irregularly irregular F (Fibrillatory) waves No clear P waves Rapid QRS complex absence of [isoelectric] baseline variable ventricular rate

Answer 81

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)***

Answer 82

“ 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.

Answer 83

* 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

Answer 84

* 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

Answer 85

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**

Answer 86

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

Answer 87

- **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

Answer 88

Looks to see if bronchodilators can **improve FEV1** In asthma, use of bronchodilators should lead to improvement of FEV1 by ≥12% and increase ≥200ml in volume post-bronchodilator An improvement of less than 12% is indicative of COPD

Answer 89

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,

Answer 90

1st line - SAB2A, eg **Salbutamol**, PRN 2nd line - **SABA** ; e.g. salbutamol + **low dose ICS**e.g. beclomethasone.

Answer 91

OSHITME: **O**2 if oxygen sats are low **S**aba (Salbutamol nebulised) **H**ydrocortisone IV **I**pratropium bromide added to nebulizer *remember, ipratropium is a SAMA* **T**heophyline IV - Bronchodilator **M**gSO4 - Magnesium sulphate, **E**scalate

Answer 92

3a. Before adding more drugs assess inhaler technique and compliance 3b. SABA + ICS + Leukotriene Receptor Antagonist (LTRA = montelukast) 4th - SABA + ICS + LABA (Salmeterol) +/- LTRA

Answer 93

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***

Answer 94

Morning lower, evening higher. Diurnal variation

Answer 95

* 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.

Answer 96

itching (pruritus) is the main symptom, -> results in scratching and exacerbation of the rash The excoriated areas become erythematous, weeping, and crusted.

Answer 97

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.

Answer 98

Thin creams: E45 Diprobase cream Thick, greasy emollients: 50:50 ointment (50% liquid paraffin) Hydromol ointment Diprobase ointment Steriods

Answer 99

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%)

Answer 100

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

Answer 101

Bacterial - staphylococcus aureus. Treat with flucloxacillin. Viral - herpes simplex virus (HSV) or varicella zoster virus (VZV). - treat with aciclovir.

Answer 102

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).

Answer 103

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

Answer 104

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!!*

Answer 105

Vaginal **lubricants** can help symptoms of dryness. Examples include Sylk, Replens and YES. **Topical** oestrogen - Estriol Cream or pessaries - Estradiol Tablets or a ring

Answer 106

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.

Answer 107

- 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

Answer 108

Loss of lactobacilli which produce lactic acid and keep the vaginal pH low Gardnerella vaginalis (most common) Mycoplasma hominis Prevotella species

Answer 109

Fishy-smelling watery grey or white vaginal discharge. Half of women with BV are asymptomatic.

Answer 110

Clue cells

Answer 111

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.

Answer 112

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.

Answer 113

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)

Answer 114

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

Answer 115

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

Answer 116

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’).*

Answer 117

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.

Answer 118

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.

Answer 119

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).

Answer 120

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

Answer 121

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

Answer 122

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)*

Answer 123

steroids - prednisolone antivirals - acyclovir eye-care - reduced eye closing can lead to dry eye and corneal damage

Answer 124

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.**

Answer 125

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)**

Answer 126

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

Answer 127

In BPH, the enlargement feels **smooth and firm** while in prostate cancer, the gland may feel **hard and lumpy** - Enlarged in Both though

Answer 128

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

Answer 129

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.

Answer 130

α-1 antagonists: eg tamulosin - Postural hypotension, dizziness, dry mouth and depression 5-α reductase inhibitors eg Finasteride - reduced libido, erectile dysfunction, and gynaecomastia

Answer 131

**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)

Answer 132

Prostate adenocarcinoma - ***ARISE IN THE PERIPHERAL ZONE***

Answer 133

- **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

Answer 134

BRCA1 and BRCA2 have been linked to prostate cancer

Answer 135

They most often results from a **genetic mutation in a luminal cell,** but can also be a basal cell, and it results in that cell dividing uncontrollably forming a tumour. Early on, prostate cancer cells depend heavily on androgens for survival, but eventually, the **cancer cells mutate and find a way to keep multiplying without relying on androgens.**

Answer 136

Spreads to the bines of the vertebrae and pelvis resulting in hip and in back pain

Answer 137

**On DRE**Asymmetrical, hard and nodular prostate with the loss of the median sulcus Urinary retention Palpable lymphadenopathy: indicates metastatic disease

Answer 138

***Early prostate cancers may not cause symptoms as they usually start in posterior area*** - **Frequency** - **Hesitancy** - **Terminal dribbling** - **Nocturia** - **Haematuria or haematospermia** - **Dysuria** - **Constitutional symptoms: e.g. weight loss, fatigue** - **Bone pain**: e.g. lumbar back pain: suggests metastatic disease

Answer 139

Prostate-specific antigen (PSA) **Multiparametric MRI is now first-line** Previously, **transrectal ultrasound (TRUS)-guided needle biopsy** was the gold-standard diagnostic investigation

Answer 140

***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.

Answer 141

A Gleason score of: 6 is considered low risk 7 is intermediate risk (3 + 4 is lower risk than 4 + 3) 8 or above is deemed to be high risk

Answer 142

**External beam radiotherapy** directed at the prostate Brachytherapy ***placing radioactive seeds into the prostate to continuously deliver radiotherapy*** Hormone therapy - **anti-androgen eg Flutamide**

Answer 143

**Radical prostatectomy** Removal of the prostate, seminal vesicles, ampulla, and vas deferens, **+/- pelvic lymph node dissection;** often performed robotically **Option 4: Docetaxel chemotherapy with anti-androgen therapy** - Chemotherapy must not be used alone - Also used to treat metastatic cancer - Docetaxel is an anti-microtubule agent that block cell proliferation

Answer 144

- Metastatic cancer - Treated with docetaxel chemotherapy **and** **anti-androgen therapy** - **Bilateral orchidectomy (removal of testes to cause androgen deprivation)** should be offered as an alternative to LHRH agonists

Answer 145

**Cancer-related:** - **Urinary retention** - **Metastasis:** most commonly to bone **Procedure or treatment-related:** - **TRUS biopsy**: haematuria and rectal bleeding, pain, sepsis (1%) - **Surgery:** urinary incontinence, erectile dysfunction (common) - **Radiotherapy**: proctitis, cystitis, colorectal cancer, bladder cancer - **Hormone therapy**: gynaecomastia, hot flushes - **Surgery, radiotherapy or hormones**: erectile dysfunction

Answer 146

benign prostatic hyperplasia or BPH inflamed or infected prostate (prostatitis). Digital rectal examination. High levels of physical activity. Ejaculation. Also, PSA levels normally increase with age ***Obesity has been shown to actually lower PSA levels from the expected ranges in some cases***

Answer 147

A breast abscess is a collection of pus within an area of the breast, usually caused by a bacterial infection. This may be a: Lactational abscess (associated with breastfeeding, - usually peripheral in the breast) Non-lactational abscess (unrelated to breastfeeding - usually associated with duct ectasia and therefore central.)

Answer 148

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.

Answer 149

Lactational mastitis caused by blockage of the ducts is managed conservatively, with **continued breastfeeding, expressing milk and breast massage**. Heat packs, warm showers and simple analgesia can help symptoms. Antibiotics **(flucloxacillin or erythromycin/clarithromycin** where there is penicillin allergy) are required where infection is suspected or symptoms do not improve.

Answer 150

Management of non-lactational mastitis involves: Analgesia Antibiotics Treatment for the underlying cause (e.g., eczema or candidal infection) Antibiotics for non-lactational mastitis need to be broad-spectrum. The NICE clinical knowledge summaries (last updated January 2021) recommend either: **Co-amoxiclav Erythromycin/clarithromycin (macrolides) plus metronidazole** (to cover anaerobes)

Answer 151

If redness/inflammation hasn’t improved after one antbx course - refer to a breast specialist on suspicion of cancer!

Answer 152

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

Answer 153

Most common – RSV. prematurity, Downs syndrome or cystic fibrosis, Congenital heart disease or immunodeficiency.

Answer 154

Typically patients only require supportive management. This involves: Ensuring adequate intake. This could be orally, via NG tube or IV fluids depending on the severity. It is important to avoid overfeeding as a full stomach will restrict breathing. Start with small frequent feeds and gradually increase them as tolerated. Saline nasal drops and nasal suctioning can help clear nasal secretions, particularly prior to feeding Supplementary oxygen if the oxygen saturations remain below 92% Ventilatory support if required There is little evidence for treatments such as nebulised saline, bronchodilators, steroids and antibiotics.

Answer 155

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.

Answer 156

Occupation causing mechanical stress on bursa Rheumatoid arthritis Gout/pseudogout Penetrating injuries (route of entry for infective microorganisms ->infective bursitis) Repetitive stress or acute trauma Crystal deposition 2y to gout/pseudogout Autoimmune disease e.g. RA, ankylosing spondylitis, scleroderma, SLE Infection - acute/chronic OA of hip (possible cause of trochanteric bursitis)

Answer 157

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

Answer 158

Non-septic bursitis: Modified physical activity Rest, elevation Analgesia, NSAIDs Corticosteroid injections reserved for cases not responding to conservative management Bursal excision = last resort When infection is suspected or cannot be excluded, management involves: Aspiration of the fluid for microscopy and culture Antibiotics The NICE CKS recommend flucloxacillin first-line, with clarithromycin as an alternative.

Answer 159

By GFR and by the degree of **persistent Albuminuria** Goes G1-G5 and A1-A3

Answer 160

The **A score** is based on the **a**lbumin:creatinine ratio: - A1 = < 3mg/mmol - A2 = 3 – 30mg/mmol - A3 = > 30mg/mmol

Answer 161

- Albuminuria (ACR > 3 mg/mmol) - Electrolyte and other abnormalities due to renal dysfunction (e.g. hyperkalaemia) - Structural abnormalities on imaging - A history of kidney transplantation

Answer 162

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**

Answer 163

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**

Answer 164

Elderly Ileostomy/colostomy Short bowel syndrome Bowel obstruction Diuretics

Answer 165

Walls **thicken in order to withstand pressure** 🡪 less blood and O2 to kidney 🡪 ischaemic injury to glomerulus Diminishes ability for nephron to filter blood

Answer 166

Excess glucose in blood stick to proteins (particularly affects **efferent arteriole making it stiff and narrow** Creates **obstruction for blood to leave glomerulus 🡪 hyperfiltration** 🡪 supportive mesangial cells secrete more structural matrix increasing size of glomerulus Glomerulosclerosis 🡪 CKD

Answer 167

Hypertension (second most common) Diabetes (most common)

Answer 168

Systemic disease e.g., Rheumatoid arthritis Infections (HIV) SLE Medications, PPI, ACE inhibitor, NSAIDs, lithium Toxins (in smoking) Age-related decline Glomerulonephritis Polycystic kidney disease

Answer 169

Diabetes Hypertension Age Gender – M

Answer 170

Can be asymptomatic early on - **Nausea** - **Anorexia** - **Loss of appetite** - **Frothy urine** Malaise, oliguria, - *decreased urine output* haematuria, nocturia

Answer 171

- **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

Answer 172

FBC – shows anaemia, raised creatinine and urea, decreased Ca2+, raised phosphate, PTH, K+ and renin Estimated glomerular filtration rate (eGFR), checked with U and E blood test Urinalysis, on dipstick = Haematuria and proteinuria suggest GN Leukocytes and nitrites suggest infection Mid-stream urine sent for microscopy and sensitivity Albumin to creatinine ratio (ACR)

Answer 173

Renal ultrasound – excludes obstruction, gives assessment of kidney size (small kidneys favour CKD) and also looks for other abnormalities such as cysts and masses

Answer 174

Treat underlying cause Antibiotics for sepsis Correct volume depletion with fluids Immunosuppressive agents for vasculitis Treat hypertension Give statins Tight metabolic control in diabetes Stop nephrotoxic drugs

Answer 175

Diet – Na+ and K+ restriction, supply Vitamin D - **need to reduce CKD Mineral bone disease, by REDUCING SERUM PHOSPHATE AND PTH LEVELS** Smoking Alcohol Exercise

Answer 176

A – ACE-Inhibitor (e.g. Ramipril) or Angiotensin II receptor blocker e.g. valsartan B – Beta Blocker e.g. bisoprolol C – Calcium channel blocker e.g. amlodipine D – Diuretic e.g. oral Bendroflumethiazide **ACE-Inhibitors – reduce urinary protein** Half urinary protein = half chance of kidney failure and dialysis First line treatment in patients who are proteinuric and diabetic

Answer 177

**SGLT -2 inhibitors like dapagliflozin are particularly used in CKD** - USED IN PATIENTS WITH HEART FAILURE As it decreases renal intraglomerular pressure and inhibits the renin-angiotensin-aldosterone system.

Answer 178

Because ACE inhibitors dilate efferent arterioles to the kidney, And NSAIDs vasoconstrict the afferent arterioles going to the kidney Can be really bad for renal perfusion!

Answer 179

- **Swollen ankles/ oedema** - **Increased bleeding:** excess urea in the blood makes platelets less likely to stick to each other Bone disease – osteomalacia, osteoporosis - ***Less 1, 25-dihydroxyvitamin D from kidneys = less Serum calcium - more PTH and bone remodelling** Lethargy - due to anaemia

Answer 180

**Serum potassium needs to be monitored as chronic kidney disease and ACE inhibitors, both cause hyperkalaemia.** *NOTE: do not routinely offer a renin–angiotensin system antagonist in CKD if the pretreatment potassium is > 5 mmol/L.*

Answer 181

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!!!

Answer 182

Chronic Bronchitis Emphysema

Answer 183

Cigarette smoking - **MOST INPORTANT CAUSE** Air pollution - Exposure to air pollutants e.g. **sulfur and nitrogen dioxide** Occupational exposure to dusts, chemical agents, and fumes, silica A1AT deficiency - can lead to early onset COPD Family history of chronic bronchitis

Answer 184

FEV1 = volume of air that can be forcefully expired in 1 second FVC = total volume of air that can be forcibly exhaled after maximum inhalation The normal value for the FEV1/FVC ratio is 70% (and 65% in persons older than age 65).

Answer 185

**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

Answer 186

**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.

Answer 187

**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.

Answer 188

- **Wheeze:** due to narrowing of the passageway available for air to move in and out - **Crackles or rales:** caused by the popping open of small airways - **Cyanosis (blue bloaters):** if there is buildup of CO2 in blood - **Productive cough, lots of mucous** - **Dyspnoea** - Signs of CO2 retention - **Drowsy** - **Asterixis** - **Confusion**

Answer 189

A lung disease characterised by **dilatation and destruction of the lung tissue** causing enlarged air spaces **distal to the terminal bronchioles**

Answer 190

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.

Answer 191

Related to loss of Elastin: Collapse: the alveoli are prone to collapse. Dilation and bullae formation: alveoli dilate and may eventually join with neighbouring alveoli forming bullae

Answer 192

- **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 CO2 retention - **Drowsy** - **Asterixis** - **Confusion**

Answer 193

Clinical Dx with Spirometry Test for confirmation Spirometry shows Obstruction: FEV1/FVC ration <0.7 **Global Initiative for COPD (GOLD)** FEV1% - compared to predicted value Stage 1 - > 80% (mild) Stage 2 – 50-79% (moderate) Stage 3 – 30-49% (severe) Stage 4 - < 30% (very severe) Multiple peak flow measurements to exclude asthma

Answer 194

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

Answer 195

FEV1/FVC ratio less than 0.7 Important to note that it does not show a dramatic response to reversibility testing with salbutamol (beta-2 agonist). If it does then consider asthma as a differential Bronchodilator (salbutamol) will increase **FEV1 by >12%** in asthma, FEV1 would increase less than 12% or not at all in COPD

Answer 196

STOP SMOKING Annual flu vaccine and the pneumococcal vaccine (this is a one off vaccine)

Answer 197

SABA:short-acting beta-agonist (e.g. salbutamol) SAMA: short-acting muscarinic antagonist (ipratropium) LABA: long-acting beta-agonist (e.g. salmeterol) LAMA: long-acting muscarinic antagonist (e.g. tiotropium)

Answer 198

Initial medical treatment recommended by the NICE guidelines (updated 2019) involves: Short-acting beta-2 agonists (e.g., salbutamol) Short-acting muscarinic antagonists (e.g., ipratropium bromide)

Answer 199

long acting beta agonist (LABA) plus a long acting muscarinic antagonist (LAMA) - LABA: long-acting beta-agonist (e.g. salmeterol) LAMA: long-acting muscarinic antagonist (e.g. tiotropium)

Answer 200

combined long acting beta agonist (LABA) plus an inhaled corticosteroid (ICS) LABA (i.e. salmeterol) ICS (i.e. budesonide) . If these don’t work then they can step up to a combination of a LABA, LAMA and ICS.

Answer 201

- Nebulisers - eg Salbutamol - **Phosphodiesterase-4 inhibitors** eg Roflumilast - (blocks the breakdown of cyclic adenosine monophosphate) - **Long-term oxygen therapy (LTOT)** - Oral corticosteroids (e.g., prednisolone)

Answer 202

H.Influenzia S.Pneumoniae TREAT BOTH WITH AMOXICILLIN

Answer 203

CO2 will make blood more acidotic. This will show as a type 2 respiratory acidosis high CO2 and low oxygen with low pH If this chronic there will be some metabolic compensation by kidneys releasing more bicarbonate to try and neutralise pH

Answer 204

Prednisolone for 7-14 days Regular inhalers or home nebulisers Antibiotics if there is presence of infection

Answer 205

Nebulised bronchodilators (e.g. salbutamol 5mg/4h and ipratropium 500mcg/6h) Steroids (e.g. 200mg hydrocortisone or 30-40mg oral prednisolone) Antibiotics if evidence of infection Physiotherapy can help clear sputum

Answer 206

IV aminophylline Non-invasive ventilation Intubation and ventilation -Doxapram can be used as a respiratory stimulant if ventilation not appropriate

Answer 207

Too much oxygen in someone that is prone to retaining CO2 can depress their respiratory drive. Venturi masks are designed to deliver specific percentage concentrations of oxygen If retaining CO2 aim for oxygen saturations of 88-92% titrated by Venturi mask If not retaining CO2 and their bicarbonate is normal (meaning they do not normally retain CO2) then give oxygen to aim for oxygen saturations > 94%

Answer 208

Hyperexpanded, enlarged lungs, air pockets (bullae) or a flattened diaphragm, and saber sheath trachea Barrel shaped chest

Answer 209

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)

Answer 210

Low mood Loss of energy (anergia) Anhedonia (loss of enjoyment of formerly pleasurable activities)

Answer 211

Depressed mood, diurnal variation of mood (lowest in morning) Weight change, change in appetite Libido changes Sleep disturbance - early morning waking (classic Sx) Agitation Poor concentration Hopelessness Memory loss Unlike dementia however, the memory loss will have a more rapid, and global whereas dementia affects recent memory first - Suicidal ideation (assess risk) Psychotic Sx: Nihilistic and guilty delusions 3rd person auditory hallucinations - derogatory in nature

Answer 212

Carry out mental state examination - **Appearance may be normal**, or evidence of self beglect. substnace abuse, tearfulllness, anxious, fidegty **Speach may be monotonic and slow** - patient may appear distracted **Psychotic features** - eg auditory hallucinations, loss of insight Baseline tests for FBC and TFT may be useful for ruling out anaemia and hypothyroidism, that can lead to depression

Answer 213

The Patient Health Questionnaire-9 (scored out of 27) is used to grade depression – It asks patients to report over the last 2 weeks how often they have been experiencing symptoms – Made of 9 items which is scored from 0-3 – Mild = 5-9 – Moderate = 10-14 – Moderate/Severe = 15-19 – Severe = >19

Answer 214

Mild depression * Watchful waiting (GP monitoring progress post diagnosis) * Guided self-help: workbook/online course + therapy support * Exercise * Talking therapies - CBT, interpersonal therapy (IPT), psychodynamic psychotherapy ○ CBT: § Aim to help understand thoughts/behaviour + how they affect you § Recognises events in past but concentrates on how can change thinking/feeling/behaviour in present § Available on NHS for depression/mental health problems ○ IPT: § Focus on relationships with others and problems within them § E.g. issues with communication, coping with bereavement

Answer 215

Moderate/severe depression * Antidepressants (SSRIs, TCAs) - continued for 6+ mths after Sx stop * Combination therapy e.g. meds + talking therapy SSRI - Selective serotonin reuptake inhibitors eg Sertraline, paroxetine, fluoxetine, citalopram *Fluoxetine 1L in children* TCAs (Tricyclic antidepressants): Imipramine, amitriptyline SNRIs (Serotonin-noradrenaline reuptake inhibitors): Venlafaxine, duloxetine, Mirtazapine

Answer 216

* NSAIDs - add PPI if giving SSRI * Warfarin/heparin - avoid SSRI, consider mirtazapine * Aspirin - give PPI * **Triptans** - avoid SSRI **nb - fluoxetine and paroxetine have higher risk interaction

Answer 217

SSRIs - headaches, dry mouth, tiredness, sleeping problems, problems with sex, risk GI bleed if taking NSAIDs, weight gain, feeling more apathetic TCAs - SE: dry mouth, blurred vision, constipation, sweating, lightheadedness, urinary retention (anticholinergic effects), lethargy

Answer 218

Resistant depression Tx w/ combo of antidepressants + Lithium Atypical antipsychotic Another antidepressant ECT very effective in severe cases (Electroconvulsive Therapy)

Answer 219

* Psychological dependence - feelings of loss of control, cravings, pre-occupation with obtaining substance * Physiological dependence - physical consequences of withdrawing from substance

Answer 220

Addiction liability - depends on: How substance taken: orally, injection, inhaling Rate substance crosses blood brain barrier and triggers reward pathway in brain Time takes to feel effect of substance Substance ability to induce tolerance ± withdrawal symptoms Male Aged ~ 18-25 Mental health conditions: ADHD, bipolar, depression, GAD, panic disorder, PTSD Adverse childhood experiences: childhood abuse/neglect, witnessing domestic violence, family members with SUD

Answer 221

Opioid SAD: methadone, buprenorphine, naltrexone ((blocks opioid receptors in the body, stopping the effects)

Answer 222

Alcohol SAD: naltrexone acamprosate, (reduces GABA) disulfiram (deterring you from drinking by causing unpleasant physical reactions eg nausea, vommting dizziness)

Answer 223

Tobacco SAD: nicotine patch/spray/gum, bupropion, varenicline Varr En Ick Cline

Answer 224

Primary: - Hashimoto's disease - most common cause of primary. - Iodine deficiency - common in developing world and mountainous areas - Sub-acute granulomatous (De Quervain's - Other infections - **Drug induced** Central: Pituitary adenomas (most common) Other infections Radiation

Answer 225

Iodine deficiency, female, middle age, family history, treatment, - turners and down syndrome. - radiation therapy to head and neck, amiodarone and lithium use (both interfere with Thyroid hormone synthesis)

Answer 226

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.

Answer 227

**Bradycardia** Unexplained weight gain **Slow reflexes, Ataxia** Round Puffy face **Immobile Ileus** - temporary arrest of Intestinal peristalsis **ASCITES** - fluid in abdomen

Answer 228

**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

Answer 229

Thyroid function test Measure Free T4 and TSH levels ○ Primary - High TSH, low free T4 ○ Secondary – inappropriately low TSH, low T3/T4 (since issue is in pituitary) In Hashimoto’s Thyroid antibodies ○ Thyroid antibodies (TPO) - **Look for Thyroperoxidases and Thyroglobulin antibodies** ***(TPO antibody more common than antithyroglobulin)***

Answer 230

Look for serum chloresterol and Blood glucose Serum Cholesterol would be high, *as T3 moves it from the blood* Fasting blood glucose may also be elevated (Hypothyroidism can be assosiated with T1DM)

Answer 231

Thyroid hormone replacement agents such as **levothyroxine** Life long, oral, Start 25mcg (microgram) LEVOTHYROXINE IS SYNTHETIC T4 With primary, Primary – titrate dose *until TSH normalises* Aim is to get **TSH to >0.5** IN secondary, treat underlying pituitary issue!

Answer 232

Check TSH every 8 weeks after adjusting a dose - it takes that long for synthetic T4 to have an effect. Primary - Stable patients need TSH measured every 12 months Secondary – TSH will always be low, **monitor T4**

Answer 233

Graves' disease Other causes are: - multinodular goiter, toxic adenoma - inflammation of the thyroid, - --eating too much iodine, -too much synthetic thyroid hormone. A less common cause is a pituitary adenoma.[

Answer 234

Stimulation of the thyroid by **TSH receptor antibodies** Combination of genetic and environmental risk factors.

Answer 235

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)

Answer 236

Serum **IgG antibodies called TSH receptor stimulating antibodies (TRAb)** bind to TSH receptors on the thyroid and stimulate T3/4 production This results in excess secretion, hyperplasia of the thyroid follicular cells, hyperthyroidism and goitre TSH receptor autoantibodies cause thyroid hormone hyperproduction as well as thyroid hypertrophy and hyperplasia of thyroid follicular cells. ===> Leads to clinical manifestations of hyperthyroidism

Answer 237

- **Tremor** - Tachycardia/AF - Goitre - **Hair loss/thin hair** - **Lid lag/retraction** - Hyperkinesia - increased muscle activity - **Exophthalmos** – bulging of the eye out of the orbit

Answer 238

**** Weight loss * Irritability * Heat intolerance*** * Insomnia * Diarrhoea * Sweats * Palpitations Anxiety ***Pretibial myxedema*** specific to Grave's

Answer 239

TSH levels test - it would be low, as lots of T3 and T4 being produced that is leading to the symptoms - so negative feedback.

Answer 240

If serum TSH is normal or even (slightly) elevated in the presence of hyperthyroid symptoms and elevated free T4 level, consider other causes of hyperthyroidism such as a TSH-producing pituitary tumour and partial resistance to thyroid hormone

Answer 241

Toxic multinodular goitre (benign tumour on thyroid gland,) Gestational hyperthyroidism Iodine induced hyperthyroidism TSH producing pituitary adenoma

Answer 242

**Beta blockers** for rapid system control in attacks Decreases SNS activation ***Carbimazole*** – anti-thyroid drug decreases the synthesis new thyroid hormone **Potassium iodide** – to acutely block release of thyroid hormone from gland - Damage follicular cells (ionisation) **Thyroidectomy** – removal of the thyroid gland leaving a small remnant in order to maintain thyroid function

Answer 243

* Carbimazole – anti-thyroid drug ○ Blocks thyroid hormone synthesis and also have immunosuppressive effects which affect Graves’ disease

Answer 244

Severe side effect is agranulocytosis --- a deficiency of granulocytes in the blood, causing increased vulnerability to infection. Due to the fact is depresses the activity of the bone marrow ***YOU MUST TELL THE PATIENTS THIS, AND THAT THEY MUST STOP THIS IF THEY GET SIGNS OF INFECTIONS EG SORE THROAT***

Answer 245

monitor replacement thyroxine therapy with serum TSH at 6-week intervals until stable, then with serum TSH at least annually.

Answer 246

It should not be prescribed to pregnant women, as it can be toxic. Prescribe Propylthiouracil (a different Anti thyroid drug, also inhibits T4==> T3

Answer 247

Formation of **IgG** antibodies to the TSH receptors on the Thyroid Gland

Answer 248

Graves Disease, makes up for 50-80% of cases

Answer 249

Lithium (used to treat Bipolar) Amiodarone (used to treat arrhythmias - can cause either Hyper or Hypo) Interferons (used to treat cancer)

Answer 250

Stimulates the release of it as it stimulates TSH receptors, which can lead to Gestational hyperthyroidism - resolves in second trimester

Answer 251

Symptoms of Diabetes (3Ps) + Fasting plasma glucose > 7 mmol/l OR No symptoms - GTT (75g glucose) fasting > 7 or 2h value > 11 mmol/l (repeated on 2 occasions) HbA1c of > 48mmol/mol (6.5%)

Answer 252

Coxsackie B virus and Human enterovirus

Answer 253

- 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

Answer 254

Gluconeogenesis, Glycogenolysis and ketogenesis. Patients as a result present with ketoacidosis and hyperglycaemia.

Answer 255

- Hyperglycaemia (above 11.1). - Polyuria (passing urine frequently). - Polydipsia (drinking water frequently) - Weight loss - Tiredness

Answer 256

young age, weight loss, blurred vision, nausea, and vomiting, Abdo pain,

Answer 257

Random glucose tolerance test if at GP - blood sugar of >11.1mmol/L a glucose tolerance test. In this test, a fasting blood glucose is taken after which a 75g glucose load is taken. After 2 hours a second blood glucose reading is then taken If the patient is symptomatic: • fasting glucose greater than or equal to 7.0 mmol/l • random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test) If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.

Answer 258

Glycohemoglobin test (HbA1c) It measures Glycated haemoglobin, a form of haemoglobin that is measured to identify the three month average plasma glucose concentration Reflects the degree of hyperglycaemia over the **preceding 3 months greater than 6.5% (48 mmol/mol)** indicates diabetes

Answer 259

o **Basal-bolus insulin** (insulin glargine s/c) o Pre-meal insulin correction dose 2nd line: Metformin and fixed insulin dose

Answer 260

hypoglycaemia, weight gain, lipodystrophy Lipodystrophy - where you loose fat in some regions, but gain it in others, like on Organs like the Liver

Answer 261

- Microvascular: retinopathy, peripheral or autonomic neuropathy - Cardiovascular disease, diabetic kidney disease. - Potential for depression and eating disorder# - Foot amputations - Blindness

Answer 262

A progressive disorder defined by deficits in insulin secretion and insulin resistance that lead to abnormal metabolism and related metabolic derangements

Answer 263

Family History of it - genetics Obesity and poor exercise - Ageing and being overweight (body mass index [BMI] 25.0 to 29.9 kg/m²), and obesity (BMI >30 kg/m²) Age ***Low birth weight has been shown to predisposose***

Answer 264

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

Answer 265

Having the risk factors eg Older age Overweight/obese Being of a certain ethnic groups inc Black, south asiain, And coming in with: Fatigue Polydipsia and polyuria (thirsty and urinating a lot) ***Unintentional weight loss Opportunistic infections Slow healing***

Answer 266

Polyphagia - Eating lots, Polydipsia, Drink, Polyuria - wee lots, unexplained weight loss

Answer 267

Fasting plasma glucose - **Order after a minimum 8-hour fast.** Positive result is ≥7.0 mmol/L (≥126 mg/dL) 2 hour post load glucose test after 75g oral glucose - Plasma glucose is measured 2 hours after 75 g oral glucose load Positive result is ≥11.1 mmol/L (≥200 mg/dL) Random Plasma glucose - positive test is >11mmol/L ***Bear in mind that a repeat confirmatory test is required for diagnosis in most cases.***

Answer 268

Patient education about their condition and the lifestyle changes, advise that there is a possible cure. Exercise and weight loss, stop smoking Regarding food: - Include **high-fibre, low-glycaemic-index** sources of carbohydrate in their diet, such as fruit, vegetables, wholegrains, and pulses - Eat **low-fat dairy products and oily fish** - Limit their intake of foods containing saturated and trans fatty acids. **Needs annual reinforcement and review** Optimise treatment for other illnesses, eg hypertension

Answer 269

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%.

Answer 270

If HbA1c rises to 58mmol/mol, consider dual therapy or metformin and one of either a sulfonylurea, - **(Gliclazide)** DPP-4 inhibitor **(Sitagliptin)** or SGLT-2 inhibitor **(Dapagliflozin)**, or Glitazone. **(Pioglitazone)** The decision should be based on individual factors and drug tolerance. **Most commonly metformin and an SU**

Answer 271

It does not cause weight gain (and may cause some weight loss). It does not cause hypoglycaemia. Notable side effects of metformin: Gastrointestinal symptoms, including pain, nausea and diarrhoea (depending on the dose) Lactic acidosis (e.g., secondary to acute kidney injury) Patients with gastrointestinal side effects with standard-release metformin can try modified-release metformin.

Answer 272

* Diabetic retinopathy * Kidney disease Diabetic foot - due to neuropathy Cardiovascular disease - atherosclerosis, stroke TIA, CHD Glucose sticks in the vessels everywhere - eyes, brains, Kidney, 3rd line to add a sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.

Answer 273

***Eg - Gliclazide*** Sulphonurea - Eg Gliclazide - Stimulates insulin release - gives an extra kick to beta cells - lowers Hba1c - SE - Weight gain, increased risk of heart failure and fractures, and can cause hypoglycaemia - CI in pregnancy and breastfeeding

Answer 274

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***

Answer 275

Just once a day, (Basal) sometimes twice (BD)

Answer 276

The two main ways to take insulin are bolus and basal. Bolus insulin is the *quick-acting* delivery that you often take before mealtimes. Basal insulin is *longer-acting* and helps keep your glucose levels steady day and night

Answer 277

Insulin. Start with Basal Dose

Answer 278

he primary ketone body involved in diabetic ketoacidosis is **acetoacetate**

Answer 279

Gliclazide Sitagliptin Dapagliflozin Pioglitazone

Answer 280

eg Sitagliptin Inhibit DPP4 (so increase effect of **incretins (GLP-1 and GIP) which stimulates insulin secretion** Incretin = A group of hormones released after eating & augment secretion on insulin (inhibited by DPP4) DOES NOT CAUSE weight gain or weight loss Side effects: Headaches Low risk of acute pancreatitis

Answer 281

If HbA1c still 58mml/mol, consider triple therapy with: Metformin + SU + DPP4 inhibitor Metformin + SU + pioglitazone Metformin + SU/pioglitazone + SGLT-2i Insulin-based therapy

Answer 282

nsulin deficiency leads to release of free fatty acids from adipose tissue (lipolysis), hepatic fatty acid oxidation, and formation of ketone bodies), which result in ketonaemia and acidosis, as the bicarbonate buffer from the kidneys is used up

Answer 283

**Known to have diabetes, and are unwell** **Hyperkalaemia** Polydipsia polyuria, recent unexplained weight loss, or excessive tiredness, **Acetone smell on breath** Secondary: Nausea Abdominal pain[4][49] Hyperventilation Reduced consciousness.

Answer 284

**Venous blood gas** of: pH ≥7.0 indicates mild or moderate DKA. pH <7.0 indicates severe DKA Diabetes - blood glucose is >11.0 mmol/L blood ketones are >3.0 mmol/L - Ketonemia ketonuria (2+ or more on standard urine sticks)

Answer 285

IV fluids. 1. Give a fluid bolus of 500 mL of normal saline (0.9% sodium chloride) over 10 to 15 minutes if the initial systolic blood pressure (SBP) is <90 mmHg. If BP is >90mmHg, give 1L of normal saline over 60 minutes.

Answer 286

**Potassium and Insulin!!** 1. Add potassium to the **second litre of intravenous fluid** if serum potassium is ≤5.5 mmol/L ***(Insulin makes you hypokalaemic), as it move postassium into your cells *** 2. Start a fixed-rate intravenous insulin infusion (FRIII) according to local protocols; continue FRIII until DKA has resolved Ensure intravenous fluids have already been started before giving a FRIII.

Answer 287

he primary ketone body involved in diabetic ketoacidosis is **acetoacetate**

Answer 288

The HbA1c test Pre-diabetes is an indication that the patient is heading towards diabetes. They do not fit the full diagnostic criteria but should be educated about the risk of diabetes and lifestyle changes. An HbA1c of 42 – 47 mmol/mol indicates pre-diabetes.

Answer 289

Reflux of stomach contents into the oesophagus, due to pressure of the LOS getting lower = so the reflux persists for longer, becoming pathological

Answer 290

- **High BMI** - **Genetic association** - **Pregnancy** Male - **Smoking** - **NSAIDs, caffeine & alcohol** Hiatus hernia – LOS sphincter can’t close properly - **Other medication (may lower LOS pressure)**

Answer 291

Sliding Hiatus hernia - Acid reflux often happens as the lower oesophageal sphincter becomes less competent in many cases. In Rolling, the gastro-oesophageal junction remains intact, gross acid reflux is uncommon.

Answer 292

Symptoms Heart burn – burning chest pain Odynophagia – painful swallowing Hoarse throat Wheezing Regurgitation Acidic taste in mouth Signs Chest pain aggravated by bending, stooping and lying Nocturnal asthma – due to aspiration of gastric contents into lungs

Answer 293

Prescribe an 8 week trail of a PPI - and suspect GORD if symptoms improve - **first line** Also can do ambulatory pH monitoring - *insertion of pH capsule at gastro-oesophageal junction during endoscopy.* === demonstrate abnormal exposure to oesophageal acid in the absence of oesophagitis

Answer 294

• Anaemia • Loss of weight • Anorexia (loss of appetite) • Recent onset of progressive symptoms • Masses / Melena (black stools) → or bleeding from any part of GI tract • Swallowing difficulties (Dysphagia) • + > 55 y/o, new onset dyspepsia ALARMS - *(also nausea, raised platelet count)*

Answer 295

Endoscopy oesophagitis, Barrett’s oesophagus or an alternative diagnosis (i.e. oesophageal/gastric malignancy). Oesophageal adenocarcinoma

Answer 296

PPI- this will lower acid production within the stomach H2 receptor antagonist e.g., ranitidine reduces stomach acid Antacids e.g., Gaviscon *surgery - Nissen Fundoplication*

Answer 297

Outpouching of the colon wall, most frequently in the sigmoid colon.

Answer 298

Diverticulosis: the presence of diverticula (out-pouching) in an asymptomatic patient

Answer 299

Diverticular disease: where diverticula **cause symptoms,** such as intermittent lower abdominal pain, **without inflammation and infection**

Answer 300

Diverticulitis: where diverticula become **inflamed and infected,** typically causing severe lower abdominal pain, fever, general malaise, and occasionally rectal bleeding

Answer 301

- **Increasing age:** > 50 years; peak age is 50-70 years old - **Low dietary fibre** - **Obesity**: particularly in younger people - **Sedentary lifestyle** **Connective tissue disorders** like Maarfans - **Smoking:** increases the risk of complicated diverticular disease - **NSAIDs:** increases the risk of perforation in diverticulitis

Answer 302

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**

Answer 303

Can happen due to erosion of the diverticular wall from higher luminal pressures. Inflammation can happen when fecal matter, or fecaliths, become lodged in the diverticula (less common)

Answer 304

Bowel habits changed Bloating / flatulence Left lower quadrant pain N&V

Answer 305

**Symptoms of diverticular disease** = aka Bowel habits changed Bloating / flatulence Left lower quadrant pain N&V **AND** + FEVER + Blood in stool - Haematochezia

Answer 306

FBC - would see polymorphonuclear leukocytosis - *diverticulitis in older patients with abdominal pain and leukocytosis, because the presentation can be atypical in this group* C reactive protein/ESR - should be raised U and Es - to check kidney function Contrast CT scan **gold standard**, imaging modality of choice

Answer 307

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

Answer 308

Dietary and lifestyle modifications. Offer laxatives if constipation *increasing dietary fibre, including fruit and vegetables*

Answer 309

1ST LINE – dietary and lifestyle modifications CONSIDER – analgesia - Paracetamol, avoid NSAIDs CONSIDER – antispasmodic - dicy**clover**ine

Answer 310

1ST LINE – analgesia CONSIDER – antispasmodic - dicycloverine CONSIDER – oral antibiotic - eg **Amoxicillin/clavulanate** (co amoxcilcav)

Answer 311

Pain: Dysfunction in the brain-gut axis results in disorder of intestinal motility and/or **enhances visceral sensitivity** - *nerve endings in GI wall have abnormally strong response to stimuli like stretching during/after a meal* Abnormal motility: Eating FODMAPs (fermentable oligo-, di-, mono-saccharides and polyols) can bring water into GI tract, ===> excess water can **cause smooth muscle lining in GI tract to spasm,** can lead to **diarrhoea if the excess water is not reabsorbed** ***Recurrent abdominal pain with NO inflammation***

Answer 312

- 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*

Answer 313

**Abdominal pain / discomfort:** - Relieved on opening bowels, or - Associated with a change in bowel habit **AND 2 of:** - Abnormal stool passage - Bloating - Worse symptoms after eating - PR mucus

Answer 314

- Normal FBC, ESR and CRP blood tests - **Faecal calprotectin** negative, *excludes inflammatory bowel disease* - Negative coeliac disease serology (**IgA tissue transglutaminase antibodies**) - Cancer is not suspected or **excluded if suspected: colonoscopy**

Answer 315

- **Loperamide** for diarrhoea - **Laxatives** for constipation - **Linaclotide** is a specialist laxative, 2nd line - Antispasmodics for cramps e.g. **hyoscine butylbromide** (**Buscopan**) - Second line - Tricyclic antidepressants (i.e. amitriptyline 5-10mg at night), reduce pain, help mood, **CBT may also be offered**

Answer 316

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**

Answer 317

**Faecal calprotectin** (released by intestines when inflamed) **C-reactive protein** is a good indication of current inflammation FBC: leukocytosis during a flare; anaemia due to vitamin B12, folate or iron deficiency **Stool sample** to rule out infectious diseases - **U&Es**: to assess for electrolyte disturbance and signs of dehydration - **Coeliac serology**: to exclude coeliac disease

Answer 318

Colonoscopy will show mucosal inflammation (deep ulcers, skip lesions and **cobblestone appearance)** Histology will show **transmural inflammation with granulomas and increased number of goblet cells**

Answer 319

Oral corticosteroids e.g. budesonide and prednisolone, as well as an **elemental diet** - pre-digested nutrients

Answer 320

**IV hydrocortisone** in severe flare ups Add **anti-TNF antibodies e.g. Infliximab** if no improvement Consider adding **other immunosuppressive drugs** Surgery – doesn’t cure disease

Answer 321

**azathioprine or methotrexate** to remain in remission if there are frequent exacerbations. *Thiopurine methyltransferase level should be measured before using*

Answer 322

Antibodies found - **p-ANCAs - Perinuclear antineutrophilic cytoplasmic antibodies.** *just remember anti neutrophilic antibodies* antibodies that target antigens in the body’s own neutrophil Maybe party due to immune reaction to gut bacteria that have to **structural similarity to own neutrophils == cross react.**

Answer 323

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*

Answer 324

**Stool studies for infective pathogens** - rule out infection Faecal calprotectin: will be raised, helps differentiate between irritable bowel disease **pANCA antibodies** - often a feature of UC FBC - **may show leukocytosis, thrombocytosis, and anaemia** **LFTs** - check every 6 to 12 months for surveillance of primary sclerosing cholangitis. Lead pipe appearance on a barium enema - indicative of chronic UC

Answer 325

Colonoscopy - - Red and raw mucosa with widespread **shallow 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 abscesses** due to neutrophil migration through gland walls - **Goblet cell depletion**, with **infrequent** granulomas *picture taken from netters illustrated human pathology*

Answer 326

First line: Anti-inflammatories such **as Aminosalicylates (like mesalazine or sulfasalazine)** Second line corticosteroid (prednisolone) **(THINK SALAZINES)** Anti-TNF drugs - infliximab

Answer 327

Hospital admission + A **high-dose intravenous corticosteroid**, eg hydrocortisone

Answer 328

Pseudopolyps **Crypt abscess** Goblet cell depletion, Infrequent granulomas Increased plasma cells in lamina propria

Answer 329

Take BP reading, and Repeat BP in the other arm * Repeat again at the end of the consultation *If it remains high, then arrange home BP monitoring; either: **Ambulatory BP monitoring (ABPM)** – the patient is fitted with a BP recording device, which takes their BP every hour (or more) throughout a 24 hour period. -> *tell them to keep doing their daily activities* *Home blood pressure monitoring (HBPM)* – Ask the patient to keep a diary of their BP: * **Twice daily * For 7 days** * Take two consecutive readings and record the lowest * Discard the first day and take an average of the rest of the readings at a follow-up appointment

Answer 330

When you see high BP in someone under 40 ROPED Renal disease Obesity Pregnancy/Pre eclampsia Endocrine Drugs

Answer 331

- Urinalysis to check for Kidney damage (Proteins/blood in wee, Albumin to creatine ratio) - ECG/Echo for LV hypertrophy - Fundoscopy for retina damage - Bloods - Serum creatine, eGFR, Glucose (Hba1c) - Take clinical history Lipid Profile and QRISK

Answer 332

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!**

Answer 333

calcium channel blocker e.g. amlodipine **Anyone with diagnosed hypertension, even if its under control, need an annual review!**

Answer 334

ACE-inhibitor + CCB Or if afro Caribbean - CCB and ARB **Anyone with diagnosed hypertension, even if its under control, need an annual review!**

Answer 335

○ Third line = ACE-inhibitor + CCB + **Thiazide like diuretic** e.g. Bendroflumethiazide or indapamide

Answer 336

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.

Answer 337

ACEi, eg Ramipril **Anyone with diagnosed hypertension, even if its under control, need an annual review!**

Answer 338

Calcium-channel blockers such as amlodipine commonly cause peripheral oedema **Anyone with diagnosed hypertension, even if its under control, need an annual review!**

Answer 339

eg Candesartan It's given instead of an ACE-inhibitor, if a ACE-i is contraindicated. You give ACE-i to anyone who is younger than 55, or not Black afro Caribbean, or someone with Diabetes at any age .

Answer 340

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**

Answer 341

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

Answer 342

‘Punched out’ ischaemic ulcers – usually on the toes and heels, rarely higher up the limb. These tend to occur after a localised traumatic event. . Gangrene – often black necrotic gangrenous tissue surrounds the punched out ulcer lesions. Infection of this areas can occur (wet gangrene). Reduced / absent peripheral pulses – start distally, and work your way up until you find the pulse Skin atrophy – in chronic disease Hair loss – in chronic disease Cyanosis Excessive sweating – due to overactivity of the sympathetic nerves Erectile Dysfunction – Amputation may be necesscary!

Answer 343

Ankle Brachial pressure index - Compares Blood pressure in Arms and legs, as reduced blood flow to legs is more common than arms in PVD. **Used alongside a suggestive examination and history to diagnose PVD**

Answer 344

No medications proven to help with claudication **Walking therapies** and exercise encouragement! Statin (Atorvastatin) Ace Inhibitor - Ramipril Beta blockers - should be avoided, unless PAD is severe Antiplatelet agent - Aspirin, clopidogrel

Answer 345

initially - dual antiplatelet = Aspirin and clopidogrel Then, long term Aspirin, 75mg Beta Blocker, Ramipril 5mg , and statin (secondary prevention) Atorvastatin 80mg

Answer 346

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)**

Answer 347

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

Answer 348

Occur in the gaiter area (between the top of the foot and bottom of the calf muscle), and medial malleolus Are **larger and more superficial**than 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

Answer 349

Left sided heart failure Cardiomyopathy is a chronic disease of the heart muscle which **causes the heart to become weak and enlarged., as it attempts to increase preload and stroke volume via Frank-starling law** This can lead to heart failure, where the heart is unable to effectively pump enough blood to meet the body's needs.

Answer 350

The hypertrophy that is created by hypertension is concentric, which means that the new sarcomeres are generated in parallel with existing ones. This means that heart muscle **encroaches on the ventricular chamber space, resulting in less room for blood** in there -> *Can't fill up as much* ==> Therefore contributes to systolic but can also cause diastolic heart failure

Answer 351

***Now more commonly known as heart failure with reduced ejection fraction (or HFrEF)*** Ejection fraction <40% (SV/EDV) Caused by IHD MI Hypertension Cardiomyopathy

Answer 352

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

Answer 353

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

Answer 354

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)

Answer 355

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

Answer 356

ECG Chest X ray BNP B-type Natriuretic Peptide levels Echocardiogram

Answer 357

Should be performed on all suspected heart failure patients **May indicate the underlying cause of the heart failure such as**; Myocardial infarction/ischemia Bundle Branch Block Ventricular hypertrophy Pericardial disease Arrhythmias Signs of previous MI - pathological Q waves ***A normal ECG makes heart failure unlikely (sensitivity 89%)*** *taken from almostadoctor*

Answer 358

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

Answer 359

B-type Natriuretic Peptide (BNP) are peptides that cause natriuresis, diuresis and vasodilation. HF - released in response to increased pressure on heart - BNP signals to the body that it needs to **reduce the amount of fluid in the body, and help reduce the strain on the heart.** == **They are the body’s “natural defence” against hypervolaemia** A marker of heart failure Released when the myocardial walls are under stress Levels directly correlated to ventricular wall stress and severity of heart failure **RELEASED FROM THE VENTRICLES**

Answer 360

***ECHOCARDIOGRAM*** Can confirm the diagnosis Can calculate the **ejection fraction, ventricular wall thickness** etc *An ejection fraction (EF) of <40% strongly indicated heart failure EF of 41-49% is not diagnostic, but suggestive of heart failure* Can confirm any underlying structural abnormalities – such as valve disease Helps to **stratify the type of HF present and therefore guides management**

Answer 361

A diuretic, like furosemide **The following flashcards will be asking about heart failure medication for when there is a** ***reduced*** **ejection fraction**

Answer 362

- 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)*

Answer 363

A mineralocorticoid receptor antagonist - eg Spironolactone

Answer 364

K+ sparing diuretic, like Spironolactone - Aldosterone receptor antagonist ABAL Also a drug like ***Digoxin*** - good for arrhythmias and AF, and helps symptoms of **LVSD** *(Left Ventricular Systolic Dysfunction.)* ---> *Helps strengthen heart muscle contractions*

Answer 365

shortness of breath (and must say specifically at least one of; paroxysmal nocturnal dyspnoea, orthopnoea), Ankle swelling, Fatigue

Answer 366

A diuretic, like furosemide

Answer 367

distended superficial veins measuring more than 3mm in diameter, usually affecting the legs When the valves in the veins become incompetent, the blood is drawn downwards by gravity and pools in the veins and feet.

Answer 368

Tap test – apply pressure to the saphenofemoral junction (SFJ) and tap the distal varicose vein, feeling for a thrill at the SFJ. Cough test is same as above but with a cough Trendelenburg’s test

Answer 369

– 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**

Answer 370

Simple treatment measures include: Weight loss if appropriate Staying physically active Keeping the leg elevated when possible to help drainage Compression stockings (exclude arterial disease first with an ankle-brachial pressure index) Surgical options: Endothermal ablation – inserting a catheter into the vein to apply radiofrequency ablation Sclerotherapy – injecting the vein with an irritant foam that causes closure of the vein Stripping – the veins are ligated and pulled out of the leg