Med 1 LO's Flashcards

1
Q

list relevant conditions that can cause angina (chest pain)

A
  • Carcinoma in the bronchus
  • Pneumothorax- pleuritic chest pain
  • Pericardial disease
  • Respiratory tract infection (pneumonia, influenza, TB)
  • PE
  • Ischaemic heart disease
  • Pleurisy (sharp pain when breathing- inflamed pleural membranes)
  • Aortic dissection
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2
Q

what is VTE

what are the risk factors?

A

VTE- venous thromboembolism. Term for blood clots that form in the (typically deep) veins

Risk factors-

  • Vein wall damage
    • Fractures
    • Severe muscle injury
    • Major surgery
  • Slow blood flow
    • Confinement to a bed (hospitalisation)
    • Limited movement (e.g., cast)
    • Sitting for a long time
    • Paralysis
    • Dehydration
    • Varicose veins
  • Increased oestrogen
    • Birth control
    • Hormone replacement therapy, sometimes after menopause
    • Pregnancy
  • Certain chronic medical illnesses
    • Heart disease
    • Lung disease
    • Cancer and its treatment
    • Inflammatory bowel disease
  • Other factors include
    • Previous DVT or PE
    • Family history of DVT or PE
    • Age increasing
    • Obesity
    • Catheterisation of central vein
    • Inherited clotting disorders
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3
Q

symptoms of VTE

A

Many people have none at all.

Following are the most common in their affecting areas:

  • Swelling (may be unilateral)
  • Tenderness
  • Pain
  • Redness
  • Dilated veins
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4
Q

What is a pulmonary embolism

rfxs

A

Is when a blood clot in the pulmonary arterial vasculature develop, usually from an underlying DVT of the lower limbs.

Always suspect in someone <2 weeks post op

Rfxs:

  • Malignancy- myeloproliferative disorder like polycythaemia vera
  • Surgery - especially pelvic and lower limb
  • Immobility
  • Pregnancy, COC
  • Previous thromboembolism or thrombophilia disorder
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5
Q

Symptoms of PE

A
  • Sudden onset SOB, pleuritic chest pain and haemoptysis (may have these as a triad or individually)
  • Massive PE may present with syncope or shock
  • You can have these without any DVT symptoms
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6
Q

Signs of PE

A
  • Tachypnoea
  • Tachycardia
  • Hypoxia
  • Irregular heartbeat (gallop rhythm)
  • Signs of right sided heart strain (raised JVP, right ventricular heave and loud P2 sound)
  • Pleural rub
  • Cyanosis
  • AF
  • Severe hypotension
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7
Q

ECG findings in PE

A
  • Normal or sinus tachycardia
  • Evidence of right heart strain- right axis deviation, RBBB, non-specific T wave changes
  • Classic S1Q3T3 (deep S waves in lead I, pathological Q waves in lead III, and inverted T waves in lead III) is relatively uncommon (<20% of patients).
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8
Q

pathophysiology of PE

A

Caused by

  • damage to blood vessels
  • blood flow turbulence
  • hypercoagulability

Most common in the lower limb area below the knee in low-flow sites such as the soleal sinuses and behind venous valve pockets. Valves are a site for venous stasis and hypoxia. Hypoxia decreases antithrombotic proteins and increases the expression of procoagulants.

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9
Q

Blood tests in PE

A

ABG: will be normal or show a type 1 respiratory failure (hypoxia w/o hypercapnia) and/or respiratory alkalosis (hyperventilation secondary to hypoxia).

FBC: rule out anaemia, raised CRP, clotting (important in case patient is started on LMWH/ warfarin)

D-dimer- highly non-specific but a negative result means that 95% of the time you can rule out PE

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10
Q

imaging investigations in PE

A

CTPA- diagnostic test of choice for a PE and will show a defect in the pulmonary vasculature.

CXR- usually normal apart from a few specific signs

V/Q scan if the patient has renal impairment

Lower limb duplex: if DVT is thought to be the cause

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11
Q

Wells scoring system

criteria and meaning

A

3 points:

  • Clinical signs and symptoms of a DVT
  • If no alternative diagnosis is more likely than a PE

1.5 points:

  • Tachycardia (HR>100bpm)
  • Patient has been immobile for >3 days or has had major surgery in last month
  • Previous DVT or PE

1 point:

  • Presents with haemoptysis
  • Active malignancy

IF wells score is <4 then D-dimer should be measured. Low D-dimer excludes PE, high prompts diagnostic imaging by CTPA or V/1 scan

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12
Q

Management of PE

A
  • ABCDE approach
  • Thrombolysis- IV alteplase bolus for massive PE if in A and E
  • Antiplatelets like warfarin/ DOACs in general practice- rivaroxaban, dabigatran
  • LWMH for 5 days
  • Morphine 5mg/10mg IV if in pain or distress
  • Oxygen if hypoxaemic 10-15L/min
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13
Q

what is an aortic aneurysm

what is a psuudoaneurysm

A

aneurysm dilatation of diameter > 3.0cm or +50% of its original diameter. Involve all layers of the vessel wall.

only involves a collection of blood only in the adventitia (outer layer).

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14
Q

causes of an aortic aneurysm

common sites for an aneurysm

which group is invited for screening

A

causes

  • Atheroma
  • Trauma
  • Infection (mycotic aneurysm in endocarditis)
  • Connective tissue disorders (e.g., marfans)
  • Inflammatory

common sites of aneurysm

  • Aorta (infrarenal most common)
  • Iliac
  • Femoral
  • Popliteal arteries

invited for screening: all males aged 65 are invigted for screening

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15
Q

Signs and symptoms of AAA (unpopped)

A
  • ¾ asymptomatic (often incidental finding via X-ray, CT or MRI)
  • Pain in the abdomen, chest, lower back or groin. Can be severe or sudden.
  • Pulsing sensation in the abdomen
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16
Q

signs of ruptured AAA

A
  • Intermittent or continuous abdominal pain (radiates to back, iliac fossae or groin)
  • Expansile abdominal mass
  • Clammy, sweaty skin
  • Dizziness
  • Fainting
  • Tachycardia
  • Nausea and vomiting
  • SOB
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17
Q

rfx for developing AAA and Rfx for ruptured AAA

A

developing AAA

  • Tobacco use
  • Age increasing (typically 65 or over)
  • Being male
  • Being white
  • Family history
  • Other aneurysms
  • Atherosclerotic risk factors
  • Food and alcohol consumption

rfx for rupture

  • Baseline aortic diameter
  • Rapid expansion
  • Tobacco use
  • Hypertension
  • Etc.
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18
Q

pathophysiology of AAA

A
  • Thick wall with low elastin content, high wall tension and few vasa vasorum
  • Atherosclerosis
  • Damage to media (ischaemic)
  • Tunica media revascularisation causes influx of inflammatory cells
  • Inflammatory cells secrete proteases and degrade elastin and collagen
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19
Q

complications of AAA

A
  • rupture
  • thrombosis
  • embolism
  • fistulae
  • pressure on other structures
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20
Q

pathophysiology of atheroma

A

atheroma- physiological term for a build-up of materials that adhere to arteries

  • Hypercholesterolaemia
  • LDLs accumulate in the arterial intima where they may be modified by oxidation and aggregation.
  • Modified LDLs act as chronic stimulators of the innate and adaptive immune response.
  • Endothelial cells and smooth muscle cells to express adhesion molecules, chemoattractants, growth factors (e.g., macrophage colony stimulating factor) and interact with receptors on monocytes.
  • Monocytes are stimulate to home, migrate and differentiate into macrophages and dendritic cells.
  • Macrophages and dendritic cells are stimulated into differentiating into foamy cells.
  • Foam cells act as deposits for lipids.
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21
Q

How does atheroma ruptuere lead to an MI?

A

In ST elevated MI, the thrombus is typically occlusive and sustained.

In plaque rupture, a gap in the fibrous cap exposes the highly thrombogenic core to the blood. Therefore the plaque forms a new thrombus, causing further stenosis

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22
Q

heart failure definition

systolic vs diastolic

A

AKA CHF and congestive heart failure

when the heart is unable to pump sufficiently to maintain blood flow to meet the body’s needs. can be classified into that caused by: pump failure, arrhythmias, excess after-load or excess pre-load

pump failure can be further divided into systolic or diastolic dysfunction

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23
Q

causes of systolic and diastolic heart failure

A

causes of systolic heart failure

  • ischaemic heart disease
  • dilated cardiomyopathy
  • myocarditis
  • infiltration (e.g., haemochromatosis or sarcoidosis)

causes of diastolic heart failure

  • Hypertrophic obstructive cardiomyopathy
  • Restrictive cardiomyopathy
  • Cardiac tamponade
  • Constrictive pericarditis
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24
Q

clinical features of left heart failure

symptoms

signs

A

causes pulmonary congestion and systemic hypoperfusion

symptoms:

  • SOB on exertion
  • orthopnea
  • paroxysmal noctural dyspnoea
  • nocturnal cough (pink, frothy, sputum)

signs:

  • tachypnoea
  • bibasal fine crackles on ausculatation of the lungs
  • cyanosis
  • prolonged CRT
  • hypotension
  • s3 gallop rhythm due to stiffened ventricle
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25
clinical features of right sided heart failure signs and symptoms
RSHF causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced r heart output) ***_symptoms_*** * ankle swelling * weight gain * abdominal distension and discomfort ***_Signs_*** raised JVP pitting oedema/ sacral oedema tender smooth hepatomegaly ascites transudative pleural effusion
26
investigations in heart failure
* _**ECG**-_ underlying cause * **_NT-proBNP_**- released in response to myocardial stretch. has a high negative predictive value, so if BNP is low then theres a low chance that cardiac failure has occured. If raised over 400 refer for trans-thoracic echocardiogram. if \>2,000 then 2 week referral for specialist and echo. * **_echocardiogram_**- helps measure the ejection fraction. \<40%= heart failure with reduced ejection fraction. \>40% but raised BNP =HF with REF * **_blood tests_**- U+E for renal function, LFTs for hepatic congestion, TFTs for hyperthyroidism, glucose and lipids for assessing CV rfs * ***_CXR_***- ABCDEF (go into more detail in future)
27
* lifestyle modification ofr heart failure * smoking cessation * salt and lfuid restriction * supervised cardiac rehabilitation
28
pharmacological management of HF
1. ACEi and Bblocker (ARB if intolerant to ACEi) 2. Loop diuretics (furosemide or bumetanide) for symptoms ***_if symptoms persist consider:_*** * aldosterone antagonists like spironolactone or eplerenone * hydralazine or nitrate in afro-caribbeans * ivabradine if sinus rhythm but impaired EF * ARB * Digoxin- in those with AF, worsens mortality but improves morbidity
29
Surgical/ device management options for HF
***_surgical/ device management options for HF_*** cardiac resynchromisation therpy ICDs are indicated if the following criteria are fulfilled QRS interval \<120ms, high risk sudden cardiac death, NYHA class I-III QRS interval 120-149ms without LBBB, NYHA class I-III QRS interval 120-149ms with LBBB, NYHA class I
30
intial management of acute ehart failure
1. Sit the patient up 2. Oxygen therapy (aiming saturations \>94% in normal circumstances) 3. IV furosemide 40mg or more (with further doses as necessary) and close fluid balance (aiming for a negative balance) 4. SC morphine - this is contentious with some studies suggesting that it might increase mortality by suppressing respiration
31
advanced management of acute heart failure
1. ***_CPAP_*** - reduces hypoxia and may help push fluid out of alveoli 2. ***_Intubation and ventilation_*** 3. ***_Furosemide infusion_*** - continuous IV furosemide given over 24 hours to maximise diuresis 4. ***_Dopamine infusion_*** - Continuous IV dopamine given over 24 hours. It works by inhibiting sympathetic drive and thereby increasing myocardial contractility. 5. ***_Intra-aortic balloon pump_*** - if the patient is in cardiogenic shock 6. ***_Ultrafiltration_*** - If resistant to or contraindicated diuretics
32
adverse effects of HF medications ## Footnote beta blockers ACE inhibitors spironolactone furosemide hydralazine/ nitrate digoxin
***_beta blockers-_*** bradycardia, hypotension, fatigue, dizziness ***_ACE inhibitors-_*** hyperkalaemia, renal impairment, dry cough, light headedness, fatigue, GI disturbances, angioedema ***_spironolactone-_*** hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/ hair growth in women, hyponatraemia ***_furosemide-_*** hypotensio, hyponatraemia/kalaemia ***_hydralazine/ nitrate-_*** headaceh, palpitation, flushing ***_digoxin-_*** dizziness, blurred vision, GI disturbances
33
Atrial fibrillation +causes
* most commonly sustained rhythm * no p waves * absence of isoelectric baseline * cariable ventricular rate * QRS complexes \> 120ms * fibrillatory waves may mimic P waves causes of a fib * [Ischaemic heart disease](https://litfl.com/myocardial-ischaemia-ecg-library/) * Hypertension * Valvular heart disease (esp. mitral stenosis / regurgitation) * Acute infections * Electrolyte disturbance ([hypokalaemia](https://litfl.com/hypokalaemia-ecg-library/), [hypomagnesaemia](https://litfl.com/hypomagnesaemia-ecg-library/)) * [Thyrotoxicosis](https://litfl.com/hyperthyroidism-ecg-library/) * Drugs (e.g. sympathomimetics) * Alcohol * [Pulmonary embolus](https://litfl.com/ecg-changes-in-pulmonary-embolism/) * [Pericardial disease](https://litfl.com/pericarditis-ecg-library/) * Acid-base disturbance * [Pre-excitation syndromes](https://litfl.com/pre-excitation-syndromes-ecg-library/) * Cardiomyopathies: [dilated](https://litfl.com/dilated-cardiomyopathy-dcm-ecg-library/), [hypertrophic](https://litfl.com/hypertrophic-cardiomyopathy-hcm-ecg-library/). * Phaeochromocytoma
34
***_Wheeze_*** * what is it * common causes
* wheeze is a relatively high-pitched shound produced by movement of air through a narrowed or compressed **SMALL LOWER** airway (stridor = higher) * **expiratory** noise ***_Causes:_*** * Asthma * COPD * Heart failure * Anaphylaxis * Taxic inhalation * Acute bronchitis * Bronchiolitis * Foreign body aspiration
35
what is pneumonia
Lower respiratory tract infection in which the alveoli and terminal bronchioles are infected
36
likley bacterial pathogens for pneumonia
***_Typicals_***- called so because of their rapid onset of symptoms, inc. high fever and productive cough; * **Strep pneumoniae-** 80% of acases (gram +ve coci) * **Staph aureus** * Haemophilius influenzae (gram -ve rod) ***_Atypicals-_*** more gradual onset of symptoms, may be non-specific initially (fever, myalgia, dry cough) * **Mycoplasma pneumoniae** * Chlamydia pneumoniae * Legionella pneumophila * Coxiella burnetti
37
viral causes of pneumonia
viral much less common influenza A
38
symptoms of pneumonia Signs of pneumonia
***_Symptoms_*** * Cough * Sputum * Dyspnoea * Chest pain; may be pleuritic on inspiration * Fever * Rigors * Confusion (elderly) ***_Signs_*** * systemic inflammatory response (fever, tachycardia, CRP) * reduced oxygen saturations * reduced chest expansion * dull percussion * ausculatation (reduced breathing sounds, bronchial breathing, inreased vocal resonance)
39
treatment for pneumonia
antibiotics if bacterial ***_non-severe: (CURB-65= 2)_*** * 1st line- amoxicillin * alternative e.g., COPD use doxycycline ***_Severe; (CURB-65\> 3)_*** co-amoxiclav+ consider clarithromycin in addition
40
What method is used for risk stratification when assessing pneumonia
***_CURB-65_*** * Confusion * Urea\> 7mmol/L * Respiratpry rate \> 30/min * Blood pressure (systolic \<90mmHg or diastolic \<60 mmHg) * Age \>65 years score 1 point for each feature present * 0-1 low mortality 1.5% treat at home * 2 mortality intermediate 9.2% short stay inpatient * 3+ 22% mortality risk manage in hospital * 4/5 ICU
41
* What is COPD * what is it usually caused by
COPD is an umbrella term encompassing the older terms: * Chronic bronchitis * Emphysema Vast majority of cases is caused by smoking
42
Multisystem effects of COPD
***_Mutlisystem effects of COPD_*** * **_Cardiovascular_**; heart failure, ischaemic heart disease, pulmonary hypertension, arrhythmias * **_Brain;_** depression, anxiety * **_Bone abnormalities:_** osteopenia and osteoporosis present in 89% of COPD cases * **_Skeletal muscle_** atrophy * **_Sleep:_** obstructive sleep apnoea
43
Features of COPD
* dyspnoea * cough; often productive * wheeze * in severe cases: weight loss, fatigue, right sided heart failure possible to have an infective exacerbation
44
typical history of COPD patient
Smoking history- are they still smoking Occupational and industrial exposures History of exacerbations Presence of comorbidities Impact on patient’s life Typically \>20 pack years
45
how to calculate packyears of smoking
(how many packs smoked per day) x (how many years smoked)
46
signs of COPD
* Raised Resp rate * **Hyperextended/ barrel ches**t * Prolonged expiratory time \>5s with pursed lip breathing * Use of accessory muscles on respiration * Quiet breath sounds (especially in apices) +/- wheezing * Quiet heart sounds (due to overlapping hyperinflated lung) * Basal crepitations * Signs of cor pulmonale (Raised JVP, ankle odema, warm peripheries, bounding pulse) * CO2 retention flap
47
Investigations for COPD
***_post-bronchodilator spirometry_*** to demonstrate airflow obstruction--\> FEV/FCV ratio \<70% is diagnostic ***_CXR:_*** hyperinflated, bullae, flat hemidiaphragm
48
how do we grade severity (bar CURB-65)
looking at post-bronchodilator FEV1
49
What is the MRC scale
scale to measure severity of pneumonia * **Grade 0**= not troubled by breathlessness except on strenuous exercise * **Grade 1**= short of breath when hurrying or walking up a slight incline * **Grade 2**= Walks slower than contemporaries on ground level * **Grade 3**= Stops for breath every 100m * **Grade 4**= Too breathless to leave the house
50
pathological changes seen
* **Airflow limitation and gas trapping-** chronic inflame and fibrosis of airways leads to air trapping in the small airways * **Destruction of alveoli-** permanent enlargement of airspaces * **Mucous gland hyperplasia** * **Thickened pulmonary arteriolar wall** and **remodelling** occur with hypoxia, leading to increased pulmonary vascular resistance, pulmonary hypertension and impaired gas exchange * **Increased pul resistance--\>**more force needed for RV contraction--\> dilation and hypertrophy --\> loss of RV function --\> backing up of blood into RA and subsequently systemic venous circulation
51
Non-pharmalogical management of stable COPD
* Smoking cessation * Education * Pulmonary rehabilitation * Diet * Self-management therapy * Psychosocial support
52
pharmacological management of COPD
Stepwise approach (one is carried onto the next, higher step) 1. Short acting beta2 antagonist (salbutamol) or short acting muscarinic antagonist (ipratropium) 2. LABA (salmeterol) and LAMA (glycopyrronium)/ inasthmatics ICS 3. LABA+LAMA+ICS
53
What is bronchiectasis main organisms involved
Bronchiectasis is permanent dilation of the bronchi and bronchioles due to chronic infection. ***_The main organisms include_***: Haemophilius Influenzae, Pseudomonas aeruginosa, Streptococcus Pneumoniae, Staphylococcus aureus
54
causes of bronchiectasis
Post-Infection: Tuberculosis; HIV; Measles; Pertussis; Pneumonia * Bronchial Pathology: Obstruction by foreign body or tumour * Allergic Bronchopulmonary aspergillosis (ABPA) * Congenital: Cystic fibrosis; Kartagener's syndrome; Primary ciliary dyskinesia; Young syndrome * Hypogammaglobulinaemia * Idiopathic
55
presenting symptoms of bronchiectasis
Begin insidiously and gradually get worse with periods of exacerbation * (Most common) **Chronic cough** that produces **thick, tenacious**, often **purulent sputum** * **Dyspnoea** * **Wheezing** * Hypoxia * **Haemoptysis** (can be massive) * Fever and constitutional symptoms * Exacerbations are common and often triggered by new infection
56
signs of bronchiectasis
Abnormal breath sounds (crackles, rhonchi, wheezing) Digital clubbing Pulmonary hypertension Nasal polyps
57
risk factors for bronchiectasis
* Previous childhood respiratory infections due to viruses * Previous infections by TB or severe bacteria pneumonia * Immunodeficiency * CF * Alpha-1-antitrypsin deficiency- also causes COPD and emphysema * Aspiration or inhalation injury * CT disorders- rheumatoid arthritis * IBD
58
management of bronchiectasis
***_conservative_*** * Patient Education * Support Group * Chest Physiotherapy – Postural drainage at least twice daily to aid mucous drainage * Smoking Cessation ***_Medical_*** * Antibiotics – recurrent exacerbations may require long term antibiotic treatment * Bronchodilators – Including salbutamol can be given to patients with symptoms of dyspneoa and wheeze such as COPD, ABPA, asthma * Corticosteroid - Prednisolone is used in ABPA treatment * Carbocysteine - Mucolytic which reduces the viscosity of sputum ***_surgical_*** * Surgical excision of localized area of disease or cessation of haemoptysis. * Lung transplant may be indicated in certain patients
59
* aortic dissection * what is it * most common site
* Blood splits the arotic media with **sudden tearing chest pain** (with or without **radiation to back**) . Surging of blood through a tear I the intima. Forms a false lumen (channel) through which blood can flow. * Hypertension is an important contributor. * Most common site is the **proximal ascending aorta**- within 5cm of the aortic valve
60
what are the 2 classification systems for aortic dissections
***_deBakey_***- * **type 1-** 50%- ascending aorta through to aortic arch and below * **type 2**- start in and are confined to ascending aorta * **type 3**- dissections start in the descending aorta ***_Stanford_*** **Type A:** Involves the ascending aorta, arch of the aorta **Type B:** Involves the descending aorta.
61
Rfxs for AAA
* Hypertension * Connective tissue disease e.g. Marfan's syndrome * Valvular heart disease * Cocaine/amphetamine use
62
Symptoms of AAA
Usually presents in men over the age of 50 * **Sudden onset 'tearing' chest pain** or **interscapular pain radiating to the back.** * It can also present with (depending on how far the dissection extends): * Bowel/limb ischaemia * Renal failure * Syncope
63
Signs of AAA
* Unequal arm pulses * Acute limb iscahemia * Paraplegia if spinal arteries affected * Anuria if renal arteries affected
64
diagnosis
* Transoesophageal echocardiography * CT angiography * MRA (Magnetic Resonance Angiography) * ECG and CXR * Bloods- troponin, D-dimer
65
intial management definitive management
* reuscitation * Cardiac monitoring * Strict blood pressure control (e.g. IV metoprolol infusion) ***_definitive treatment_*** * Type A: Usually requires surgical management (e.g. aortic graft) * Type B: Normally managed conservatively with blood pressure control. If there is evidence of end organ damage then endovascular/open repair may be performed.
66
what are cardiomyopathies? broad classifications
**heterogenous group** of diseases of the **myocardium,** characterised by mechanical and/ or electrical dysfunction that typically results in **inappropriate ventricular hypertrophy or dilatation** due to multiple causes (usually genetic). ***_classifications_*** * Primary cardiomyopathies- predominantly confined to the heart * Secondary cardiomyopathies- typically part of generalised multisystem diseases
67
divided also into 3 other groups:
1. dilated 2. hypertrophic 3. restrictive
68
dilated cardiomyopathy ## Footnote causes
Myocardial dysfunction causing heart failure in which dilation causes **systolic dysfunctio**n predominate. Most common form ***_causes_*** * **Ischaemic** changes can over time particularly post-myocardial infarction * **Hypertensive** * **Genetic and congenital** * **Toxin-related** - excessive alcohol consumption Cocaine is also associated with ischaemia and DCM.Clozapine * **Infiltrative** - haemochromatosis, amyloidosis and sarcoidosis are known to cause DCM * **Peripartum** - * **Thyrotoxicosis** * I**nfectious** - DCM can occur secondary to myocarditis, or as a direct result of infection from HIV, Lyme disease and Chagas disease * **Stress induced cardiomyopathy** (Takotsubo cardiomyopathy) refers to transient left ventricular ballooning precipitated by intense psychologic stress. Almost all patients recover completely * **Idiopathic** - when other potential causes have been ruled out ***_presentation_*** * Mostly gradual onset * Fatigue * Acute pulmonary oedema * Progressive symptoms of heart failure: * Nocturnal dyspnoea * Orthopnea * Paroxysmal nocturnal dyspnoea * Swelling ***_management_***
69
dailated cardiomyopathy signs and symptoms
***_symptoms_*** * Exertional dyspnoea * Orthopnoea * Proxysmal nocturnal dyspnoea * Peripheral oedema ***_Signs_*** * displaced apex beat * S3 gallop rhythm (rapid ventricular filling) * Murmur of mitral regurgitation (due to displacement of the valve leaflets) * Signs of heart failure (such as oedema, hepatomegaly, ascites, raised JVP).
70
treatment for dilated cardiomyopathy
(Standard treatment for heart failure with reduced ejection fraction) * Diuretics * ACE inhibitors * Angiotensin II receptor inhibitors * B-blockers * Spironolactone * Digoxin * Nitrates * Aldosterone antagonists * Antiarrhythmic agents * Device therapy * Cardiac resynchronisation +anticoagulants when AF present
71
hypertrophic cardiomyopathy patho
Hypertrophic cardiomyopathy (HCM) is a **genetic condition** characterised by left ventricular hypertrophy of varying degrees. a mutation in one of several myocyte sarcomere genes such as myosin and troponin. ratio of vessels to tissue is low so widespread low grade ischaemia, leads to fibrosis
72
hypertrophic cardiomyopathy presentation
* Found alongside acromegaly, pheochromocytoma, neurofibromatosis * Symptoms appear between 20 and 40 and are exertional but symptoms may be highly variable * Dyspnoea * Chest pain (resembling typical angina) * Palpitations * Syncope * (ejection fraction is preserved so fatigue isn’t often felt- abnormal diastolic function responsible for symptoms) * Mitral regurgitation sound heard at the apex * Bifid carotid pulse
73
management of hypertrophic cardiomyoapthy
Symptoms B-blockers- mainstay for angina, dyspnoea, giddiness and syncope treatment Calcium channel antagonists- verapamil and diltiazem Arrythmias B blockers Amiodarone (both for SVTs) Radiofrequency ablation
74
restrictive cardiomyopathy causes
* Characterised by non-compliant ventricular walls that resist diastolic filling * One (most commonly the left) ventricle is usually involved * Least prevalent form of cardiomyopathy * Genetic abnormality * Fabry disease * Gaucher disease * Haemachromatosis * CT disorders * Amyloidosis * Other * Carcinoid tumours * Radiation * Sarcoidosis
75
presentation of restrictive cardiomyopathy
* Exertional dyspnoea * Orthopnea * Peripheral oedema * AF and ventricular arrhythmia * Fatigue * LV +/- RV failure * Functional AV valve regurgitation
76
what is takatsubo cardiomyopathy symptoms diagnosis treatment
"stress induced cardiomyopathy" * Weakening of the left ventricle because of severe emotional or physical stress such as sudden illness or the loss of a loved one. * Left ventricle changes shape, having a narrow neck and a round bottom. * Typically affects more women than men, **Symptoms:** mimics MI- sudden intense angina and SOB **Diagnosis;** ECG, echocardiogram, MRI, angiogram **Treatment**; diuretics, B blockers and ACEi, anti-coagulation
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infective endocarditis rfx and comorbid disease
Infection of endovascular structures causes infective endocarditis- think valves ***_rfx:_*** * Age \> 60 years * Male sex * Intravenous drug use - predisposition to Staph. aureus infection and right-sided valve disease e.g. tricuspid endocarditis * Poor dentition and dental infections ***_co-morbid conditions:_*** * Valvular disease * Congenital heart diseases * Prosthetic valves * Intravascular devices * Haemodialysis * HIV infection
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common infective organisms of infective endocarditis symptoms of endocarditis
* ***Staph. aureus*** * ***Strep. viridans\*\*\*\* (most common)*** * Enterococci * Coagulase negative *staphylococci* e.g. *Staph. epidermidis* * *Strep. bovis* - often in patients with colonic lesions, e.g. IBD or carcinoma * Fungi * HACEK organisms - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella ***_Symptoms_*** * **Fever** (most common) * Anorexia * **Weight loss** * Headache * Myalgia * **Night sweats** * Cough * Pain made worse by leaning forwardss??
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signs of infective endocarditis complications
***_signs of infective endocarditis_*** * Murmurs are common * Janeway lesions- nontender macules on plasms and soles * Osler nodes- tender subcutaneous nodules on finger pads and toes * Roth spots- exudative haemorrhagic retinal lesions with pale centres * Microscopic haematuria and glomerulonephritis * Splinter haemorrhages * PR prolongation or complete av block ***_complications_*** * May often be the presenting complaint * Valvular insuffiency causing heart failure * Neurological complications * Embolic complications causing infarction of kidneys, spleen or lung * Infection e.g., osteomyelitis
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Investigations for infective endocarditis which criteria is used to help diagnose infective endocarditis
* ECG * CXR * Blood tests: FBC, UE, LFT, CRP * 3 sets of cultures * Transthoracic echocardiogram * Transoesophageal echocardiogram **_duke's criteria_** * Blood positive for IE * Imaging positive for IE * + 1 minor point (predisposing condition, fever, vascular phenomena, immunological phenomena, microbiological evidence)
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which score is used to calculate your chance of having a DVT and therefore of having a PE?
Well's score
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what is central cyanosis common causes in neonates and adults
* Caused by diseases of the heart, lungs, or abnormal haemoglobin * Seen in the tongue, lips and is due to desaturation of central arterial blood resulting from cardiac and respiratory disorders associated w shunting of deoxy venous blood into systemic circulation * Often peripherally cyanosed also ***_common causes: neonates_*** * Transposition of great arteries * Fallots tetralogy * Stenosis of pulmonary valve * Tricuspid valve * Truncus arteriosus ***_In adults_*** * Birth injury * Haemorrhage * Pulmonary oedema * Pleural effusion * Pulmonary oedema * PE * Severe pneumonia * COPD
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peripheral cyanosis causes
* Caused by decreased local circulation and increased extraction of oxygen in peripheral tissues * Isolated peripheral cyanosis occurs in conditions with peripheral vasoconstriction and stasis of blood in the extremities- e.g., congestive heart failure, circulatory shock, exposure to cold temperatures and abnormalities of the peripheral circulation * Bluish tinge to affected area all the same causes as central + * Peripheral arterial disease- e.g., thrombosis, atheroma or embolism * Vasoconstriction * Cold exposure * Raynauds * Beta blocker drugs * Venous obstruction
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what info is included in an ABG?
* **Blood pH** (normal range **7.35 - 7.45**) - high indicates alkalosis; low indicates acidosis. * **Blood carbon dioxide** level (PaCO2 level; normal range **4.7 - 6.5** KPa) - this may indicate a breathing problem. * **Bicarbonate** level (represents levels of alkali; normal range 22-26 mEq/L). * **Blood oxygen** levels (PO2 level; normal range **10.5 - 13.5** KPa) - if the PO2 level is low, it indicates an abnormally low concentration of blood oxygen (hypoxaemia).
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When would you see metabolic acidosis and metabolic alkalosis respiratory acidosis and alkalosis
***_metabolic acidosis_*** * Build-up of lactic acid; seen in shock, infection, hypoxia * Acute or chronic kidney injury * Build up of ketones; diabetes mellitus, alcohol poisoning * Severe diarrhoea ***_metabolic alkalosis_*** * Vomiting * Hypokalaemia * Excessive amounts of alkali-containing medication * Burns ***_respiratory acidosis_*** * depression of central resp centre by stroke * inability to ventilate properly- myasthenia gravis, muscular dystrophy * acute asthma exacerbation of COPD ***_resp alkalosis_*** * hyperventailtion- anxiety, stroke, meningitis, altitude, pregnancy
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Cough reflex
**_afferent pathway-_** * cough receptors activated, receptor potential to afferent nerves, info reaches vagus nerve and is passed to medulla oblangata **_central pathway-_** * sensory info to nucleus tractus solitarius of the medulla * vagus nerve passes info to effector muscles **_motor efferent pathway-_** * diapragm, laryngeal muscles, rectus abdominus
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causes of cough
* smoking * heartburn (acid reflux) * allergies – for example, hay fever * infections like bronchitis * mucus dripping down the throat from the back of the nose * cancer * ACEi
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What are interstitial lung diseases? symptoms signs
This is a generic term used to describe a number of conditions that primarily affect the lung parenchyma in a diffuse manner. Characterised by chronic inflammation and/ or progressive interstitial fibrosis. ***_symptoms_*** * paroxysmal (sudden attack of) dry hacking cough * SOB at rest or aggravated by exertion * reduced exercise tolerance ***_Signs_*** * Alveolar septal thickening * Fibroblast hyperproliferation * Collagen deposition * Pulmonary fibrosis * Abnormal breath sounds
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***_common causes of interstitial ling diseases_***
* **CT disorders**: ankylosing spondylitis, SLE * **Drug**s: carbamazapine, nitrofurantoin, dexamethasone * **Occupational**/ **environmental**: aluminium, asbestos, bird fanciers lung, charcoal * **Infections**: pneumonia, TB * **Vasculitis**: eosinophilic granulomatosis * **Sarcoidosi**s * pulmonary lymphoma
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effect of ILD on lung function
restrictive ventilatory effect due to decreased distensibility of lung parenchyma * FEV1 normal or decreased * Decreased FVC * Normal or decreased FEV1/FVC reduced total lung capacity reduced diffusing capacity
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what is pulmonary hypertension
***_Pulmonary hypertension_***- type of high blood pressure that affects the arteries in the lungs and the right side of the heart
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groups of pulmonary hypertension (5)
1. pulmonary arterial hypertension- mutations, CHD, HIV 2. due to left sided heart disease- valvular disease 3. hypoxia+/- COPD- pul fibrosis, obstructive sleep apnoea 4. chronic thromboembolic pulmonary hypertension - PE, clotting disorder 5. unclear or multifactorail aetiologies- sarcoidosis, kidney disease
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management of pulmonary hypertension
* Calcium channel blockers- amlodipine * Anticoagulants- apixaban, dabigatran, rivaroxaban, warfarin * Diuretics * Oxygen treatment
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Give examples of anti-coagulants and their drug class
***_Antiplatelets_*** **Cox inhibitors**- aspirin, NSAIDs (nurofen) **P2Y12 inhibitors**- clopidogrel, ticagrelor ***_Anticoagulants_*** **Direct thrombin inhibitors**- dabigatran **Indirect thrombin inhibitors**- dalteparin, fondaparinux **Direct factor X inhibitors**- apixaban, rivaroxaban **Thrombolytics**- plasminogen activators, alteplase, streptokinase
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What is a penumothorax rfxs
A pneumothorax is defined as air within the pleural space. ***_Rfxs_*** * Previous PTX * COPD * Alpha-1 antitrypsin deficiency * Underlying lung disease * Smoker * Valvular heart disease * Tall and thin * Marfan’s syndrome
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causes of pneumothroax
***_spontaneous_*** 1. **_primary-_** (no underlying lung pathology - typically tall thin young men) 2. **_secondary_**- (underlying lung pathology) CT disorders (Marfan's syndrome), obstructive lung disease (such as asthma and COPD), infective lung disease (such as TB and pneumonia), fibrotic lung disease (such as cystic fibrosis and idiopathic pulmonary fibrosis), and neoplastic disease (such as bronchial carcinoma ***_Traumatic_*** causes 1. ***_iatrogenic causes (_***such as insertion of a central line or positive pressure ventilation) 2. **Non-iatrogenic causes** (either a penetrating trauma or blunt trauma with rib fracture).
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Symptoms of pneumothorax Signs of pneumothorax
* sudden-onset SOB * Pleuritic chest pain * Important to note in the history whether there are any risk factors for a spontaneous primary pneumothorax (tall and thin young male, smoker), spontaneous secondary pneumothorax (COPD, asthma, Marfan's syndrome), or traumatic pneumothorax (recent chest trauma, recent invasive medical procedure). ***_signs:_*** * tachypnoeac * respiratory distress * reduced chest expansion * hyper resonant percussion note * reduced or absent breath sounds * Additional signs in a tension pneumothorax include: signs of haemodynamic compromise (tachycardia and hypotension) and tracheal deviation to the contralateral side.
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investigations for pneumothorax what is a pleural aspiration
* History and exam * Bloods * U+E, LFT, FC, CRP * ESR, autoantibodies * Amylase * CXR- should not be ordered in tension pneumothorax as it will delay immediate treatment , otherwise look for area devoid of lung markings at the periphery of lungs * Pleural ultrasound * Consider CT chest * Pleural aspiration ***_pleural aspiration_*** * Ultrasound guided * Pass needle into pleural fluid * Aspirate sample * Investigations * Colour, viscosity, smell * Biochemistry: protein, LDH, glucose * Fluid pH * Microbiology * Cytology
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***_management of pneumothorax_***
* Observation- if rim of air \>2cm on CXR then… * Aspiration if not successful then… * Chest drain * Pleural vent ***_Chronic management_*** * reoccurance at 3 years is 50% * main treatment is surgical where blebs are stapled
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what is a tension pneumothorax signs treatment
***_what is a tension pneumothorax_*** * Air drawn into the pleural space w every inspiration and has no route of escape. Mediastinum gets pushed over to the contralateral hemithorax, kinking and compressing the great veins. Unless air is removed, cardiorespiratory distress will occur. ***_signs_*** * resp distress, tachycardia, hypotension, distended neck veins, deviated trachea ***_treatment_*** * To remove air, large bore caneedle with syringe, partially filled with 0.9% saline intp 2nd intercostal space in the midclavivular line on the side of the suspected pneumothorax * Remove plunger to allow air to bubble through the syringe until a chets tube can be placed
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pulmoanry effusion what is the pleural space
**pleural space**- potential space between the visceral and parietal pleura which naturally contains 10-20ml of fluid. the aim is the lubrication of the pleura to maintain apposition of the membranes ***_pleural effusion_*** increased accumulation of pleural fluid in the pleural space
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factors causing increased fluid accumulation ***_increased entry:_*** * Increased permeability – inflammation, infection, malignancy. * Increased microvascular pressure – CCF, mitral stenosis. * Decrease pleural pressure – atelectasis/collapse of lung. * Decrease oncotic pressure – Hypolbuminaemia (Nephrotic syndrome, liver cirrhosis) ***_Decreased exit (affecting the lymphatics):_*** * Hypothyroidism * Yellow nail syndrome * Radiation injury
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classifications of pleural effusions (2) is done via which critera? review this and google
done via ***_Light's criteria_*** **_transudative effusions_**- caused by increase in hydrostatic pressure and decreased plasma oncotic. Can be treated without extensive investigations. 1. Plural fluid protein/serum protein \>0.5 2. Pleural fluid LDH/serum LDH \> 0.6 3. Pleural fluid LDH \> 2/3 upper limit of lab normal value for serum LDH ***_exudative effusion_***s- caused by local changes to capillary wall permeability. * High fluid protein- fluid: serum \>0.5 * High LDH- fluid: serum LDH \>0.6 * Haemothorax- blood in pleural space
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causes of transudates and exudates
tr***_ansudate causes_*** * Fluid leaks in to pleural space from elsewhere * Too much fluid in the body * Heart failure or pericarditis * Renal failure * Liver cirrhosis * Fluid leaking from elsewhere * Hypoalbuminaemia * Ascites/ peritoneal dialysis * Other stuff * Infections e.g., pneumonia * TB * PE * Swelling of the pancreas ***_exudate causes_*** * Too much fluid produced/ failure of reabsorption due to damage to pleural surface * Pleural malignancy * Pneumonia * Empyema- infection in pleural space * Connective tissue disease * Benign asbestos pleuritis * Pancreatitis * Drug induced
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rfx signs and symptoms of pleural effusion
***_rfx pleural effusion_*** * Chest injury * Radiation therapy * Surgery (especially to the: heart, lungs, belly, organ transplants) ***_symptoms_*** * Dyspnoea * Tachypnoea * Pleuritic chest pain * Stomach pain * Cough * Haemoptysis * Weight loss * Fever or chills ***_signs_*** * Absent tactile fremitus * Dullness on percussion * Reduced chest wall movements * Decreased breath sounds on the affected side * Rapid and shallow breaths in big effusions * Pericardial rub
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* tests * initial management * chronic management of pleural effusion
***_tests_*** * CXR * LFTs, U&Es, FBC, CRP, LDH * Thoracentesis (procedure to remove fluid or air from around the lungs) looking at: LDH and protein, cytology, pH, ADA, AFB and TB culture, amylase, haematocrit and glucose ***_management_*** * Pleural aspiration (thoracentesis)- Treat underlying cause e.g., pneumonia or heart failure * Consider contrast enhanced CT thorax * Pleural biopsy (radiologically guided VATS) * NSAID’s for pain ***_chronic management_*** * Pleurodesis- artificially obliterating pleural space * Intermittent drainage with indwelling catheter
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* What is cystic fibrosis? * Which systems are affected by it? * When are babies screened for it?
***_Cystic fibrosis-_*** inherited disease of the exocrine glands affecting primarily the GI and respiratory systems. Leads to chronic lung disease, exocrine pancreatic insufficiency, hepatobiliary disease and abnormally high sweat electroytes. All babies screened at birth
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Explain the genetics of Cystic fibrosis
* autosomal recessive inheritance * responsible gene found on the long arm of chromosome 7 * this genes ecnodes for thr DF transmembrane conductance regulator (CFTR) * **CFTR** is a c**AMP-regulated chloride channel**, **regulating chloride and sodium transport across epithelial membranes** multisystem disease as the CFTR gene is found within multiple organ systems
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pathopshyiology of CF
Nearly all exocrine glands are affected in varying distribution and severity. Increased sodium absorption and abnormal chloride secretion. This leads to thicker mucous that impairs the function of cilia. Glands may be: * Obstructed by viscid or solid eosinophilic material in the lumen (pancreas, gall bladder etc.) * Produce excessive secretions (tracheobronchial and Brunner glands) * Secrete excessive sodium and chloride (sweat, parotid and salivary glands)
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Effect of cystic fibrosis on lungs and GI system
***_Lungs-_*** comes on as child * Mucous plugging * Chronic lower resp bacterial infection * Damage to airways- eventual bronchiectasis * Nasal Polyps * Symptoms including cough, wheeze, haemoptysis * Pneumothorax * Cor pulmonale ***_GI-_*** * Pancreatic insufficiency resulting in diabetes mellitus and steatorrhea * Cirrhosis * Portal hypertension * Gallstones Male infertility * Duodenal- viscous and lacks bicarbonate
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neonatal features of cystic fibrosis
* Failure to thrive * Meconium Ileus * Rectal prolapse
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Diagnosis of cystic fibrosis conservative management of CF
* Neonatal heel prick day between day 5 and day 9 * Sweat test: sweat sodium and chloride \>60mmol/L * Faecal elastase: this can provide evidence for abnormal pancreatic exocrine function. * Genetic screening: This can identify CF mutations ***_Conservative management_*** * Education about the condition * Fertility and genetic counselling * Dietician * Psychosocial counselling * Chest physiotherapy: postural drainage and active cycle breathing techniques * Screening for complications of Cystic Fibrosis such as osteoporosis
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Medical treatment of CF surgical treatment of CF
***_infective exacerbations_***: antibiotics, nebulised mucolytics, bronchodilators ***_pancreatic insufficiency_***: insulin replacement regime, exocrine enzymatic replacement, vitmains A,D,E,K ***_Liver_***: ursodeoxycholic acid ***_Worsening progressive lung disease:_*** oxygen, non-invasive ventilation, diuretics if signs of cor pulmonale ***_Surgical treatment of CF_*** cirrhosis eventual liver tranplant, lung transplant
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Causes of hyperventilation
* Anxiety * Haemorrhage * Drug overdose (aspirin for example) * Severe pain * Pregnancy * Lung infection * Lung diseases- COPD, asthma * Diabetic ketoacidosis
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What is the most common form of lung cancer?
non-small cell carcinoma
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symptoms of lung cancer
* Cough * Haemoptysis * Chest pain * Weight loss * SOB * Hoarse voice and other features of direct intrathoracic invasion * Hoarseness (left recurrent laryngeal) * SVC obstruction from tumour or thrombosis * Dysphagia from oesophageal compression * Elevated diaphragm * Pericardial involvement * Recurrent or slowly resolving pneumonia
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SOE of lung cancer:
* Fixed monophasic wheeze * Cachexia * Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy * Finger clubbing * Pleural effusion * Tracheal deviation (lobar collapse/ whole lung collapse) * Osetoarthropy * Confusion * Fits falls
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Lung cancer is largely grouped into 2:
small cell lung cancer (SCLC)- about 15% non-small cell lung cancer (NSCLC)- 85%
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Info on small cell lung cancer
* **highly aggressive** * almost always occurs in smokers * **starts from** **endocrine cells** (Klutchisky cells) so often secrete polypeptide hormones resulting in **paraneoplastic syndromes** * rapidly growing and disseminating * 80% have evidence of metastasis at diagnosis * **not amenable to surgery** * often very chemosensitive/ radiotherapy
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what are the 4 groups within non-small cell lung cancer? which features do they share?
* squamous 30% * adenocarcinoma 27% * large cell 10% * adenocarcinoma in situ (rare) 1% ***_Shared features:_*** * early stage is curable by surgery * radiotherapy and cehmotherapy can help symptoms * immunotherapy pr biological egnts possible
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in paraneoplastic syndrome of small cell lung cancer which hormones are often screted
based on the secretion of; * antidiuretic hormone (**ADH**) resulting in hyponatremia * secretion of adrenocorticotropic hormone (**ACTH**) or rarely corticotropin-releasing hormone (**CRH**) resulting in Cushing syndrome * secretion of growth hormone-releasing hormone
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risk factors for lung cancer
* Smoking (tobacco and cannabis) * Passive smoking * Occupation exposure (asbestos, silica, welding fumes, coal) * HIV * Organ transplantation * Radiation exposure (X-ray, gamma rays). * Beta-carotene supplements in smokers.
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common metastatic destinations of lung cancer
brain, breast, adrenals and bone.
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important features of squamous cell carcinoma
squamous cell carcinoma tends to cause early symptoms **usually begins in the bronchial tubes** * 2nd most common type of lung cancer in the UK * presents as obstructive lesions of the bronchus leading to an infection * most likely lung cancer to cavitate * hypercalcaemia- bone degradation or PTH
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***_imprtant features of adenocarcinoma_***
***_imprtant features of adenocarcinoma_*** most common type in the UK Usually starts in the outer border of the lungs * arises from the mucous cells in the bronchial epithelium * commonly invades mediastinal lymph nodes and the pleura, and soreads to the brain and bones * does not cavitate * most likely to cause pleural effusion
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important features of large cell carcinoma
***_important features of large cell carcinoma_*** * tends to grow rapdily and cause late symptoms * usually begins in the outer edges of the lungs
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how would you investigate for lung cancer?
* CXR * Urgent referral to clinic * CT or combined PET-CT- also used to guide biopsy * Pleural tap-cytopathology examination of pleural fluid or sputum * Usually bronchoscopy-guided biopsy and core biopsy * Sometimes open lung biopsy * PET scan if curative treatment feasible
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complications of lung cancer
* Pancoast syndrome * Recurrent laryngeal nerve palsy * Phrenic nerve palsy * Rib erosion * Pericarditis * AF
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what is pancoast syndrome?
Occurs when apical tumours, usually NSCLC invade the branchial plexus, pleura or ribs causing shoulder and upper-extremity pain and weakness or atrophy of the ipsilateral hand. May also include Horner’s syndrome.
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what is Horner's syndrome
Horner's syndrome is characterised by ptosis, meiosis with or without anhydrosis. It is due to an interruption of the sympathetic nerve supply to the eye * *Ptosis**- drooping of the upper eyelid (due to oculomotor palsy levator palpebri superioris * *Miosis**- pupil constriction **Anhidrosis**
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when light levels drop what happens to the pupil? what is the name for this? which muscles contract? and if light shines into the eye?
pupil dilates mydriosis radial muscles contract pupil constricts miosis sphincter muscle innervated by parasympathtic fibres constricts
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what is mesothelioma what causes it
Only known pleural cancer Caused by asbestos exposure- asbestos was heavily used historically in the shipbuilding and construction industries due to its fire resistant qualities.
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* signs and symptoms of mesothelioma * diagnosis * treatment
***_Signs and symptoms_*** * Dyspnoea * Non-pleuritic chest pain * Constitutional symptoms are uncommon * Pain * Hoarseness * Dysphagia * Horner syndrome * Brachial plexopathy * Ascites ***_Diagnosis_*** * CXR * Pleural fluid cytology// pleural biopsy * Staging via- CT chest, mediastinoscopy, MRI ***_Treatment_*** * Supportive care * Pleurectomy * Analgesia with opioid’s * Chemotherapy
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Systemic inflammatory response syndrome (SIRS) definition sepsis diagnosis severe sepsis septic shock
***_SIRS_*** ≥ 2 of: * \> 38°C or \< 36°C * Heart rate \> 90 * Respiratory rate \> 20 * WBC \> 12,000/mm³ or \< 4,000/mm³ ***_Sepsis-_*** SIRS+ suspected or confirmed infection ***_Severe sepsis_***- Sepsis plus evidence of organ dysfunction: confusion, hypoxia, oliguria, metabolic acidosis ***_Septic shock_***- severe sepsis with hypotension, despite adequate fluid resuscitation, or lactic acidosis (lactate \> 4mmol/L)
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"sick person" bloods ## Footnote lactate bicarb CRP LFTs coag platelets
lactate \>2 bicarb \<18 CRP raised LFTs off coag deranged (PT\>20) platelets low
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red flags for sepsis * responds to * mental state * systolic bp * HR * RR * Sp02 * rash * urine * lactate * recent chemotherapy
* responds to voice/ pain/ unresponsive * mental state- acute confusional state * systolic bp- 90mmHg or drop of \>40% of normal * HR- \>130 * RR- \>25/min * Sp02- oxygen needed to maintain above 92% * rash- non-blanching, cyanotic, mottled * urine- not passed urine in the last 18 hrs * lactate- \>2 mmol.L * recent chemotherapy
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what is the sepsis 6?
***_3 in_*** * administer **oxygen**, aim to keep sats \>94% * administer **broad spectrum antibiotics** * give **IV fluid** ***_3 out_*** * take **blood cultures** * measure **serum lactate** (via ABG) * measure accurate **hourly urine output**
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additional tests for diagnosing sepsis
Imaging e.g chest xray, echocardiogram, abdominal ultrasound Viral PCR for e.g. influenza Urinalysis +/- culture Lumbar puncture
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symptoms and signs of sepsis
***_symptoms_*** * Fever, sweats or chills * Breathlessness * Headache * Nausea and vomiting * Diarrhoea ***_signs_*** * Tachycardia * Hypotension * Pyrexia * Peripherally vasodilated * Hypoxia * Tachypnoea
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Which score is used to calculate someones sequential risk of sepsis related organ failure
qSOFA and SOFA * O2 * platelets * bilirubin * cardiovascular * GCS * creatinine * urine output Score of more than 3 in any parameter then think sepsis
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normal values for ABG * pH * paCO2 * HCO3- * PaO2
* **pH** 7.35-7.45 * **paCO2** 35-45 * **HCO3-** 21-28 * **PaO2** 80-110
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Pathology of inflammation in sepsis
* Antigen pro-inflammatory stimulus is found in the intravascular compartment. * Innate immune system is activated--- pro-inflammatory response and coagulative cascade produces microemboli * Initial hypotension in response to arteriole dilation, cardiac output increases for a time “warm shock” * Eventually hypotension increases further due to dilatation and increased permeability of vessels * Distributive shock as oxygenated blood is shunted away from capillary beds and tissues become hypoxic * Micro-emboli also block capillary beds
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Common sites of infection
* Mouth and throat * Skin * Lungs * Kidneys and bladder, especially if you have a catheter to drain urine * Cannula sites * Wounds or where wound
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identify sources of common infection
* Person to person contact * Person to animal contact (e.g., bites) * Contaminated surfaces * Contaminated food * Environment into open wounds * Hospital setting
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name 3 ways that antibiotics can be used what is empiric therapy
***_targeted-_*** when you know the exact causative organism ***_empirical_***- when you don't the precise organism but you have a good idea of what it will be and its sensitivities ***_Prophylactic_***- use before the fact in anticipation of infection
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how can we manage antimicrobial resistance
***_infection prevention and control_*** * prevent spread- vaccines, antiseptic technique ***_antimicrobial stewardship_*** * reduce broad spectrum use * reduce treatment regime * reduce antibiotic use when no infection present
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5 forms of acquired resistance
* Efflux pumps- remove the active substance * Limiting uptake of drug- * Modification of target- make it so antibiotic cant bind * Inactivation of a drug * Bypassing the targeted process- e.g., metabolism routes
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What is HIV? how is it transmitted?
HIV is a **retrovirus** which infects and **replicates within human lymphocytes** (**CD4+ T cells**) and macrophages. This leads to **progressive immune system dysfunction**, **opportunistic infections** and **malignancy** --\> AIDS (acquired immunodeficiency syndrome). Transmission is via? --\> blood, sexual fluids and breast milk * Sexual * Perinatal * Blood transfusion * Sharing needles
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what are the 2 kinds of HIV? which is more common in the UK? Pathophysiology of HIV? if hIV is a retrovirus, what is the key enzyme?
* HIV-1 (global epidemic) * HIV-2: less common, mostly in West Africa, less transmissible ***_Pathophysiology_*** HIV binds, via its GP120 envelope glycoprotein, to CD4 receptors on helper T cells, monocytes and macrophages. These infected cells migrate to lymphoid tissue where the virus replicates producing millions of virions. They are released as they burst out of the cell, in turn infecting more CD4+ cells, leading to ↓ immune function. key enzyme? **reverse transcriptase**
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presentation of HIV in which stage is HIV most infectious?
early/ primary infection- asymptomatic in 80% coryzal symptoms: fever, rash, myalgia, pharyngitis, lymphadenopathy, headache most infectious in primary infection
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what are the 3 stages of HIV infection?
* Acute HIV infection- 0-12 weeks * Chronic HIV infection- clinical latency * Acquired immunodeficiency (AIDS)- constitutional symptoms and opportunistic infections each stage gets worse
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stage 1 of HIV infection- acute/ primary stage
* Generally, develops **within 2-4 weeks after infection** with HIV. * Flu-like symptoms: headache, rash, fever, sore throat * As infection slowly weakens the immune system, * Swollen lymph nodes * Weight loss * Diarrhoea * cough * HIV multiplies rapidly and spreads throughout body * Virus invades, replicated within and destroys CD4+ cells * **HIV levels in blood** (viral load) **very high**- **very infectious** * **Start RT here** to experience health benefits
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Stage 2 of HIV infection- AKA asymptomatic or clinical latency
* HIV continues to divide but at a much lower rate * May not have any HIV symptoms it will present with deranged lab results- e.g., anaemia, neutropenia, lymphopenia, thrombocytopaenia, diffuse hypergammaglobulinaemia * Possible to stay in this stage for 10+years if on ARTs * If well medicated- very small chance of passing on disease via sex
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AIDS- acquired immunodeficiency syndrome
* Cannot fight off opportunistic infections- PCP, CMV, MAI, non-Hodgkins lymphoma * High viral load and very infectious * 3 year survival rate if unmedicated * Constitutional symptoms may present like: night sweats, malaise, fatigue, diarrhoea, weight loss of more than 10kg
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common opportunistic infections with HIV
* **Karposi's sarcoma**- herpes virus 8 * **Oral hairy leukolakia**- caused by EBV * **Oesophageal candiasis**- white plaques on the buccal and pharyngeal mucosa
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* What is a UTI * what is cystitis * symptoms
***_UTI-_*** infection of the urinary tract (anywhere from the kidney to the urethra) ***_Cystitis-_*** infection from UTI that affects urinary bladder ***_Symptoms_*** * dysuria- pain on urination * frequency- increased fequency of urination * urgency- abrupt, strong overwhleming need to urinate * haematuria in older patients
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***_rfx for UTIs in women_*** ***_likley pathogens_***
***_Rfxs_*** * Sexual intercourse * Diaphragm and spermicide use * Antibiotic use * New sex partner within the past year * History of UTIs within 1st degree female relatives * History of recurrent UTIs * First UTI at early age * Catheter insertion ***_Likely pathogens_*** abx use can kill off native flora and allow commensal **E.coli** to overgrow staph saprophycitcus likely pathogens for cystis: enteric gram negative (enterobacteria, klebsiella, pseudomonas auruginosa)
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investigations for UTI
***_NEWS monitoring_*** * Urine dip (check for presence of leukocytes or nitrate positive * Urine cultures (to confirm epirical treatment) * consider bloods if unwell ***_treatment options for UTI_***
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how would you treat a woman with a UTI without haematuria, who is not pregnant or catheterised?
advice on self care- paracetamol, intake of fluids to avoid dehydration, don't encourage cranberry products immediate abxs take into account local guidelines: * Nitrofurantoin 100mg modified-release twice a day for 3 days * Trimethoprim 200mg twice a day for 3 days
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how would you treat a woman who gets recurrent uncomplicated UTIs?
* discuss behavioural and personal hygiene advice * in post menopasual women consider prescribing vaginal oestrogen * abx prophylaxis: trimethoprim or amoxicillin
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how would you treat a pregnant woman with a UTI?
pain relief AVOID nitrofurantoin at term (39 weeks?) use amoxicillin or cefalexin
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cryptosporidium
Protozoan infection Acquired through ingestion of contaminated water or food Self-limiting in immunocompetent people, but causes * chronic diarrhoea * abdominal cramps and weight loss in people with HIV * diagnosed on stool microscopy or PCR
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toxoplasmosis
Protozoan parasite, commonest cause of brain lesion in people with HIV Usually due to reactivation of previous infection, causes focal neurological symptoms, fever , seizures Can also cause chorioretinitis
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Shingles
caused by **herpes zoster** infection painful vesicular lesions that occur in a **dermatomal distribution** *_complications:_* post-herpetic neuralgia, blindness, meningitis
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***_Pneumocystis jiroveci pneumonia_***
Commonest cause of infection in patients with HIV ***_Presents with_*** * Progressive dyspnoea * Fever * Malaise * Desaturation on exertion, CXR shows diffuse alveolar infiltrates * Diagnosis is by PCR of induced sputum or BAL or histology
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***_Progressive multifocal leukocephalopathy_***
Rare brain and spinal cord disease caused by JC virus, seen almost exclusively in people with HIV Symptoms include: * Loss of muscle control * Paralysis * Blindness * Speech problems * Altered mental state Progresses rapidly and can be fatal
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CMV
Herpes virus Viral infection that can cause pneumonia, colitis, encephalitis and retinitis Can cause blindness if not treated promptly
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***_Cryptococcus neoformans_***
Common cause of meningitis in HIV ***_Presents with insidious onset:_*** * Fever * Headache * Visual change * Neck stiffness * Seizures
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***_Features of septic arthritis_*** ***_initial investigtions_***
* Singular acute, painful, swollen joint * Restricted movement in 80% of patients * Pain on active and passive movemnts * Examination findings: warm to touch/ fluctuant * Fever- present in the majority of patients * Unable to weight bear * Symptoms more obvious and florid in native joint infection ***_initial investigations for septic arthritis_*** * Synovial fluid sampling- look for white cells and bacteria -\> send for gram stain * Done prior to administration of antibiotics ideally * Blood cultures * FBC + CRP+ ESR+ urate levels * Plain radiograph- nothing in early disease, capsule and soft tissue swelling, fat pad shift or joint space widening in later disease * CT or MRI in specific joints- e.g., sternoclavicular joint
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pathophysiology of septic arthritis causative agents
usually bacterial Due to either: * Hematogenous spread (most common) * Direct inoculation. **Staphylococcus aureus** (including MRSA) - 50% of cases **Streptococci** - (group A, B, C or G) 2nd **Neisseria gonorrhoeae** - particularly in young, sexually active patients **Pseudomonas aeurginosa** - usually healthcare associated **Salmonella** - those with sickle cell anaemia particularly at risk.
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risk factors for septic arthritis:
* IV drug users * Diabetes Mellitus * Older age * Underlying joint injury * Underlying joint disease (e.g. osteoarthritis, rheumatoid arthritis) * Prosthetic joint * Immunosuppression (due to medications or disease e.g. HIV) * Unprotected sex (gonococcal arthritis) * Peripheral vascular disease * Alcoholism
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ibvestigations for septic arthritis
* ***_Synovial fluid sampling_***- look for white cells and bacteria  send for gram stain * Done prior to administration of antibiotics ideally * Blood cultures * FBC + CRP+ ESR+ urate levels * Plain radiograph- nothing in early disease, capsule and soft tissue swelling, fat pad shift or joint space widening in later disease * CT or MRI in specific joints- e.g., sternoclavicular joint
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* May need aspiration for small joints or arthroscopy and arthrotomy for large joints. Artificial joints replaced ***_Empirical antibiotics:_*** * Gram-positive cocci (staph and strep): * **Vancomycin** * Alternatives: clindamycin, cephalosporin ***_Gram-negative infection:_*** * ceftriaxone (or other 3rd generation cephalosporins) * Alternative: ciprofloxacin (give gentamicin if associated with sepsis) ***_Confirmed organism:_*** * Staph aureus/strep: flucloxacillin (or clindamycin) * MRSA: Vancomycin
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Understand and list causes of immunodeficiency and how they relate to host defence mechanisms.
***_Primary immunodeficiencies-_*** genetically determined and may appear alone or as part of a syndrome. Usually present during childhood. Defined by which part of the immune system they interact with. ***_Secondary immunodeficiencies_***- occur in older or sick patients * Endocrine- diabetes mellitus * GI- hepatic insufficiency * Haematologic- aplastic anaemia, multiple myeloma * Iatrogenic- certain drugs such as chemotherapeutics, immunosuppressants * Infectious- HIV, EBV, measles * Nutritional- alcoholism, undernutrition * Physiologic- physiological immunodeficiency * Renal- nephrotic syndrome * Rheumatologic- SLE
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what kind of bacterium is TB? how are they distinguished in the lab? where in the lung do they like to grow?
mycobacteria- slow growing aeorbic bacilli ## Footnote Distinguished by a **complex, lipid rich cell envelope** responsible for characterisation as acid-fast (i.e. resistant to decolourisation by acid after staining) and their relative resistance to gram stain. **STAINS BRIGHT RED** **aerobic** so like to grow in the apices
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risk factors for TB spread
Have to be in contact for a while cramped conditions and residents * **T**ight living quarters * **B**elow or at the poverty line * **R**efugees or immigrants * **I**mmune system issues (HIV, immunosuppressants) * **S**ubstance abusers * **K**ids\< age of 5 * via droplets that can survive in their environment for a long time
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Natural history of TB
***_Primary and secondary infection:_*** * **Infection-** In 90% the immune system contains the infection, through macrophages that engulf bacteria and localize them to the hilar lymph nodes. Here, they are eliminated or may be encapsulated by a barrier of granulation tissue (considered to be in a dormant state). * A **small proportion progress to active TB**, with an increased risk in those who are immunosuppressed (e.g. HIV). This is known as Secondary TB and usually occurs in the apex of the lungs. From here it can spread locally or to distant sites. * Some patients are not able to contain the primary infection, and it disseminates widely via the bloodstream. This is known as **miliary TB** (due to the characteristic pattern on Chest X-ray like 'millet-seeds' when re-infection of lungs occurs after passing through circulation). * When immune system is weak you see **secondary infection of TB**
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general presentation of TB
* Subacute to chronic in onset * Symptoms depend on the main site of infection, but are usually accompanied by; * night sweats * fever * weight loss * other systemic symptoms
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respiratory presentation of TB Cns Presentation Additional presentation
* Most common * Chronic cough productive of purulent sputum +/- hemoptysis. * Can get bronchiectasis, pneumonia and pleural effusions. ***_CNS_*** * TB meningitis or tuberculoma * Headache * Meningism * Focal neurological signs * Decreased consciousness ***_Additional presentation_*** * May get palpable tender, firm superficial lymphadenopathy. * Causes 'sterile' pyuria, kidney pathology, abscesses, salpingitis and infertility, epididymo-orchitis.
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comparison of active and latent TB contagious? signs and symptoms? CXR? Sputum sample positive? Result of mantoux test? Purpose of treatment?
***_Latent TB_*** ***_Active TB_*** Not contagious Contagious No signs and symptoms Signs and symptoms Normal CXR Abnormal CXR Negative sputum Positive sputum for mycobacterium Mantoux + blood test positive Mantoux + blood test positive Still needs Tx to prevent active status Can spread via lymphatic system to other organs
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tests for TB
* **CXR**- look for multinodular infiltrate behind the clavicle. Calcified hilar nodes. * **Acid**-fast stain and culture from sputum culture- use ZE stain. Drug susceptibility tests. * **Mantoux test**- indell will appear if you are positive for infection. This doesn’t specify whether active, latent or from inoculation. 6-15mm is a positive test * **Bronchoscopy** * **IGRA**- blood test. Interferon Gamma Release Assay- * **PCR**- quick and easy + helps detect sensitivity to rifampicin
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Treatment for TB which TB medication makes your urine red?
RIPE * **R**ifampicin * **I**soniazid * **P**yrazinamide * **E**thambutol rifampicin makes your urine red
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what is osteomyelitis presentations
* inflammation and destruction of bone,caused by bacteria, mycobacteria and fungi ***_presentations_*** Peripheral bones * Weight loss * Fatigue * Fever * Localised warmth * Swelling * Erythema * Tenderness Vertebral osteomyelitis Localised back pain Tenderness with paravertebral muscle spasm
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likley pathogens for osteomyelitis investigations
Staphylococcus bacteria in most cases **Staph. Aureus** Staph. Epidermidis ***_investigations_*** * Definitive diagnosis - need a **bone biopsy** for pathology and culture. ***_Supportive diagnostic tests:_*** * Blood inflammatory markers ***_Imaging:_*** * **X-ray** - may be negative early on as periosteal reaction cannot be seen until about 7 days and bone necrosis after 10 days. It is useful in the diagnosis of chronic osteomyelitis. * **MRI** - good for viewing bone and soft tissue. Imaging modality of choice. * **CT** - good for identifying necrotic bone and for guiding needle for biopsy. ***_Other tests;_*** * Blood cultures, and culture of any expressed pus (but note that samples from sinus tracts are unreliable)
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measles description
* **Unvaccinated child** * **Fever \>40** * Cough * Coryza * **Conjunctivitis** * **White spots in the mouth** (koplik spots) * MEASLES- e**rythematous maculopapular rash** across **head, neck, torso** and **limbs**
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roseola infantum
3-5 day high fever Followed by a maculopapular rash Caused by human herpes virus 6
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henoch schonlein purpura
Child 2-10 years ***_Triad of:_*** 1. Purpura over extensor surfaces of the lower limb 2. Abdominal pain 3. Arthritis Urinalysis and blood pressure to check renal involvement
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malaria 1. which species 2. spread by 3. which cells are destroyed 4. particularly dangerous for
* An infection caused by a few Plasmodium species * Caused by single celled parasites that are spread by mosquito * Once plasmodium enters the blood stream it infects and destroys mainly liver and red blood cells. Particularly dangerous for: * Young children under 5 * Pregnant women * Patient with other conditions like HIV/ AIDS * Travellers with no prior exposure to malaria
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malaria is prevalent in which part of the world? multiple infections leads to most common plasmodium that infects humans?
tropical areas premunition- tolerance plasmodium vivax
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life cycle of the mosquito (9)
1. Plasmodium infected **female anopheles mosquito** hunts for a blood meal in the evening- night. Mosquitos are drawn to CO2. 2. Plasmodium is in a stage of development called a **sporozoite** in the mosquito’s **salivary gland**. 3. When mosquito pierces skin, worm like sporozoites enter our bloodstream. 4. Reach **liver** and go **dormant for months**/ years before engaging in **asexual reproduction** (reason for gap in infection  symptoms) 5. **Merozoites** are released into blood where each one **enters a RBC** (young RBCs) 6. Undergoes **asexual reproduction** and **changes form**. 7. **Gametocytes** released within RBC. 8. Infected RBC collected by a **different mosquito** taking a blood meal. 9. Gametocytes reach the **mosquitos gu**t where they fuse into a mature **zygote**. 10. Zygote matures into **oocyst** and ruptures **releasing sporozoites into the mosquito gut** 11. Migration into salivary gland to repeat cycle.
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Symptoms of malaria infection
incubation period for months asymptomatic then * haemolytic anaemia- extreme fatigue, headaches, jaundice, splenomegaly * tertian fever every 48 hours * rigors * muscle pains * chills * ischaemic damage from RBC clumping together *
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diagnosis of malaria
* **Thick blood smear**- locates parasites sitting in RBCs * **Thin blood smear-** directly identifies plasmodium species * **FBC** * Important to know percentage of RBCs affected * Thrombocytopaenia * Normochromic + normocytic anaemia (few RBC but normal in size and colour)
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treatment divided by stage of infection (4) which medication for non-severe infections
1) **_Suppressive treatment or chemoprophylaxis_** Kills sporozoites before they infect hepatocytes Given to travellers before they go 2) ***_Therapeutic treatment_*** Aimed at eliminating merozoites in the erythrocytic phase (while replicating in RBCs) Given during active infection ***_3) Gametocidal treatment_*** Aimed at killing gametocytes Prevents spread of disease and creation of resistant forms of the parasite ***_4) Radical treatments_*** Aimed at killing hypnozoites in the liver for non-severe--\> ***_Chloroquinone, doxycycline, quinine_***
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what is valvular heart disease what does stenosis mean what does regurgitation mean what does insufficiency mean
**Valvular heart disease**- one or more of the valves in your heart doesn’t work properly stenosis- narrowing or constriction of valve regurgitation- when blood travels back through a valve when it shouldn't insufficiency - when a valve doesn't close properly
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* Where is the tricupsid valve found? * pulmonary? * mitral? * aortic?
**_Tricuspid valve-_** located between the right atrium and right ventricle. **_Pulmonary valve-_** located between the right ventricle and the pulmonary artery **_Mitral valve_**- located between the left atrium and the left ventricle **_Aortic valve_**- located between the left ventricle and aorta
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what is the management of vlavular disease?
***_options:_*** **_Valvuloplasty-_** balloon valvuloplasty is a procedure done to open a stenosed heart valve. **_Valve replacemen_**t- annuloplasty or valvuloplasty. Important procedure as it can preserve heart function. ***_valve replacement_*** ***_treatment of secondary heart failure to manage symptoms_***
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causes of valvular disease
* Changes in heart valve structure due to aging * Coronary heart disease and heart attack * Heart valve infection * Birth defect * Rheumatic disease- happens after infections from bacteria that cause strep throat. Causes valvular scarring * **Endocarditis**- disease in the blood leads to endocarditis. Therefore IV use can cause it. * Heart failure * Hypertension * MI * Autoimmune diseases- lupus * Marfan syndrome- disease of connective tissue * Syphilis (a sexually transmitted infection)
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Symptoms of valvular disease
* Angina * Palpitations caused by irregular heartbeats (atrial flutter or fib) * Fatigue * Exertional syncope * Dizziness * Low or high blood pressure * SOB * Abdo pain (hepatomegaly if tricuspid failure) * Leg swelling * Orthopnea * Heart murmur * Heart failure symptoms essentially
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possible causes of angina/ chest pain
* Carcinoma in the bronchus * Pneumothorax- pleuritic chest pain * Pericardial disease * Respiratory tract infection (pneumonia, influenza, TB) * PE * Ischaemic heart disease * Pleurisy (sharp pain when breathing- inflamed pleural membranes) * Aortic dissection
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possible causes of pyrexia of unknown origin
* Lymphoproliferative disease- lymphadenopathy * Malaria * Myeloproliferative disorders- problems with bone marrow e.g., polycythemia vera * Thromboembolic disease * TB * Endocarditis
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* which 1st line antihypertensive would you give to someone \<55 years old? * which 1st line antihypertensive would you give to someone \>55 years old or originates from an afro-caribbean heritage? what would you do if you've already maxed out this dose? what would you do if this doesn't work?
* **ramipril**- ACE inhinitor * **Nefedipine-** DHP-Calcium Channel Blocker * Combine CCB and ACE-I/ARB * Add a thiazide like diuretic (Indapamide)
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what is a delta wave? what is it indicative of?
slurred upstroke of the QRS complex Wolff parkinson syndrome
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What is the indication of adenosine?
it is an AVN blocking drug used in SVTs