CR2 Revision 4 Flashcards
Nasopharyngitis is mostly commonly caused by which of the following?
Adenoviruses
Echoviruses
Coronaviruses
Rhinoviruses
Nasopharyngitis is mostly commonly caused by which of the following?
Adenoviruses
Echoviruses
Coronaviruses
Rhinoviruses
Beyond common symptoms, name 2 major cold symptoms of nasopharyngitis [2]
- Rhinorrhea (XS mucus in nasal cavity)
- Nasal obstruction (mucosal lining)
Explain how human rhinovirus infection occurs:
- Name the type of receptors that rhinovirus is detected by [2]
- What does activation of these receptors cause the release of? [3]
- HRV infects airway epithelial cell
- Recognise by Toll-like and retinoic acid-inducible gene-I like (RIG) receptors
- Activation of these receptors causes release of pro-inflam mediators: TNF-alpha, IFN & CXCL8
- This causes recruitment and activation of inflam and immuno-effector cells: neutrophils, eosinophils, dendritic cells, basophils
Explain the pathophysiology behind RSV / HRV virus causing the rhinorrrhea & nasal obstruction symptoms xx
- After release of pro-inflam cytokines like TNF-alpha, IFN & CXCL8, get neutrophil inflammation
- Causes increase in vascular permeability and mucus hypersecretion
How do viruses impede host immune recognition?
Have high glycosylation and structural variability of surface G-protein: favours an easy escape from neutralising antibodies.
Causes a decrease in virus-specific antiobody concentrations
How could a HRV nasopharyngitis infection impact asthma patients?
The host reaction to HRV in atopic asthmatic subjects is characterised by a T-helper (Th)2-type immune response.
Causes increased synthesis and release of cytokines, such as interleukin (IL)-4, IL-5, IL-10 and IL-13, which are capable of increasing the expression of intercellular adhesion molecule (ICAM)-1, the major HRV receptor, on the surface of bronchial epithelial cells (BECs)
Causes BECS more sus. to infection.
How would decide if you need to treat an acute sore throat from pharyngitis?
Use FeverPAIN or Centor scoring systems:
- If FeverPAIN score is 0-1 or Centor score 0-2: No antibiotic
- FeverPAIN score 2-3: back up antibiotic / no antibiotic prescription
- FeverPAIN score 4-5 or Centor score 3-5: immediate antibiotic or backup antibiotic prescription
- If symptoms are systemic (e.g. fever) and not resolved by immediate antibiotic refer to hospital.
(more common symptoms are likely to be viral, but if hospitlisation occurs then likely to be bacterial)
Which drugs would you use to treat a Ptx who had acute sore throat with pharnygitis?
Start of treatment is determined by hospital’s microbiology protocol
But:
First choice: Phenoxymethylpenicillin
If allergic:
Clarithromycin
Erythromycin
Pathogenesis of TB?
- Inhaled bacteria in droplets carried into lungs:
typically settle in subpleural area mid or lower lung zones - Engulfed by alveolar macrophages form Ghon Focus
- TB laden macrophages travel to local lymph nodes
- Form Primary complex (aka Ghon Complex) = primary TB lung infection in non-immune host (Ghon Focus, TB granuloma), plus draining lymph nodes.
- 5% Ptx have primary pulmonary TB
- 5% will control TB temporarily, but it will be reactivated later (latent): post primary TB
- 90 % have no more disease progression
What is a ghon focus? [1]
What is a ghon complex? [1]
A small lung lesion known as a Ghon focus develops. The Ghon focus is composed of tubercle-laden macrophages.
The combination of a Ghon focus and hilar lymph nodes is known as a Ghon complex
What is biggest risk factor for mTB reactivating? [1]
All suspected and confirmed cases of TB must have an WHAT test? [1]
HIV / AIDs (due to both infections impacting T helper cells)
All suspected and confirmed cases of TB must have an HIV test
Treatment of which drug type is a risk factor for TB re-activation?
Prolonged therapy of corticosteroids
Why would post-primary TB / reactivation of latent TB occur? [1]
Where is post primary TB most likely to be found ? [1]
Reactivation of latent TB causes: Post primary TB
- If the host becomes immunocompromised the initial infection may become reactivated. Reactivation generally occurs in the apex of the lungs and may spread locally or to more distant sites.
- In lungs characterized by cavitary lesions, typically in oxygen rich upper lobes. Relates to hosts previous exposure to MTB and immune response.
Signs and symptoms of pulmonary TB?
SYMPTOMS
Fever
Night sweats
Weight loss and anorexia
Tiredness and malaise
Cough (most common symptom) > 3 weeks duration
Haemoptysis (occasionally)
Dyspnoea (Breathlessness) if pleural effusion
Signs
- Pyrexia
- Often no chest signs despite CXR abnormality
- Maybe crackles in affected area
- In extensive disease:
i) signs of cavitation (if large) – hyperresonance
ii) fibrosis – decreased lung expansion
- If pleural involvement: typical signs of effusion – decreased breath sounds over effusion, stony dullness to percussion, loss of tactile fremitus
Investigations for TB? [5]
CXR (mainstay)
Sputum sample: ZN stain AND culture
Histology
Mantoux test
IFN-y assay
What vaccination do you give for TB? [1]
Which population do you give it to? [1]
BCG: Bacille Calmette-Guerin vaccine
Given to children: little evidence protecting adults
How do you diagnose if you’ve got latent TB or not? [2]
Tuberculin sensitivity Test – aka PPD (Purified Protein Derivative) (Manteux) test:
- Tuberculin is injected between layers of the dermis, tuberculin is a component of the bacteria, and if a person has previously been exposed to TB, the immune system reacts to the tuberculin and produces a small, localized reaction within 48 to 72 hours; if the reaction creates a large enough area of induration (rather than just redness), it’s considered to be a positive test.
DOESNT DISTINGUISH BETWEEN LATENT AND ACTIVE TB
IFN-γ assay
- If patient has had TB infection, T lymphocytes produce interferon gamma in response – measured and compared with control sample.
Which stain do you use for Tb? [2]
What colour do they appear when using this stain? [2]
Ziehl–Neelsen stain: bright- red colored rods when a is used.
Auramine: flourescent coloured
Which populations do we screen for latent TB? [1]
High risk populations: HIV / Immunocompromised. Test for reactivation
Would would CXR of Ptx with TB present like? [3]
Apex of the lung often involved (more aerobic!)
Ill defined patchy consolidation
Cavitation usually develops within consolidation
Healing results in fibrosis
Hilar lymphadenopathy
First line treatment for TB? [4]
Standard treatment of TB disease is four-drug therapy - treatment with single drug can lead to development of a bacterial population resistant to that drug:
RIPE !
- Rifampicin
- Isoniazid
- Pyrazinamide
- Ethambutol
Second line Treatment medications for TB?
Quinolones (Moxifloxacin)
Injectables
Capreomycin, kanamycin, amikacin
Ethionamide/Prothionamide
Cycloserine
PAS (Para-aminosalicylic acid)
Linezolid
Clofazamine
How long do you treat TB for if there is no suspected CNS involvment or drug resistance? [1]
Which drugs do you give and when? [4]
6 months total treatment duration
First two months: Rifampicin, Isoniazid (with pyridoxine), Pyrazinamide, Ethambutol
Next 4 months – if MTB drug susceptibility conforms- isoniazid (with pyridoxine) and rifampicin
What is miliary TB?
When does it occur? [1]
Miliary TB:
- systemic spread of bacilli through blood stream
- during: primary infection or reactivation
- lungs are always involved
- Often multiple organs involved
Headaches suggest meningeal involvement
Pericardial,pleural effusions
Ascites(involvement of peritoneum)
Retinal involvement (choroid tubercles in the eye)
Adrenal galnds – may causes adrenal insufficiency
Name 5 places that extra-pulmonary TB likely spread to [3]
Lymphadenitis
Cervical LNs most commonly
Abscesses & sinuses
Gastrointestinal
Swallowing of tubercles in mucous coughed up – any part gut
Peritoneal
Ascitic or adhesive
Genitourinary
Slow progression to renal disease
Subsequent spreading to lower urinary tract
Bone & joint Haematogenous spread
Spinal TB most common- called Pott’s disease
Tuberculous meningitis
Chronic headache, fevers
CSF – markedly raised proteins, lymphocytosis
What would CXR look like in:
- Primary TB
- Reactivated TB
- Millary TB
Primary TB may show patchy consolidation, pleural effusions and hilar lymphadenopathy
Reactivated TB may show patchy or nodular consolidation with cavitation (gas filled spaces in the lungs) typically in the upper zones
Disseminated Miliary TB give a picture of “millet seeds” uniformly distributed throughout the lung fields
What is normal pH range of arterial blood? [1]
What is normal pH range of venous blood? [1]
What is typical arterial blood pH? [1]
What is typical venous blood pH? [1]
What is normal pH range of arterial blood? [1]
7.35-7.45
What is normal pH range of venous blood? [1]
7.31-7.41
What is typical arterial blood pH? [1]
7.40
What is typical venous blood pH? [1]
7.35
Hessel bank equation xxx
What are the two leading causes of respiratory acidosis? [2]
Name 3 others causes [3]
Hypoventilation and ventilation-perfusion mismatch resulting in inadequate excretion of CO2
Drugs suppress breathing (powerful pain medicines, such as narcotics, and “downers,” such as benzodiazepines), especially when combined with alcohol
Brain injury impairing CNS respiratory centres
Diseases of gas exchange (such as asthma and chronic obstructive lung disease)
Diseases of the chest (such as scoliosis), which make the lungs less efficient at filling and emptying
Diseases affecting the nerves and muscles that drive lung ventilation
Severe obesity, which restricts how much lungs can expand
What is a CNS symptom of resp. acidosis? [1]
Increased CO2 causes cerebral arterial vasodilation increased intracranial pressure with oedema – net result is a dreceased brain blood flow
How do you treat respiratory acidosis? [4]
Treat cause !:
- Bronchodilator drugs to reverse some types of airway obstruction
- Noninvasive positive-pressure ventilation (sometimes called CPAP or BiPAP) or mechanical ventilation if needed
- Opioid drug overdose reversal with naloxone
- Oxygen if the blood oxygen level is low – BUT must be careful with oxygen
Why do you need to monitor when giving O2 to Ptx with respiratory acidosis? Especially if have COPD
- Giving oxygen to these patients may lead to worsening CO2 retention from ventilation-perfusion mismatch: causes more acidosis.
- Can lead to CO2 narcosis and cardio-pulmonary arrest
How should you treat hypoxaemia in Ptx with COPD and chronic hypercapnia? [2]
- Controlled oxygen therapy with 24% or 28% O2
- with target haemoglobin saturation of 88 – 92% as hypoxaemia is life threatening.
- If CO2 does go up and pH falls may need to mechanically ventilate patient.
How does metabolic compensation to respiratory acidosis occur? [3]
- Increase HCO3- reabsorbtion at PCT
- Produce and excrete more ammonia
- Produce and excrete more phosphate ions
What disease does excessive excretion of phosphate ions lead to? [1]
This requires phosphate which comes from breakdown of calcium phosphate in bone, which can lead to bone weakening and osteoporosis.
When does respiratory alkalosis occur? [1]
Respiratory alkalosis generally occurs when person hyperventilates. Increased breathing produces increased alveolar respiration, expelling CO2 from circulation
Effect of resp. alkolosis / acidosis on free Ca2+ ions? [1]
Increase in pH (alkaemia), promotes increased calcium protein binding, which decreases free calcium.
Acidaemia decreases protein binding, resulting in increased free calcium.
How does resp. alkalosis cause syncope? [1]
What happens to O2 dissociation curve in resp alk? [1]
Describe what happens to Ca2+ levels during alkalosis and what effect this has [2]
1) Decrease CO2 content: of blood causes constriction of cerebral blood vessels – may cause syncope
2) Alkalaemia shifts the haemoglobin O2 dissociation curve to the left:, impairing O2 delivery to tissues.
3) pH related changes in free Ca2+ blood levels can lead to an increase in neuromuscular excitability- increased risk arrythmias and tetany (involuntary and sustained muscle contractions)
Explain the mechanism of renal compensation of chronic resp. alkalosis [2]
- Kidney increases bicarbonate excretion by reducing levels of carbonic anhydrase.
- The minimum plasma [HCO3-] achievable is about 12 mmol/L).
Name common causes of type 1 resp. failure [3]
Name one common cause of type 2 resp. failure [1]
Name common causes of type 1 resp. failure [3]
3 Ps: PE, Pulmonary oedema, Pneumonia
Name one common cause of type 2 resp. failure [1]
Severe COPD
Name 3 reasons that could be the pathology behind mitral valve prolapse [3]
Describe the physiology occuring in mitral valve prolapse [1]
What are symptoms and severity of mitral valve prolapse? [1]
Whats a sign of mitral valve prolapse? [1]
Pathology:
- histologically normal valves
- myxomatous degeneration (efect in the mechanical integrity of the leaflet due to the altered synthesis and/or remodeling by type VI collagen)
- Marfan, Ehlers danlos
Physiology:
- valve leaflet(s) prolapses back into LA during systole, sometimes producing Mitral Rerguit.
Symptoms:
- Usually asymptomatic
Sign:
- Late ejection click
Define aortic stenosis [1]
Name 3 causes of aortic stenosis [3]
Definition:
Narrowing of the aortic valve resulting in obstruction to the left ventricular stroke volume, leading to symptoms of chest pain, breathlessness, syncope and fatigue
Causes:
- Calcific disease (hardening of aortic valve)
- Congenital bicuspid aortic valve (BAV) (valve has 2 leaflets instead of 3 due to genetic disease - this is the most common congenital heart disease) resulting in stenosis
- Rheumatic heart disease
Signs [5] & Symptoms [4] of Aortic stenosis?
Symptoms:
- Dyspnoea - increase in diastolic pressure in stiff non-compliant LV. LV is thicker because has to use more energy to expel blood (hypertrophy)
- Angina - increase O2 demand of hypertrophied LV
- Syncope - either paroxysmal ventricular arrhythmias or exertional cerebral hypoperfusion (less blood is leaving)
- LVF - contractile failure as ventricle dilates – causes heart failure
- Sudden death - ventricular arrhythmias
Signs:
- slow rising carotid pulse
- S4 ejection click
- Late diastole (trying to eject blood)
What are the 4 heart sounds? [4]
What are they caused by and when do they occur? [4]
S1:
closure of AVN (tricuspid and mitral valve) at start of systolic contraction of ventricles
S2:
closure of semi-lunar valves (aortic and pulmonary valves) at the end of systole
S3:
0.1 secs after S2. Caused by rapid ventricular filling causing chordae tendinae to twang close.
S4:
Directly before S1. Always abnormal: indicates stiff / hypertrophic ventricle. Turbulent flow from atria trying to get blood in
Describe the murmur that occurs from aortic stenosis [4]
Systolic ejection murmur (S1 –> S2)
Prominant S4 ejection click
High pitched
Crescendo / decresendo
Radiates to carotids
What investigations would you conduct (and see) for aortic stenosis? [4]
Echocardiogram
- area of valve: if less than 1cm2
- Speed / gradient of LV into aorta more than 64 mm Hg
ECG:
- Inverted T wave in lateral leads (LV hypertrophy)
CXR
- imaging of valve
Pressure signals: (put a catheter into LV and measure gradient of LV –> aorta)
- prominant a wave
What would indicate need for surgery for AS? [3]
- Any symptoms of AS
- Echocardiographic evidence of worsening LV dilatation
- Peak systolic pressure gradient (the difference between peak left ventricular [LV] and peak aortic systolic pressures) >50 mmHg
TAVI now taking over from heart surgery for people not suitable (frail).
What are two overiding causes of aortic regurgitation? [2]
Aortic leaflet disease [1]
Aortic root dilating disease [1]
What are 4 causes of aortic valve lealeft disease [4]
Calcific disease – stiffness of valve (hard to open / close)
Congenital bicuspid valve
Rheumatic disease
Infective endocarditis. Infection of aortic valve
What are 3 causes of aortic regurgitation caused by aortic root dilating disease? [3]
Ankylosing spondylitis (is an inflammatory disease that, over time, can cause some of the bones in the spine (vertebrae) to fuse)
Marfan syndrome (cant make strong CT)
Aortic dissection
Describe signs of aortic regurgitation
Heart murmur:
- Early diastolic, soft / subtle murmur at left sternal border
- Systolic ejection murmur; due to increased flow across the aortic valve
- Corrigans pulse / collapsing pulse: rapidly appears then dissapears
- Apex beat displaced laterally
What investigations for aortic regurgitation?
Echocardiogram:
- Aortic root size compared to LV. Aortic root often much larger than normal)
- LV dimensions (LV dilation)
Doppler
- detection and quantification of regurgitant flow
What would indications would trigger surgery for AR? [2]
Any symptoms of AR
Echocardiographic evidence of worsening LV dilatation
Describe the pathophysiology behind aortic rurgigation
Aortic regurgitation is reflux of blood from the aorta through the aortic valve into the left ventricle during diastole
- If net cardiac output is to be maintained, the total volume of blood pumped into the aorta must increase and, consequently, the left ventricular size must enlarge resulting in left ventricle dilation and hypertrophy
- Progressive dilation leads to heart failure
- Furthermore due to the fact that the remaining blood in the root of the aorta supplies the coronary arteries via the coronary sinus during diastole - regurgitation causes diastolic blood pressure to fall and thus coronary perfusion decreases
- Also the large left ventricular size is mechanically less efficient, so that the demand for oxygen is greater and cardiac ischaemia develops
Describe the pathophysiology of mitral stenosis
- Thickening and immobility of the valve leads to obstruction of blood flow from the left atrium to the left ventricle
- In order for sufficient cardiac output to be maintained, the left atrial pressure increases and left atrial hypertrophy and dilatation occur
- Consequently pulmonary venous, pulmonary arterial and right heart pressures also increase
- The increase in pulmonary capillary pressure is followed by the development of pulmonary oedema - this is seen particularly when atrial fibrillation occurs, due to the elevation of left atrial pressure and dilatation, with tachycardia and loss of coordinated atrial contraction
What are the causes [1] and symptoms [4] of mitral stenosis?
Causes:
- Rheumatic fever
Symptoms:
- Afib - lead to palpitations
- Progressive dyspnoea - due to left atrial dilation resulting in pulmonary congestion
- Systemic emboli - due to atrial fibrillation.
- Right ventricular failure: due to the development of pulmonary hypertension
What are the signs of mitral stenosis?[5]
- Mid-diastolic rumbling murmur: low velocity of blood flow (due to narrow area - rumbles way through). LENGTH OF RUMBLE CORRELATES TO THE INTENSITY
- Loud S1 caused by thick valves closing
- Tapping apex beat that is palpatable (due to loud S1)
- Atrial fibrillation: left atrium can’t push through stenotic valve - disrupts electrical signal
- Increase in JVP, basal creps, ankle oedema
What investigations would you do to ID mitral stenosis?
ECG:
- Left atrial enlargement
Echocardiogram:
* GOLD STANDARD for diagnosis
* Assess mitral valve mobility, gradient and mitral valve area
noncalcified valve
no mitral regurgitation
LA thrombus
What are classifications of pathologies that cause mitral regurgitation? [3]
State which specific disease causes these within the classifications
Mitral valve leaflet disease
- Mitral valve prolapse (leaflets prolapse during systole)
- Rheumatic disease
- Infective endocarditis – infection. Disease / bacteria stop closure of the valve)
Subvalvar disease
- Chordal rupture (chordae tendinae)
- Papillary muscle dysfunction (usually ischaemic)
- Papillary muscle rupture
Functional MR
- LV dilatation
Describe the signs of mitral regurgitation [5]
- Pan-systolic murmur
-
Prominent third extra heart sound (S3) in congestive heart failure/left
atrium overload - High pitched whistling
- increased JVP, basal creps, ankle oedema due to backlog of blood
- radiates to the left axilla
What are symptoms of mitral regurgitation? [3]
Symptoms
Dyspnoea, orthopnoea due to increase in left atrial pressure
Palpitations due to atrial fibrillation
Systemic emboli due to static blood within dilated fibrillating left atrium predisposes to thrombosis
What would indicate someone is suitable for mitral regurgitation surgery? [3]
What medical treatment would you conduct for mitral regurgitation? [3]
Surgery:
Symptoms that fail to respond to medical treatment
Worsening cardiovascular complications
pulmonary hypertension (MS)
LV dilatation (MR)
Medication:
Fluid retention - diuretics
AF (MS, MR) - digoxin, beta-blockers, verapamil
Anticoagulants to protect against systemic embolisation (AF)
