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CR2 > CR2 Revision 4 > Flashcards

CR2 Revision 4 Flashcards

1
Q

Nasopharyngitis is mostly commonly caused by which of the following?

Adenoviruses
Echoviruses
Coronaviruses
Rhinoviruses

A

Nasopharyngitis is mostly commonly caused by which of the following?

Adenoviruses
Echoviruses
Coronaviruses
Rhinoviruses

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2
Q

Beyond common symptoms, name 2 major cold symptoms of nasopharyngitis [2]

A
  • Rhinorrhea (XS mucus in nasal cavity)
  • Nasal obstruction (mucosal lining)
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3
Q

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]
A
  1. HRV infects airway epithelial cell
  2. Recognise by Toll-like and retinoic acid-inducible gene-I like (RIG) receptors
  3. Activation of these receptors causes release of pro-inflam mediators: TNF-alpha, IFN & CXCL8
  4. This causes recruitment and activation of inflam and immuno-effector cells: neutrophils, eosinophils, dendritic cells, basophils
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4
Q

Explain the pathophysiology behind RSV / HRV virus causing the rhinorrrhea & nasal obstruction symptoms xx

A
  • After release of pro-inflam cytokines like TNF-alpha, IFN & CXCL8, get neutrophil inflammation
  • Causes increase in vascular permeability and mucus hypersecretion
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5
Q

How do viruses impede host immune recognition?

A

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

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6
Q

How could a HRV nasopharyngitis infection impact asthma patients?

A

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.

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7
Q

How would decide if you need to treat an acute sore throat from pharyngitis?

A

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)

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8
Q

Which drugs would you use to treat a Ptx who had acute sore throat with pharnygitis?

A

Start of treatment is determined by hospital’s microbiology protocol
But:

First choice: Phenoxymethylpenicillin

If allergic:

Clarithromycin
Erythromycin

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9
Q

Pathogenesis of TB?

A
  • 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
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10
Q

What is a ghon focus? [1]

What is a ghon complex? [1]

A

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

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11
Q

What is biggest risk factor for mTB reactivating? [1]

All suspected and confirmed cases of TB must have an WHAT test? [1]

A

HIV / AIDs (due to both infections impacting T helper cells)

All suspected and confirmed cases of TB must have an HIV test

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12
Q

Treatment of which drug type is a risk factor for TB re-activation?

A

Prolonged therapy of corticosteroids

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13
Q

Why would post-primary TB / reactivation of latent TB occur? [1]
Where is post primary TB most likely to be found ? [1]

A

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.
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14
Q

Signs and symptoms of pulmonary TB?

A

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

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15
Q

Investigations for TB? [5]

A

CXR (mainstay)
Sputum sample: ZN stain AND culture
Histology
Mantoux test
IFN-y assay

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16
Q

What vaccination do you give for TB? [1]
Which population do you give it to? [1]

A

BCG: Bacille Calmette-Guerin vaccine

Given to children: little evidence protecting adults

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17
Q

How do you diagnose if you’ve got latent TB or not? [2]

A

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.
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18
Q

Which stain do you use for Tb? [2]

What colour do they appear when using this stain? [2]

A

Ziehl–Neelsen stain: bright- red colored rods when a is used.

Auramine: flourescent coloured

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19
Q

Which populations do we screen for latent TB? [1]

A

High risk populations: HIV / Immunocompromised. Test for reactivation

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20
Q

Would would CXR of Ptx with TB present like? [3]

A

Apex of the lung often involved (more aerobic!)

Ill defined patchy consolidation

Cavitation usually develops within consolidation

Healing results in fibrosis

Hilar lymphadenopathy

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21
Q

First line treatment for TB? [4]

A

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
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22
Q

Second line Treatment medications for TB?

A

Quinolones (Moxifloxacin)
Injectables
Capreomycin, kanamycin, amikacin
Ethionamide/Prothionamide
Cycloserine
PAS (Para-aminosalicylic acid)
Linezolid
Clofazamine

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23
Q

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]

A

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

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24
Q

What is miliary TB?
When does it occur? [1]

A

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

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25
Q

Name 5 places that extra-pulmonary TB likely spread to [3]

A

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

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26
Q

What would CXR look like in:

  • Primary TB
  • Reactivated TB
  • Millary TB
A

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

27
Q

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]

A

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

28
Q

Hessel bank equation xxx

A
29
Q

What are the two leading causes of respiratory acidosis? [2]

Name 3 others causes [3]

A

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

30
Q

What is a CNS symptom of resp. acidosis? [1]

A

Increased CO2 causes cerebral arterial vasodilation increased intracranial pressure with oedema – net result is a dreceased brain blood flow

31
Q

How do you treat respiratory acidosis? [4]

A

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
32
Q

Why do you need to monitor when giving O2 to Ptx with respiratory acidosis? Especially if have COPD

A
  • 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
33
Q

How should you treat hypoxaemia in Ptx with COPD and chronic hypercapnia? [2]

A
  • 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.
34
Q

How does metabolic compensation to respiratory acidosis occur? [3]

A
  • Increase HCO3- reabsorbtion at PCT
  • Produce and excrete more ammonia
  • Produce and excrete more phosphate ions
35
Q

What disease does excessive excretion of phosphate ions lead to? [1]

A

This requires phosphate which comes from breakdown of calcium phosphate in bone, which can lead to bone weakening and osteoporosis.

36
Q

When does respiratory alkalosis occur? [1]

A

Respiratory alkalosis generally occurs when person hyperventilates. Increased breathing produces increased alveolar respiration, expelling CO2 from circulation

37
Q

Effect of resp. alkolosis / acidosis on free Ca2+ ions? [1]

A

Increase in pH (alkaemia), promotes increased calcium protein binding, which decreases free calcium.

Acidaemia decreases protein binding, resulting in increased free calcium.

38
Q

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]

A

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)

39
Q

Explain the mechanism of renal compensation of chronic resp. alkalosis [2]

A
  1. Kidney increases bicarbonate excretion by reducing levels of carbonic anhydrase.
  2. The minimum plasma [HCO3-] achievable is about 12 mmol/L).
40
Q

Name common causes of type 1 resp. failure [3]
Name one common cause of type 2 resp. failure [1]

A

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

41
Q

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]

A

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

42
Q

Define aortic stenosis [1]

Name 3 causes of aortic stenosis [3]

A

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

43
Q

Signs [5] & Symptoms [4] of Aortic stenosis?

A

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)

44
Q

What are the 4 heart sounds? [4]

What are they caused by and when do they occur? [4]

A

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

45
Q

Describe the murmur that occurs from aortic stenosis [4]

A

Systolic ejection murmur (S1 –> S2)

Prominant S4 ejection click

High pitched

Crescendo / decresendo

Radiates to carotids

46
Q

What investigations would you conduct (and see) for aortic stenosis? [4]

A

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

47
Q

What would indicate need for surgery for AS? [3]

A
  • 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).

48
Q

What are two overiding causes of aortic regurgitation? [2]

A

Aortic leaflet disease [1]

Aortic root dilating disease [1]

49
Q

What are 4 causes of aortic valve lealeft disease [4]

A

Calcific disease – stiffness of valve (hard to open / close)

Congenital bicuspid valve

Rheumatic disease

Infective endocarditis. Infection of aortic valve

50
Q

What are 3 causes of aortic regurgitation caused by aortic root dilating disease? [3]

A

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

51
Q

Describe signs of aortic regurgitation

A

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
52
Q

What investigations for aortic regurgitation?

A

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

53
Q

What would indications would trigger surgery for AR? [2]

A

Any symptoms of AR
Echocardiographic evidence of worsening LV dilatation

54
Q

Describe the pathophysiology behind aortic rurgigation

A

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
55
Q

Describe the pathophysiology of mitral stenosis

A
  • 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
56
Q

What are the causes [1] and symptoms [4] of mitral stenosis?

A

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

57
Q

What are the signs of mitral stenosis?[5]

A
  • 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
58
Q

What investigations would you do to ID mitral stenosis?

A

ECG:
- Left atrial enlargement

Echocardiogram:
* GOLD STANDARD for diagnosis
* Assess mitral valve mobility, gradient and mitral valve area

59
Q
A

noncalcified valve
no mitral regurgitation
LA thrombus

60
Q

What are classifications of pathologies that cause mitral regurgitation? [3]

State which specific disease causes these within the classifications

A

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

61
Q

Describe the signs of mitral regurgitation [5]

A
  • 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
62
Q

What are symptoms of mitral regurgitation? [3]

A

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

63
Q

What would indicate someone is suitable for mitral regurgitation surgery? [3]

What medical treatment would you conduct for mitral regurgitation? [3]

A

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)

CR2 (59 decks)

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