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Yr 2 EOYS > CR EOYS9 > Flashcards

CR EOYS9 Flashcards

1
Q

What is the most common cause of aortic stenosis?

Calcification
Rheumatic fever
Congenital bicuspid disease
Coarctation of aorta

A

What is the most common cause of aortic stenosis?

Calcification
Rheumatic fever
Congenital bicuspid disease
Coarctation of aorta

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2
Q

Name 4 risk factors for calcification of aortic valve? [4]

A

Risk factors: hypercholesterolaemia, hypertension, smoking and diabetes.

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3
Q

Aortic stenosis is most likely to initially cause

eccentric hypertrophy
concentric hypertrophy
dilated cardiomyopathy
no change

A

Aortic stenosis is most likely to initially cause

eccentric hypertrophy
concentric hypertrophy
dilated cardiomyopathy
no change

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4
Q

Severe aortic stenosis is most likely to cause

eccentric hypertrophy
concentric hypertrophy
dilated cardiomyopathy
no change

A

Severe aortic stenosis is most likely to cause

eccentric hypertrophy
concentric hypertrophy
dilated cardiomyopathy

With very severe aortic stenosis, the muscle of the left ventricle can convert from being too thick and stiff to becoming weak and dilated—a condition called dilated cardiomyopath

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5
Q

Respiratory acidosis and alkalosis has what effect on serum Ca2+ levels

Acidosis: increases Ca2+; Alkalosis decreases Ca2+
Acidosis: decreases Ca2+; Alkalosis decreases Ca2+
Acidosis: decreases Ca2+; Alkalosis increases Ca2+
Acidosis: increases Ca2+; Alkalosis increases Ca2+

A

Respiratory acidosis and alkalosis has what effect on serum Ca2+ levels

Acidosis: increases Ca2+; Alkalosis decreases Ca2+
Acidosis: decreases Ca2+; Alkalosis decreases Ca2+
Acidosis: decreases Ca2+; Alkalosis increases Ca2+
Acidosis: increases Ca2+; Alkalosis increases Ca2+

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6
Q

Name this symptom

Janeway lesion
Oslers node
Splinter haemorrhage
Normal wear n tear

A

Name this symptom

Janeway lesion
Oslers node: Osler’s nodes are on the tip of the finger or toes and painful
Splinter haemorrhage
Normal wear n tear

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7
Q

Name this symptom

Janeway lesion
Oslers node
Splinter haemorrhage
Normal wear n tear

A

Name this symptom

Janeway lesion transient, nontender macular papules on palms or soles. NOT PAINFUL
Oslers node
Splinter haemorrhage
Normal wear n tear

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8
Q

A 17-year-old intravenous drug user presents to the hospital with low-grade fever, lethargy, and general malaise. He has tender, red, raised lesions on his palms and soles, which he reports appeared a few days ago. Cardiac auscultation reveals a pansystolic murmur in the tricuspid area. Lab investigations reveal a white blood cell count of 19000/microlitre. What is the most likely diagnosis for the lesions described?

A. Heberden nodes
B. Bouchard nodes
C. Osler nodes
D. Janeway lesions

A

A 17-year-old intravenous drug user presents to the hospital with low-grade fever, lethargy, and general malaise. He has tender, red, raised lesions on his palms and soles, which he reports appeared a few days ago. Cardiac auscultation reveals a pansystolic murmur in the tricuspid area. Lab investigations reveal a white blood cell count of 19000/microlitre. What is the most likely diagnosis for the lesions described?

A. Heberden nodes
B. Bouchard nodes
C. Osler nodes
Janeway lesions can also occur on the palms in infective endocarditis but are not painful.
D. Janeway lesions

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9
Q

Janeway lesions and Osler nodes are supporting criteria for a diagnosis of [].

A

Janeway lesions and Osler nodes are supporting criteria for a diagnosis of infective endocarditis

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10
Q

Pott’s disease is when pulmonary TB has spread to

Lymph system
Gastrointestinal system
Genitourinary system
Bone & joints
Meninges

A

Pott’s disease is when pulmonary TB has spread to

Lymph system
Gastrointestinal system
Genitourinary system
Bone & joints - Spinal
Meninges

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11
Q

Which is the most common place pulmonary TB spreads to?

Lymph system
Gastrointestinal system
Genitourinary system
Bone & joints
Meninges

A

Which is the most common place pulmonary TB spreads to?

Lymph system
Gastrointestinal system
Genitourinary system
Bone & joints - spinal TB: Potts disease
Meninges

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12
Q

Myxomatous degeneration of the cardiac valves (MDMV) occurs due to remodelling of which type of collagen?

Collagen I
Collagen II
Collagen III
Collagen IV
Collagen V

A

Myxomatous degeneration of the cardiac valves (MDMV) occurs due to remodelling of which type of collagen?

Collagen I
Collagen II
Collagen III
Collagen IV
Collagen V

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13
Q

Cerebral oedema is associated with

Respiratory alkalosis
Respiratory acidosis
Metabolic alkalosis
Metabolic acidosis

A

Cerebral oedema is associated with

Respiratory alkalosis
Respiratory acidosis
Metabolic alkalosis
Metabolic acidosis

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14
Q

A narrow pulse pressure is associated with:

aortic stenosis
mitral stenosis
aortic regurgitation
mitral regurgitation

A

A narrow pulse pressure is associated with:

aortic stenosis
mitral stenosis
aortic regurgitation
mitral regurgitation

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15
Q

A wide pulse pressure is associated with:

aortic stenosis
mitral stenosis
aortic regurgitation
mitral regurgitation

A

A wide pulse pressure is associated with:

aortic stenosis
mitral stenosis
aortic regurgitation
mitral regurgitation

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16
Q

A low volume pulse is associated with

aortic stenosis
mitral stenosis
aortic regurgitation
mitral regurgitation

A

A low volume pulse is associated with

aortic stenosis
mitral stenosis
aortic regurgitation
mitral regurgitation

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17
Q

Ankylosing spondylitis is associated with

A
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18
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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19
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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20
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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21
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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22
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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23
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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24
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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25
Q

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

A

Prolonged therapy of corticosteroids

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26
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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27
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

28
Q

Investigations for TB? [5]

A

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

29
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

30
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.
31
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

32
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
33
Q

Second line Treatment medications for TB?

A

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

34
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

35
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

36
Q

Hessel bank equation xxx

A
37
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

38
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

39
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
40
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
41
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.
42
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.

43
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

44
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.

45
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)

46
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).
47
Q

What is the basic pathophysiology behind type 1 and 2 respiratory failures? [2]

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

A

Type 1: respiratory failure occurs when the respiratory system cannot adequately provide oxygen to the body, leading to hypoxemia

Type 2: when the respiratory system cannot adequately remove carbon dioxide from the body, leading to hypercapnia

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

48
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

49
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

50
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)

51
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

52
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

53
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).

54
Q

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

A

Aortic leaflet disease [1]

Aortic root dilating disease [1]

55
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

56
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

57
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
58
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

59
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
60
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
61
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

62
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
63
Q
A

noncalcified valve
no mitral regurgitation
LA thrombus

64
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

65
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
66
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

67
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)

Yr 2 EOYS (58 decks)

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