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Yr 2 EOYS ^2 > CR EOYS3 > Flashcards

CR EOYS3 Flashcards

1
Q

Explain changes in cell types due to smoking xx [3]

A
  • loss pseudostratified epitheluim, with transition into a fully squamous epithelium and expression of early markers of carcinogenesis.
  • change to squamous = metaplastic change (reversible)
  • change to squamous that is irreversible = dysplastic
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2
Q

Based on the quadrant diagram shown, which region would you expect the mean electrical axis to deviate towards in a patient with left ventricular hypertrophy?

A
B
C
D

A

Based on the quadrant diagram shown, which region would you expect the mean electrical axis to deviate towards in a patient with left ventricular hypertrophy?

A
B
C
D

Left ventricular hypertrophy results in a thickening of the cardiac muscle. The increase in mass increases the magnitude of the depolarisation wave on the left side of the heart. This causes the left axis deviation.

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3
Q

Based on the quadrant diagram shown, which region would you expect the mean electrical axis to deviate towards in a patient with normal heart?

A
B
C
D

A

Based on the quadrant diagram shown, which region would you expect the mean electrical axis to deviate towards in a patient with normal heart?

A : normal heart axis = -30 to 90 degrees
B
C
D

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4
Q

Based on the quadrant diagram shown, which region would you expect the mean electrical axis to deviate towards in a patient with right ventricular hypertrophy?

A
B
C
D

A

Based on the quadrant diagram shown, which region would you expect the mean electrical axis to deviate towards in a patient with right ventricular hypertrophy?

A
B
C
D = 90 to 180 degrees

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5
Q

Absent Q waves in V5-6 is most commonly due to:

LBBB
Mobitz type 1 AV block
RBBB
Wolff-Parkinson-White (WPW)
Mobitz type 2 AV block

A

Absent Q waves in V5-6 is most commonly due to:

LBBB
Mobitz type 1 AV block
RBBB
Wolff-Parkinson-White (WPW)
Mobitz type 2 AV block

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6
Q

What is the axis deviation of a healthy heart? [1]
Right axis deviation ranges between which degrees? [1]
Left axis deviation ranges between which degrees? [1]

A

Normal: -30° and +90º

Right axis deviation: +90º and +180º

Left axis deviation: -30° and -90°.

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7
Q

Which lead would you expect to see the biggest negative deflection in a healthy heart?

avL
avF
avR
Lead I
Lead II

A

Which lead would you expect to see the biggest negative deflection in a healthy heart?

avL
avF
avR
Lead I
Lead II

This is due to aVR looking at the heart in the opposite direction.

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8
Q

State the most common cause of a heart axis deviation between +90º and +180º [1]

Explain why this occurs

A

+90º and +180º: RAD. Most common cause is right ventricular hypertrophy

Extra right ventricular tissue results in a stronger electrical signal being generated by the right side of the heart.

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9
Q

Describe the changes in ECG leads seen cardiac in right axis deviation [2]

A

Deflection in lead I to become negative
Deflection in lead aVF/III to be more positive.

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10
Q

Describe the changes in ECG leads seen cardiac in left axis deviation [2]

A

Deflection of lead III becoming negative (this is only considered significant if the deflection of lead II also becomes negative).

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11
Q

Name 3 reasons left axis deviation may occur [3]

A

left anterior hemiblock
left bundle branch block
inferior myocardial infarction
Wolff-Parkinson-White syndrome- right-sided accessory pathway
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people

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12
Q

Name 3 reasons right axis deviation may occur [3]

A

right ventricular hypertrophy
left posterior hemiblock
lateral myocardial infarction
chronic lung disease → cor pulmonale
pulmonary embolism
ostium secundum ASD
Wolff-Parkinson-White syndrome- left-sided accessory pathway
normal in infant < 1 years old
minor RAD in tall people

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13
Q

Left axis deviation would occur from an MI in which part of the heart?

Septal
Anterior
Inferior
Lateral

A

Left axis deviation would occur from an MI in which part of the heart?

Septal
Anterior
Inferior
Lateral

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14
Q

Name 4 causes of systolic dysfunction [4]

A

Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Arrhythmias

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15
Q

Name a common side effect of statin use [1]

A

myalgia

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16
Q

Name the different places that haematopoiesis occurs in from embryo to neotate [4]

A

Embryo (3 weeks): Yolk sac

Fetus (6 weeks): Liver

Fetus (8 weeks): Spleen =

Neonate: Bone marrow

You Love a Smart Bunny

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17
Q

Explain the 4 different types of alpha thalassaemias

A

o1 defective alpha subunit: alpha thalassemia minima
· Minimal effect on Hb synthesis
· The other alpha globin genes produce enough subunits
· No clinical symptoms
· Slightly reduced MCV
· ‘silent carriers’

o2 alpha subunits missing or defective: alpha thalassemia minor
· Mild microcytotic hypochromic anaemia
· The remaining 2 alpha genes produce nearly normal levels of RBCs
· Can be mistaken for iron deficiency anaemia.

o3 alpha subunits missing or defective: Haemoglobin H disease (HbH)
Deletion of three alpha genes
Haemoglobin H (B4)
Moderate microcytic hypochromic anaemia
Excess beta chains cause damage by:
i) damage the red blood cell membrane, resulting in intramedullary hemolysis
ii) HbH has very high affinity for oxygen, and doesn’t release oxygen to the tissues. And a consequence of hypoxia is that it signals the bone marrow, as well as extramedullary tissues like the liver and spleen, to increase production of red blood cells.

o4 alpha subunits missing or defective:
· Foetus cannot live outside of uterus
· May not survive gestation
· Hydrops fetalis: Haemoglobin Barts (γ4) - super high affinity to O2.
Incompatible with life

18
Q

Describe how Beta-thalassemias occur [2] (be specific)

Explain why Beta-thalassemias are pathological [2]

A

Beta-thalassemias: occur from mutations within the B-gene [1]

Characterised by a reduced or absent production of haemoglobin A (which contains a2,B2)

As a result: excess α-chains precipitate in red cell precursors (as theres no beta chains) causing ineffective erythropoiesis as well as in mature red cells causing hemolysis.

Ineffective erythropoiesis and hemolysis cause anaemia

When there’s a β-globin chain deficiency, free α-chains accumulate within red blood cells, and they clump together to form intracellular inclusions, which damage the red blood cell’s cell membrane. This causes hemolysis,

19
Q

Why does hemoglobin H, or HbH, disease lead to splenomagaly or hepatomegaly? [3]

A

HbH = Hb β4. This form of Hb causes

Damage to the red blood cell membrane, resulting in intramedullary hemolysis, or red blood cell breakdown in the bone marrow; or extravascular hemolysis, when red blood cells are destroyed by macrophages in the spleen.

Second, HbH has very high affinity for oxygen, and doesn’t release oxygen to the tissues. And a consequence of hypoxia is that it signals the bone marrow, as well as extramedullary tissues like the liver and spleen, to increase production of red blood cells. This may cause the bones that contain bone marrow, as well as the liver and spleen, to enlarge.

20
Q

What are 4 causes of heart failure? [4]

A

Coronary artery disease: myocardial ischaemia or MI (as that part of the heart wont be working)

Hypertension: get left ventricular hypertrophy (LV stiffened and can’t relax)

Cardiomyopathy: dilated cardiomyopathy: reduces EF, hypertrophic cardiomyopathy leads to LV thickening, inflammatory disorders of LV, tachyarythmias (e.g. chronic afib will lead to heart failure)

Valvular heart disease: aortic and mitral regurgitation lead to LV dilatation and LV failure.

21
Q

Why might a patient develop acute decompensation heart failure and therefore present with significant symptoms? [4]

A

Cardiac arrhythmias (e.g., AF):

Hypertension

Anaemia

Infections

22
Q

How does targeting sympatho-adrenal activation and RAAS systems cause an increase in contractile function?

A
23
Q

How would you treat someone with acute failure?
a) immediately? (pharmacologically [2] & non-pharmacologically [2] )
b) after stabilisation? [4]
c) ongoing management? [3]

A

Immediately:
Pharmalogical: O2 & duiretic
Non Pharmalogical: ventilation; ultrafiltration

After stabalisation: ACE-I/ARB, beta-blocker, aldosterone inhibitor

Ongoing management: Valve surgery; revasc; transplant

24
Q

How does sympathetic system work to increase BP under heart failure?

A

Heart failure there is chronic sympathetic activation which results in the receptors being acted on by the sympathetic system to down regulate.

Causes overall less receptors to be acted on, meaning the effect of sympathetic activation is diminished and cardiac output stops increasing in response to sympathetic activation

25
Q

What can be 3 consequences of cardiomyopathies? [3]

A

Thrombus / PE [1]
Arrhthymias [1]
Heart failure [1]

26
Q

What are features of dilated cardiomyopathy? [1]

What are the physiological consequences of dilated cardiomyopathy? [3]

A

Left or biventricular dilation & systolic dysfunction in absence of CAD, hypertension valvular disease or congenital heart disease. Dilated left ventricle which contracts poorly/has thin muscle

Causes:
- Reduced stroke volume and therefore CO
- Disordered myocytes: impaired ventricular filling
- Increase in preload / end diastolic pressure

27
Q

How does the heart compensate for a reduction in CO due to dilated cardiomyopathy? [2]

A

Frank Starling Mechanism:

  • Sympathetic nervous system activates increase in HR and contractility
  • Subsequent activation of RAAS
28
Q

Which drug classes would you treat dilated cardiomyopathy with? [4]

A

ACE I / ARBs: lower BP
Diuretics: reduce fluid built up
Anti-coagulants: reduce blood clot chances
Beta blockers: control HR

29
Q

How would you treat arrhythmias caused by dilated cardiomyopathy? [3]

What is another treatment possibility? [1]

A

Medication to treat blood clots (anti coagulants)
Pacemaker: control rhythm of heart
ICD: shock heart if need to go into normal rhythm

Surgery: remove areas of heart muscle / whole heart transport

30
Q

What is the genetic reason that HCM may occur?

A

Caused by sarcomeric protein gene mutations e.g troponin T and B- myosin

Mutations in β-myosin heavy chain gene (β-MyHC) cause 30% of all cases.

31
Q

What ECG findings would you find for HOCM? [3]

A

left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
(atrial fibrillation may occasionally be seen)

32
Q

What is intrinsic restrictive lung disease caused by? [1]

Name two pathologies that cause extrinsic restrictive lung disease caused by? [2]

A

Intrinsic: Interstitial Lung Diseases

Extrinsic: Obesity & Myasthenia Gravis (rare long-term condition that causes muscle weakness)

33
Q

Describe the aetiology of IPF xx

Describe the pathophysiology of IPF

A

Occurs due to:Unknown cause [1]

Environmental factors, chronic viral infections, smoking, Fx causes scarring and honeycombing of the lungs: airway remodelling. Causes impaired oxygen transfer.

Airway remodelling cccurs due to:
- fibroblast remodelling and activation: causes fibroblast plaques occurring & collagen deposition. Causes Traction bronchiectasis: where there is irreversible dilatation of bronchi and bronchioles within areas of pulmonary fibrosis
- ↓ Epithelial cell integrity
- Accelerated ageing-associated changes
- Exaggerated fibroblast expansion

34
Q

Describe symptoms of IPF [3]

A
  • exertional dyspnoea
  • clubbing
  • dry cough
35
Q

What would the lung sound like on physical examination of a Ptx with IPF? [1]

A

Fine, high-pitched bibasilar inspiratory crackles (velcro-like sounds

36
Q

Describe the diagnostic pathway for IPF xx

A
  1. Suspected ILD
  2. ID the cause? If yes - not IPF
  3. If no, conduct Chest High Resolution CT Scan. If you see usual interstitial pneumonia (honeycombing lungs) then v likely to have IPF.
    Still unsure?
  4. Lung biopsy
  5. MDT Diagnosis
  6. IPF / Not IPF
37
Q

Which drugs would you use to manage IPF ? [3]

How would you treat IPF via non-pharmacotherapy?

A

Pharmacotherapy:
- Pirfenidone: anti fibrotic agent, decreases pyhysiological deterioration
- Nintedanib : Tyrosine kinase inhibitor. ↓FVC decline

  • Antiacid therapy:IPF with gastro-oesophageal reflux

Non-pharmacotherapy:
- Pulmonary rehab (MDT Team & QoL
- Oxygen therapy
- Lung treatment

38
Q

Which drugs should you NOT combine to treat IPF?

A

Prednisone, Azathioprine & NAC = Harmful AEs

39
Q

Define sarcoidosis

A

Caused by multi system granulomas (is a tiny cluster of white blood cells and other tissue that can be found in the lungs). Inflammation causes multi-system granulomas

Most cases are acute, self-limiting (needs no medicinal treatment)

About 90% of diagnosed cases are deemed to be pulmonary sarcoidosis.

40
Q

What pulse pressure is [1]

Explain which heart murmur has a wide pulse pressure [2]

A

Pulse pressure = Systolic Blood Pressure – Diastolic Blood Pressure

Aortic regurgitation
* Aortic valve insufficiency results in a backward, or regurgitant flow of blood from the aorta back into the left ventricle, so that blood ejected during systole returns during diastole.
* This condition leads to an increase in the systolic pressure and a decrease in the diastolic pressure, which results in increased pulse pressure.

41
Q

Which lymph nodes are most likely for TB to spread to in systemic TB cases? [1]

A

Cervical

Yr 2 EOYS ^2 (42 decks)

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