pt7 Flashcards

(50 cards)

1
Q

What does the term ‘neoplasia’ literally mean?

A

Neoplasia literally means ‘new growth,’ referring to the abnormal, unregulated proliferation of cells.

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2
Q

What is meant by tumour ‘differentiation’?

A

Tumour differentiation describes how much tumour cells resemble their normal counterparts; well-differentiated tumours closely mimic normal tissue, whereas poorly differentiated tumours do not.

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3
Q

What is pleomorphism, and in which context is it used?

A

Pleomorphism is the variation in size and shape among cells, and it is a common feature seen in anaplastic and malignant cells.

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4
Q

What are tumour giant cells?

A

Tumour giant cells are unusually large cells, often formed by the fusion of several cells, and are characteristic of anaplastic or highly malignant tumours.

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5
Q

Why is dysplasia considered a pre-neoplastic condition?

A

Dysplasia involves disordered growth and architectural disturbance; if persistent, it can progress to carcinoma in situ and eventually to invasive cancer.

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6
Q

What does metastasis indicate about a tumour?

A

Metastasis indicates that a tumour is malignant since only malignant tumours have the capacity to spread to distant sites.

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7
Q

How does lymphatic spread contribute to metastasis?

A

Tumour cells enter lymphatic vessels and travel to regional lymph nodes, where they may establish secondary tumour sites.

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8
Q

How does haematogenous spread differ from lymphatic spread?

A

In haematogenous spread, tumour cells enter the bloodstream and can form metastases in distant organs, such as the liver or lungs.

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9
Q

What are the five main components of the circulatory system?

A

Pump (heart), distributary system (aorta/arteries/arterioles), oxygenation system (pulmonary vessels/lungs), exchange system (capillaries), collecting system (veins/vena cava).

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10
Q

What is the primary function of the heart valves?

A

To maintain unidirectional blood flow through the heart chambers and great vessels.

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11
Q

Name the four cardiac valves.

A

Aortic valve, pulmonary valve, mitral (bicuspid) valve, tricuspid valve.

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12
Q

What tissue makes up the myocardium?

A

Specialized striated muscle cells called cardiac myocytes.

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13
Q

How are ventricular myocytes arranged, and why?

A

In a spiral/circumferential orientation to squeeze blood efficiently on systole and relax on diastole.

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14
Q

When does most coronary blood flow to the myocardium occur?

A

During ventricular diastole, when contracting myocardium isn’t compressing the vessels.

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15
Q

What are the three major epicardial coronary arteries?

A

Left anterior descending (LAD), left circumflex (LCX), and right coronary artery (RCA).

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16
Q

Why is the LAD artery clinically important?

A

It supplies a large portion of the left ventricle and is most often blocked in myocardial infarction.

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17
Q

What is the sinoatrial (SA) node?

A

The heart’s primary pacemaker, located at the junction of the right atrial appendage and superior vena cava.

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18
Q

What is the role of the atrioventricular (AV) node?

A

Delays impulse from atria to ventricles to allow atrial contraction and ventricular filling.

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19
Q

What does the Bundle of His do?

A

Conducts impulse from AV node into the interventricular septum before dividing into bundle branches.

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20
Q

What are Purkinje fibers?

A

Network of fibers extending through the ventricular myocardium to ensure coordinated contraction.

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21
Q

Why does the SA node set heart rate over other pacemakers?

A

It has the fastest intrinsic rate (up to ~200 bpm), overriding slower subsidiary pacemakers.

22
Q

What does the P wave on an ECG represent?

A

Atrial depolarization.

23
Q

What does the QRS complex represent?

A

Ventricular depolarization.

24
Q

What does the T wave represent?

A

Ventricular repolarization.

25
Which ECG segments can indicate myocardial ischemia?
ST-segment changes and T-wave inversions.
26
Define tachycardia and bradycardia.
Tachycardia: heart rate too fast; Bradycardia: heart rate too slow.
27
What is ventricular fibrillation, and why is it dangerous?
Uncoordinated ventricular contractions that fail to pump blood—fatal without immediate treatment.
28
State the Frank–Starling mechanism.
Greater ventricular filling (stretch) increases sarcomere overlap and stroke volume up to an optimal point.
29
How does cardiac hypertrophy compensate for increased workload?
Myocytes enlarge, increasing contractile force and maintaining output under stress.
30
Name three neurohormonal compensatory systems in heart failure.
Sympathetic (noradrenaline), renin–angiotensin–aldosterone system, atrial natriuretic peptide.
31
List four common cardiovascular diseases.
Atherosclerosis, hypertension, stroke, heart failure (also arrhythmia and valve disease).
32
How is hypertension defined clinically?
Sustained diastolic > 89 mm Hg or systolic > 139 mm Hg on repeated measurements.
33
What two factors determine arterial blood pressure?
Cardiac output and peripheral vascular resistance.
34
Which vessels contribute most to peripheral resistance?
Small arterioles (high resistance due to narrow lumen and muscular walls).
35
Give three risk factors for essential hypertension.
Age (vessel stiffness), genetics, obesity/dietary sodium intake, stress.
36
Differentiate essential vs. secondary hypertension.
Essential: idiopathic, multifactorial; Secondary: due to identifiable causes (renal, endocrine, vascular, neurological).
37
Name two renal causes of secondary hypertension.
Renal artery stenosis; chronic kidney disease impairing sodium/water excretion.
38
Which endocrine disorder can cause secondary hypertension?
Cushing’s syndrome (excess cortisol) or hyperaldosteronism.
39
List four classes of antihypertensive drugs.
ACE inhibitors/ARBs, beta-blockers, calcium-channel blockers, diuretics.
40
What is hypertensive heart disease?
Pressure overload causing ventricular hypertrophy and eventually heart failure.
41
How does systemic vs. pulmonary hypertension affect the heart differently?
Systemic → left ventricular hypertrophy; Pulmonary → right ventricular hypertrophy.
42
How can hypertensive left ventricular hypertrophy be diagnosed before symptoms?
ECG changes or echocardiography show increased wall thickness and reduced chamber size.
43
What are common symptoms of hypertension?
Often asymptomatic; may cause headache, nosebleeds, shortness of breath when severe.
44
What major complications arise from long-term hypertension?
Myocardial infarction, stroke (ischemic & hemorrhagic), renal failure, retinopathy, heart failure.
45
What is atherosclerosis?
Thickening and loss of elasticity of arterial walls due to intimal fibrofatty plaques protruding into and obstructing lumens.
46
In which arteries do atherosclerotic plaques primarily develop?
Elastic arteries (e.g., aorta, carotid) and medium/large muscular arteries (e.g., coronary arteries).
47
Which lipoprotein changes are associated with atherosclerosis?
↑ LDL-cholesterol and ↓ HDL-cholesterol.
48
Name the four non-modifiable risk factors for atherosclerosis.
Age, male gender, positive family history, genetic abnormalities (e.g., ACE gene variants).
49
List five modifiable risk factors for atherosclerosis.
Hyperlipidemia, hypertension, smoking, diabetes, obesity, physical inactivity.
50
What are the three principal cellular components of a plaque?
Smooth muscle cells, macrophages, and other leukocytes.