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Cardiovascular Pathology > CP28 - Cardiovascular Disease 1 > Flashcards

CP28 - Cardiovascular Disease 1 Flashcards

1
Q

what is ischaemic heart disease

A

inadequate blood supply to the myocardium - any imbalance in supply vs demand

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2
Q

what is the pathogenesis of ischaemic heart disease

A

acute/chronic ischaemia

Low diastolic flow especially sub -endocardial

Active aerobic metabolism of cardiac muscle-60 secs of ischaemia before function lost

myocyte dysfunction/death from ischaemia

damage is reversible in 20-30 minutes

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3
Q

what are the different ischaemic heart disease syndromes

A

angina pectoris

acute coronary syndrome,

sudden cardiac death,

chronic ischaemic heart disease

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4
Q

what are the different types of angina pectoris

A

typical/stable - fixed obstruction, predictable relationship to exertion

variant/prinzmetal - coronary artery spasm

crescendo/unstable - often due to plaque disruption

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5
Q

what are the different types of acute coronary syndrome

A

acute MI (+/- ECG ST elevation)

crescendo/unstable angina

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6
Q

how can subendocardial myocardial infarction take place?

A
  • subendocardial myocardium is relatively poorly perfused even under normal conditions
  • if there is a stable atheromanous occlusion of the coronary circulation/an acute hypertension episode
  • then the subendocardial myocardium can infarct without any acute coronary occlusion
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7
Q

what is the different between subendocardial and transmural MI?

A

subendocardial - only affect the subendocardium whereas the transmural affect the entire area of the heart

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8
Q

what does the myocardium look like macroscopically and histologically in less thank 24 hours of occurrence?

A

Macro - normal/dark

Histo - necorsis + neutrophils

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9
Q

what does the myocardium look like macroscopically and histologically in less thank 1-2 days of occurrence?

A

Macro - yellow infarct centre

Histo - necrosis + neutrophils

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10
Q

what does the myocardium look like macroscopically and histologically in less thank 3-7 days of occurrence?

A

macro - hyperaemic border, yellow centre

histo - macrophages

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11
Q

what does the myocardium look like macroscopically and histologically in less thank 1-3 weeks of occurrence?

A

macro - red/gray

histo - granulation tissue

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12
Q

what does the myocardium look like macroscopically and histologically in less thank 3-6 weeks of occurrence?

A

macro - scar

histo - collagen scarr

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13
Q

what are some blood markers which can be used to detect myocyte damage

A

troponins T & I

creatine kinase MB

Myoglobin

lactate dehydrogenase isoenzyme 1

aspartate transaminase

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14
Q

when is troponins T & I detectable ?

A

detectable 2 – 3h, peaks at 12h, detectable to 7 days

raised post MI but also in pulmonary embolism, heart failure, & myocarditis.

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15
Q

when is creatine kinase MB detectable?

A

detectable 2 – 3h, peaks at 10-24h, detectable to 3 days

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16
Q

when is myoglobin detectable?

A

peak at 2h but also released from damaged skeletal muscle

17
Q

when is lactate dehydrogenase isoenzyme 1 detectable?

A

peaks at 3 days and detectable up to 14 days

18
Q

what are some complications for MI?

A
  • contractile dysfunction and chronic cardiac failure
  • arrhythmias
  • infarct extension
  • myocardial rupture
  • pericarditis - Dressler’s syndrome
  • mural thrombus
  • ventricular aneurysm
19
Q

what is familial hypercholesterolaemia

A
  • mutation in genes which involved in cholestrerol metabolism
  • low density lipoprotein receptor gene, Apolipoprotein B
20
Q

what is primary hypertension?

A

usually benign, idiopathic

21
Q

what can cause primary hypertension

A 
Cardiac baroreceptors
Renin-angiotensin- aldosterone system
Kinin-kallikrekin system
Naturetic peptides
Adrenergic receptor system
Autocrine factors produced by blood vessels
Autonomic nervous system
22
Q

what is a common pathway for hypertension?

A

All inherited and acquired forms of share increased net salt balance as a common pathway.

Increased intravascular volume and volume delivery to the heart augment cardiac output and therefore blood pressure.

The resulting tissue perfusion exceeds metabolic demand, leading t autoregulation of blood flow to increased vasoconstriction to reduce blood flow

This results in a steady-state hemodynamic pattern of elevated blood pressure with increased systemic vascular resistance and normal cardiac output.

23
Q

what are some examples for secondary hypertension?

A

renal

endocrine - Cushing Syndrome, primary aldosteronism, phaeochromocyotma - neurotumour present in the medulla of the adrenal glands and so secrete large amount of adrenaline and noradrenaline

cardiovascular - coarction of the aorta, increased intravascular volume, increased cardiac output

neurologic - raised intracranial pressure, acute stress, sleep apnoea

24
Q

what are some effects for hypertension?

A

cardiovascular - hypertensive heart disease

renal - renal failure

cerebrovascular - cerebrovascular accident

25
Q

where does the left side of the heart pump blood to?

A

Left - aorta - body

Right - to the lungs

26
Q

what can happen to the heart if the systemic pressure is too high

A

leads to increased left ventricular blood pressure

the left ventricle undergoes hypertrophy initially without dilation in response to increased work needed to pump blood

if pressure too hight then left ventricle fails to pump and can cause sudden death

27
Q

what can happen to the kidney if hypertension exists

A

arterial intimal fibroelastosis, hyaline arteriolosclerosis - slow deterioration in renal function leading to chronic renal failure

28
Q

what can happen to the brain should hypertension be present?

A

hypertensive encephalopathy

increased risk of rupture abnormal arteries (atheromatous - intracerebral haemorrhage), berry aneurysm of the circle of willis (subarachnoid haemorrhage)

29
Q

what is another name for hypertensive crisis?

A

malignant hypertension

30
Q

what is the presentation for malignant hypertenison?

A

acute hypertensive encephalopathy, renal failure, retinal haemorrhages

31
Q

what is acute hypertensive encephalopathy?

A

Diffuse cerebral dysfunction - confusion, vomiting, convulsion, coma and death

32
Q

what can cause pulmonary hypertension?

A

loss of pulmonary vasculature - chronic obstructive lung disease, pulomary interstital fibrosis, PE, under ventilated alveoli

secondary to left ventricular failure

33
Q

what does pulmonary hypertension cause?

A

increased right ventricle workload, right ventricular myocardial hypertrophy initially without dilation, later dilation and systemic venous congestion as right ventricular failure develops

Cardiovascular Pathology (3 decks)

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