Test 2: Ben's You Tubes Flashcards
(107 cards)
1
Q
What are the two main categories of Coronary Artery Disease?
A
Chronic Ischaemic Heart Disease and Acute Coronary Syndrome
2
Q
What is the primary function of coronary arteries?
A
To supply blood to the heart muscle (myocardium) itself
3
Q
What is the most common cause of Chronic Ischaemic Heart Disease?
A
Atherosclerosis
4
Q
What causes Vasospastic/Prinzmetal Angina?
A
Vasospasm (sudden constriction) of coronary arteries due to dysregulation of vasoactive substances
5
Q
What is the key difference between ischaemia and infarction?
A
Ischaemia is decreased blood flow, while infarction is tissue death resulting from severe ischaemia
6
Q
How is pain in Stable Angina typically relieved?
A
By rest (decreasing demand) or vasodilators like GTN (increasing supply)
7
Q
Why is Silent Myocardial Ischaemia particularly dangerous?
A
Because there’s no pain to warn the patient to seek medical attention
8
Q
What causes the transition from Stable Angina to Acute Coronary Syndrome?
A
Rupture of the fibrous cap of an atherosclerotic plaque, exposing the necrotic core and forming a thrombus
9
Q
How does the pain pattern differ between Stable and Unstable Angina?
A
Stable Angina has a predictable pattern relieved by rest/GTN; Unstable Angina has changing pain patterns not relieved by rest, with GTN being less effective
10
Q
What blood marker indicates myocardial infarction?
A
Troponin
11
Q
In which conditions would you expect to find elevated troponin levels?
A
NSTEMI and STEMI (but not Stable or Unstable Angina)
12
Q
What is the key ECG difference between NSTEMI and STEMI?
A
STEMI shows ST segment elevation, while NSTEMI does not
13
Q
Why might NSTEMI have similar mortality rates to STEMI despite less occlusion?
A
Because NSTEMI may be perceived as less urgent, leading to delayed treatment, while STEMI patients receive immediate priority care
14
Q
What is the correct order of increasing severity in Acute Coronary Syndrome?
A
Unstable Angina → NSTEMI → STEMI
15
Q
What type of infarct typically occurs with NSTEMI?
A
Subendocardial infarct (partial wall thickness)
16
Q
What type of infarct typically occurs with STEMI?
A
Transmural infarct (full wall thickness)
17
Q
What is the degree of arterial occlusion in STEMI?
A
Complete (full) occlusion
18
Q
What condition commonly leads to Silent Myocardial Ischaemia?
A
Diabetes mellitus with poor glucose control causing autonomic neuropathy
19
Q
What happens to the necrotic core when a plaque ruptures?
A
It becomes exposed to blood, triggering thrombus (clot) formation
20
Q
What is the pain pattern of Stable Angina?
A
Predictable, triggered by exertion
21
Q
What is the pain pattern of Unstable Angina?
A
Unpredictable, changing pattern
22
Q
What is the pain pattern of Silent Ischaemia?
A
No pain
23
Q
How is pain relieved in Stable Angina?
A
Rest and GTN effective
24
Q
How is pain relieved in Unstable Angina?
A
Not relieved by rest, GTN less effective
25
What is the plaque status in Stable Angina?
Stable plaque
26
What is the plaque status in Unstable Angina?
Unstable plaque with ruptured fibrous cap
27
What is the plaque status in Silent Ischaemia?
Usually stable plaque
28
What is the troponin level in Stable Angina?
Normal
29
What is the troponin level in Unstable Angina?
Normal
30
What is the troponin level in Silent Ischaemia?
Normal
31
What is the risk level in Stable Angina?
Lower
32
What is the risk level in Unstable Angina?
Higher
33
What is the risk level in Silent Ischaemia?
Very high (no warning signs)
34
What are the ECG changes in NSTEMI?
No ST elevation
35
What are the ECG changes in STEMI?
ST elevation
36
What is the occlusion type in NSTEMI?
Partial
37
What is the occlusion type in STEMI?
Complete
38
What is the infarct type in NSTEMI?
Subendocardial (partial wall)
39
What is the infarct type in STEMI?
Transmural (full wall)
40
What is the troponin level in NSTEMI?
Elevated
41
What is the troponin level in STEMI?
Elevated
42
What is the treatment priority for NSTEMI?
Often delayed
43
What is the treatment priority for STEMI?
Immediate priority
44
What occurs when oxygen demand exceeds supply through coronary arteries?
Ischaemia
45
What is the progression of atherosclerotic damage?
Stable plaque → Ruptured fibrous cap → Thrombus formation → Arterial occlusion → Tissue death
46
What is the progression of tissue damage?
Ischaemia → Hypoxia → Infarction (tissue death)
47
48
What is heart failure?
The inability of the heart to generate enough cardiac output to meet the body's needs.
49
What is ejection fraction?
The percentage of blood that gets ejected from a ventricle compared to the amount that filled it. Normal is 55-70%.
50
What is systolic dysfunction?
Impairment in the heart's contractility, resulting in decreased ejection fraction despite adequate preload.
51
What is diastolic dysfunction?
Poor ventricular relaxation during diastole, resulting in normal ejection fraction but reduced preload.
52
What is preload?
The amount of blood that fills the ventricle before contraction.
53
What is afterload?
The pressure the ventricle must overcome to eject blood into the circulation.
54
What is cardiogenic pulmonary oedema?
Fluid accumulation in the lungs due to heart failure, specifically left-sided heart failure.
55
What is peripheral oedema?
Swelling in the extremities (typically legs) due to fluid buildup, often seen in right-sided heart failure.
56
What is ascites?
Fluid accumulation in the abdominal cavity, a symptom of right-sided heart failure.
57
What is ventricular hypertrophy?
Thickening of the heart's ventricular walls, often due to chronic hypertension.
58
What is a common cause of systolic dysfunction?
Myocardial infarction (heart attack), which kills heart muscle tissue, reducing contractility.
59
What is a common cause of diastolic dysfunction?
Hypertension, leading to ventricular hypertrophy and reduced chamber volume.
60
What happens when the right side of the heart fails?
Blood backs up into the systemic circulation, causing jugular vein distension, ascites, and peripheral oedema.
61
What happens when the left side of the heart fails?
Blood backs up into the pulmonary circulation, causing cardiogenic pulmonary oedema.
62
How does hypertension lead to heart failure?
Chronic hypertension increases afterload, causing ventricular hypertrophy, which decreases compliance and impairs filling, leading to diastolic dysfunction.
63
What is the most common cause of right heart failure?
Left heart failure, which increases pulmonary pressure and increases the workload on the right ventricle.
64
Compare systolic and diastolic dysfunction regarding ejection fraction.
Systolic dysfunction has decreased ejection fraction (<55%), while diastolic dysfunction has normal ejection fraction (55-70%).
65
Compare left and right heart failure symptoms.
Left heart failure causes pulmonary oedema, while right heart failure causes jugular vein distension, ascites, and peripheral oedema.
66
How do preload and afterload differ?
Preload is the volume of blood filling the ventricle before contraction, while afterload is the pressure the ventricle must overcome to eject blood.
67
What is cardiogenic pulmonary oedema?
Abnormal buildup of fluid in the lungs due to cardiac dysfunction, specifically problems with the left side of the heart.
68
Define 'pulmonary'
Relating to the lungs.
69
Define 'oedema'
Abnormal buildup of fluid in tissues.
70
Define 'cardiogenic'
Originating from or caused by the heart.
71
What structure connects the left atrium and left ventricle?
The mitral valve.
72
What structure separates the left ventricle from the aorta?
The aortic valve.
73
What is valve regurgitation?
When heart valves don't close properly, allowing blood to flow backwards.
74
What is valve stenosis?
When heart valves don't open fully, restricting blood flow.
75
What does PEEP stand for?
Positive End-Expiratory Pressure.
76
How does left heart failure lead to pulmonary oedema?
Left heart failure causes blood to back up in the pulmonary circulation, increasing pressure in pulmonary vessels, which forces fluid into the alveoli.
77
Why might a myocardial infarction lead to cardiogenic pulmonary oedema?
A myocardial infarction damages heart muscle ('dead meat don't beat'), reducing the heart's pumping efficiency and causing blood to back up into the lungs.
78
Explain how mitral valve regurgitation contributes to pulmonary oedema.
Mitral valve regurgitation allows blood to flow backwards from the left ventricle to the left atrium during contraction, causing increased pressure in the left atrium and pulmonary veins, leading to fluid accumulation in the lungs.
79
How does aortic stenosis lead to pulmonary oedema?
Aortic stenosis restricts blood flow out of the left ventricle, causing blood to back up into the left atrium and pulmonary circulation, increasing pressure and forcing fluid into the alveoli.
80
How does PEEP help treat cardiogenic pulmonary oedema?
PEEP increases pressure in the alveoli, which helps force fluid from the alveoli back into the pulmonary circulation.
81
How do vasodilators help in treating cardiogenic pulmonary oedema?
Vasodilators dilate blood vessels, reducing pressure in the pulmonary circulation and helping to move fluid from the alveoli back into circulation.
82
What is the primary goal of treatment for cardiogenic pulmonary oedema?
To reduce fluid in the alveoli by manipulating pressure gradients between alveoli and pulmonary circulation, while also addressing the underlying heart condition.
83
What are the three stimuli for RAAS activation?
(1) Decreased renal perfusion, (2) Sympathetic nervous system activation, and (3) Decreased solute concentration in the distal convoluted tubule.
84
What cells release renin and where are they located?
Juxtaglomerular cells, which are located adjacent to the glomerulus in the kidney.
85
What does ACE stand for and where is it primarily produced?
Angiotensin Converting Enzyme; primarily produced by endothelial cells in the lungs.
86
What are the four main effects of Angiotensin II?
(1) Vasoconstriction of arterioles, (2) Stimulation of thirst, (3) Release of aldosterone, and (4) Stimulation of ADH release.
87
How does aldosterone increase blood pressure?
By increasing sodium reabsorption in the distal convoluted tubule, which leads to water retention through osmosis, increasing blood volume and therefore blood pressure.
88
What are the two names for the hormone released from the posterior pituitary that helps regulate blood pressure?
Antidiuretic Hormone (ADH) and Vasopressin.
89
How does ADH help restore blood pressure?
Through vasoconstriction (increasing peripheral resistance) and increasing water reabsorption in the collecting ducts (increasing blood volume).
90
What effect does alcohol have on ADH and what is the physiological consequence?
Alcohol inhibits ADH, leading to increased urine production (diuresis) and potential dehydration.
91
What is the relationship between the RAAS system and ADH?
Angiotensin II from the RAAS system stimulates the release of ADH, making them interconnected systems for blood pressure regulation.
92
What equation represents blood pressure and how do RAAS and ADH affect its components?
Blood Pressure = Cardiac Output × Total Peripheral Resistance. RAAS and ADH increase total peripheral resistance through vasoconstriction and increase cardiac output by increasing blood volume.
93
What are the four abdominal quadrants?
Right Upper Quadrant (RUQ), Left Upper Quadrant (LUQ), Right Lower Quadrant (RLQ), and Left Lower Quadrant (LLQ).
94
What anatomical landmark is used as the centre point for dividing the abdomen into quadrants?
The umbilicus (navel).
95
Which organs are found in the Right Upper Quadrant (RUQ)?
Liver, gallbladder, right kidney and adrenal gland, and portion of transverse colon.
96
Which organs are found in the Left Upper Quadrant (LUQ)?
Spleen, left lobe of liver, left kidney, stomach, pancreas, and portions of transverse and descending colon.
97
Which organs are found in the Right Lower Quadrant (RLQ)?
Small intestine (portions), ascending colon, appendix, right side of uterus/ovary/fallopian tube (in females), and parts of rectum, right ureter, and bladder.
98
Which organs are found in the Left Lower Quadrant (LLQ)?
Small intestine (portions), descending and sigmoid colon, left side of uterus/ovary/fallopian tube (in females), and parts of rectum, left ureter, and bladder.
99
If a patient presents with pain in the RUQ, what conditions might you suspect?
Possible conditions include gallstones, hepatitis, cholecystitis, or right kidney issues.
100
If a patient presents with pain in the RLQ, what conditions might you suspect?
Possible conditions include appendicitis, right ovarian cyst, or ileocecal Crohn's disease.
101
Why is knowledge of abdominal quadrants important in clinical practice?
It helps pinpoint causes of abdominal pain, improves clinical reasoning, guides physical examinations, and facilitates communication among healthcare professionals.
102
What structure forms the boundary between the upper and lower abdominal quadrants?
An imaginary horizontal line passing through the umbilicus (navel).
103
In which quadrant would you typically find the appendix?
Right Lower Quadrant (RLQ).
104
In which quadrant would you typically find the gallbladder?
Right Upper Quadrant (RUQ).
105
In which quadrant would you typically find the spleen?
Left Upper Quadrant (LUQ).
106
In which quadrant would you typically find the sigmoid colon?
Left Lower Quadrant (LLQ).
107
How does knowledge of abdominal quadrants improve physical examination skills?
It provides a systematic approach to examining the abdomen, helps correlate physical findings with underlying anatomy, and improves diagnostic accuracy.
