Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Tutorials > Cardiorespiratory CPC? > Flashcards

Cardiorespiratory CPC? Flashcards

1
Q

What is the possible etiology of crushing chest pain?

A
  • -Unstable Angina
  • -Myocardial infarction
  • -Aortic dissection
  • -esophageal reflux/spasm if Cardiac cause excluded
  • -Pericarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do you distinguish unstable angina from myocardial infarction?

A

1) Enzymes not elevated, no ECG changes of infarction

2) Enzymes elevated, ECG changes, ST elevation or NSTEMI, look for arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What investigations would you like to perform in a patient with central chest pain?

A
  • -ECG
  • -Cardiac enzymes e.g.
  • -Troponin levels
  • -CXR
  • -FBC, U&E, lipid profile, glucose, ESR, CRP
  • -PCI urgently if STEMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is a contraindication for arterial blood gases in a patient with suspected MI?

A

hemorrhage following thrombolysis an issue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ST-segment elevation in leads II, III and aVF signifies…

A

inferior MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Q waves suggest

A

An ECG finding that represents the beginning of ventricular depolarization. Normal Q waves are narrow (≤ 40 ms). Pathologic Q waves are abnormally wide (≥ 40 ms) and/or abnormally deep (≥ 2 mV or > 25% of the R wave amplitude) and can develop due to myocardial injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the role of Troponin T in the diagnosis of MI?

A
  • -Cardiac-specific with high sensitivity for myocardial ischemia
  • -The degree of elevation often correlates with the size of the infarct.
  • -High sensitivity troponin assays (HscTn) may detect an increase in serum troponin level as early as 90 to 180 minutes after myocardial ischemia has occurred
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the role of CK-MB in the diagnosis of MI?

A
  • -CK-MB is more specific to cardiac tissue than total CK.
  • -Can be helpful for evaluating reinfarction because of its short half-life but is no longer commonly used
  • -The degree of elevation often correlates with the size of the infarct.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

when the levels of troponin T vs CK-MB normalize?

A

7-10 days vs 2-3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the significance of STEMI compared to none STEMI?

A
  • -transmural vs subendocardial
  • -Classically due to complete occlusion of a coronary artery vs Classically due to partial occlusion of a coronary artery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the contraindications to thrombolysis?

A
  • -Any prior intracranial bleeding
  • -Recent large GI bleeding
  • -Recent major trauma, head injury, and/or surgery
  • -Ischemic stroke within the past 3 months
  • -Hypertension (> 180/110 mm Hg)
  • -Known coagulopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the goal of other blood tests in a patient with MI?

A

1) CBC
- -Looking for anaemia or infection
2) Renal Function Test
- -Establishing a baseline renal function
- -Dehydration and electrolyte imbalances e.g. K
3) Liver Function Test
- -Congestion
4) Coagulation Profile
- -Baseline as anticoagulants will be introduced
5) Fasting Risk Factor Profile
- -Fasting Glucose and Lipid profile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Risk factors for coronary disease?

A
  • -Age
  • -Male
  • -Positive family history
  • -Cigarette smoking
  • -Hypertension
  • -hyperlipidemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the management of STEMI?

A
  • -Pain relief - morphine
  • -Haemodynamic stabilization
  • -O2
  • -Dual antiplatelet agent – aspirin and clopidogrel
  • -Reassurance
  • -Statin plaque stabilization
  • -Sublingual Nitrate
  • -Coronary angiography +/- intervention
  • -Cardiac bypass surgery (if above fails or contraindicated)
  • -Examine risk factors/risk factor reduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Inferior myocardial infarction is associated with acute occlusion of the …

A

right coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the other conditions associated with raised troponins?

A
  • -Cardiac surgery
  • -Cardiac contusion
  • -Myocarditis
  • -HOCM
  • -Cardiomyopathy
  • -Chemotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What factors increase the risk of complications after an MI?

A
  • -Advanced age
  • -Site of infarction
  • -Size of infarct: Transmural v subendocardial
  • -Previous myocardial infarction
  • -Heart failure
  • -Co-morbid conditions
  • -Smoker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the etiology of an MI?

A
  • -Plaque rupture/fissure
  • -Exposure of lipid, smooth muscle foam cells
  • -Thrombin generation and fibrin platelet aggregates
  • -Intra coronary thrombus
  • -Ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the complications of an MI?

A
  • -Arrhythmias
  • -LVF
  • -Pericarditis
  • -Dressler’s syndrome
  • -Death
  • -Cardiogenic shock
  • -Haemopericardium
  • -Valve dysfunction, papillary muscle rupture
  • -Left ventricular aneurysm
  • -Embolus from the left ventricle
  • -DVT. P.E.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why do patients with ischaemic heart disease suddenly drop dead from atheroma of coronary arteries?

A

Arrhythmia usually (ventricular fibrillation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Proximal left anterior descending artery (LAD) occlusion

causes which type of infarct?

A

Extensive anterior (Leads aVL and I can also be affected, V1-V6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

LAD occlusion causes which type of infarct?

A
  • -V1–V2

- -(Antero)septal

23
Q

distal LAD occlusion causes which type of infarct?

A
  • -V3–V4

- -(Antero)apical

24
Q

proximal Left circumflex artery (LCX) occlusion causes which type of infarct?

A
  • -I, aVL

- -Lateral

25
Q

RCA occlusion causes which type of infarct?

A
  • -II, III, aVF

- -Inferior

26
Q

Posterior descending artery occlusion causes which type of infarct?

A

V7-V9

Posterior/posterolateral

27
Q

Infarction of the anterior wall is caused by obstruction of the LAD or its branches. Depending on the extent of anterior wall infarction, it results in ECG changes in the anterior wall leads (V1–6) and/or I and aVL. Infarction of the inferior wall is caused by obstruction of the LCX or RCA or their branches, and ECG changes are seen in leads II, III, and aVF. T/F

A

True

Inferior both RCA or LCX

28
Q

microscopic vs macroscopic changes of myocardium after 0-24 h of MI?

A

1) Early coagulative necrosis (> 4 hours)
- -Release of inflammatory cytokines from necrotic cells → edema, hemorrhage
- -Recruitment of neutrophils (granulocytes)
- -Hypercontraction of myofibrils → wavy fibers
- -Contraction band necrosis (if reperfusion injury has occurred)
2) –0–12 hours: no gross changes
- -12–24 hours: dark mottling

29
Q

microscopic vs macroscopic changes of myocardium after 1-3 days of MI?

A

1) –Extensive coagulative necrosis (4–72 hours)
- -Neutrophilic infiltrate
- -Inflammation spreads to the tissue surrounding infarct.
2) –Hyperemia
- -Yellow pallor

30
Q

microscopic vs macroscopic changes of myocardium after 3-14 days of MI?

A

1) –Macrophage infiltration
- -Granulation tissue surrounds infarct margins (3–10 days)
- -Proliferation of blood vessels into granulation tissue (10–14 days)
2) –Hyperemic border
- -Center: yellow-brown, soft

31
Q

microscopic vs macroscopic changes of myocardium after >2 weeks of MI?

A

1) Granulation tissue becomes denser → collagenous scar formation
2) grayish-white fibrosis

32
Q

what are the causes of Poor cardiac output?

A
  • -Poor left ventricular function due to poor pumping ability of the heart
  • -e.g. MI cardiomyopathy, myocarditis, restrictive pericarditis, severe arrhythmia
33
Q

Classification of Hypertension?

A
  • -Systemic or pulmonary
  • -Essential or secondary
  • -Benign or malignant
34
Q

what are the Clinical signs of Systemic Hypertension?

A

1) Increased BP
2) LV Heave
3) Displaced apex beat
4) Hypertensive retinopathy
5) Atheroma

35
Q

what is malignant hypertension?

A
  • -Terms formerly used to describe moderate (accelerated) and severe (malignant) hypertension occurring with concomitant retinopathy (flame hemorrhages, exudates, and papilledema). The terms moderate and severe hypertensive retinopathy are now preferred.
  • -Occurs in up to 1% of patients with hypertension. There is no firm agreement on the definition of malignant hypertension; some sources also include the presence of nephrosclerosis and hypertensive encephalopathy in the definition. This term is no longer used by the AHA.
36
Q

what is the etiology of essential/systemic hypertension?

A
  • -High BMI
  • -high salt intake
  • -Genetics
  • -Lack of exercise
37
Q

Causes of secondary systemic hypertension?

A
  • -Renal
  • -Cardiac
  • -Endocrine
  • -Neurological
  • -Pregnancy-associated
38
Q

what are the Cardiovascular Causes of Hypertension?

A

–Rigidity of the aorta due to atheroma e.g.
Diabetes, hyperlipidaemia, stress, smoking etc.
–Renal Artery Stenosis
–Coarctation of the aorta

39
Q

what are the Endocrine causes of hypertension?

A 
--Adrenocortical hyperfunction
 (Cushing’s Syndrome, Conn’s Syndrome)
--Pregnancy
--Phaeochromocytoma
--Acromegaly
--Myxoedema
--Thyrotoxicosis
40
Q

Investigations to assess a possible cause of hypertension?

A
  • -Renal assessment
  • -Adrenal assessment
  • -Thyroid assessment
  • -Aortic assessment
41
Q

what is included in renal assessment of hypertension?

A
  • -Urinalysis to assess proteinuria etc.
  • -Urea and creatinine to assess renal status
  • -Renal Size
  • -Assessment of glomerular filtration rate
42
Q

What is the significance of proteinuria?

A

A condition of urinary protein excretion of > 150 mg/day. Classified as microproteinuria (≤ 300mg/day) and overt proteinuria (> 300mg/day). It can be caused by damage to the glomeruli (e.g., minimal change disease, diabetic nephropathy), damage to the tubules (e.g., Fanconi syndrome), or overproduction of proteins (e.g., multiple myeloma). Isolated (i.e. benign) proteinuria can occur in younger patients with fever or after heavy exercise.

43
Q

what is the significance of proteinuria with hypertension?

A
  • -Proteinuria indicates glomerular damage

- -It also is a serious complication of hypertension, signifying malignant hypertension

44
Q

What are the links between hypertension and renal function?

A

Hypertension causes renal failure

Renal Failure causes Hypertension

45
Q

what is the RAAS?

A

A hormonal system that regulates arterial blood pressure and sodium concentration through secretion of renin in response to renal hypoperfusion. Increased renin converts angiotensinogen to angiotensin I, which is converted to angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II both acts as a vasocontrictor and increases secretion of aldosterone, which increases renal reabsorption of sodium and water.

46
Q

The Renin-angiotensin system influences both peripheral resistance and sodium homeostasis. T/F

A

True
–renal hypoperfusion (e.g., hypotension, stimulation of β1 receptors in the kidney) → kidneys release renin → converts angiotensinogen (produced in the liver) to angiotensin I (AT I) → conversion of AT I to angiotensin II through angiotensin-converting enzyme (ACE, mostly produced in the lungs) → angiotensin II acts as a strong vasoconstrictor and induces the secretion of aldosterone by the adrenal cortex

47
Q

what are the functions of AT-II?

A

A peptide hormone that helps maintain blood pressure and blood volume. Effects include aldosterone secretion, peripheral vasoconstriction, and constriction of the efferent arterioles of the kidneys. Generated from Angiotensin I by angiotensin-converting enzyme (ACE) in the lungs.

48
Q

NB the kidney also produces vascular-relaxing or
antihypertensive compounds such as NO and prostaglandins
T/F

A

True

49
Q

What increases renin secretion?

A

–Reduced renal blood flow
–Reduced blood pressure
–Reduced NaCl in nephron
–Excess sympathetic activity
An enzyme that is secreted by renal juxtaglomerular cells in response to low renal blood pressure, beta-1 adrenergic receptor activation, and NaCl deficiency to secure a stable glomerular filtration rate.

50
Q

what is included in the endocrine assessment of hypertension?

A
  • -CT of Adrenal
  • -Urea and electrolytes
  • -Cortisol and aldosterone levels
  • -Thyroid function tests
  • -Adrenaline and noradrenaline assessment
51
Q

how aortic coarctation in assessed?

A
  • -Clinical examination
  • -Feel radial and femoral pulses to detect a lag in Aortic Coarctation
  • -CT of Aorta
52
Q

signs of End organ damage in hypertension?

A
  • -Eye changes
  • -LVH
  • -Features of atheroma
  • -U&E, creatinine, urinalysis
53
Q

what are the CVS consequences of hypertension?

A
  • -LVH
  • -LVF
  • -Renal artery narrowing due to atheroma
  • -Renal arteriolar sclerosis causing renal failure
  • -Atheroma and consequences of organ hypoperfusion ± embolic disease
  • -Blindness due to hypertensive
54
Q

what are the CNS consequences of hypertension?

A
  • -Stroke due to Micro aneurysms and arteriolar narrowing causing ischaemia
  • -Berry Aneurysm Rupture

Tutorials (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions