Brainscape's Knowledge GenomeTM

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


See full index

pharmacology > Ischaemic heart disease > Flashcards

Ischaemic heart disease Flashcards

1
Q

what is the differential diagnosis for chest pain

A
  • Angina ->MI/cardiac ischaemia
  • Asthma
    -pleuretic chest pain -> pericarditis
  • Aortic dissection
    -Pulmonary embolism
    -Gastroesophageal reflex disease
  • Musculoskeletal pain
    -Acute pneumonia
  • Biliary colic
  • Esophageal spasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the risk factors

A
  1. Obesity
  2. Age : male greater than 40 ,Postmenopause women
  3. Family history
  4. Previous MI
  5. Hypertension
  6. Diabetes
  7. Smoking
    8.Metabolic syndrome
    ( Western diet and lifestyle are a problem )
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is metabolic syndrome ,explain ?

A

Metabolic syndrome is a cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes.
- These conditions include hypertension , high blood sugar( but initially the glucose is normal because there incraesed insulin ,then the body body downregulates the insulin receptors -> insulin resistance ->increased glucose ), Central obesity , and abnormal cholesterol or triglyceride levels.

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

Define Angina

A

Clinical syndrome characterised by discomfort in the chest ,jaw,shoulders ,back or arm .
- usually last less than 20 minutes .

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

What are the aggravating factors for angina ?

A
  • exertion
  • emotional distress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what makes angina better ?

A

Relieved by rest

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

what is the most common cause of Angina ?

A

Most common cause is Atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which population has high incidence of IHD?

A
  • the incidence is increasing in all population groups
  • Large increase in number of young women
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain formation of artheroscllerotic plaque

A
  • endothelial damage
  • inflammation with plaque deposition
    (cholesterol ,fribin deposition , foam cells , etc)
  • Angina ( now with the plaque there imbalance between O2 supply to the hear muscle and demand ->chest pain ),Trabsient Ischaemic attach
  • Rupture of the plaque ( the fibrouus cap stability determines rupture and not the size)
  • leading to Cardiovascular death or MI or Ischaemic stroke or critical leg ischaemia
  • the rupture could lead to platelet activation and aggregation
    which can cause occlusive thrombus (completely blocking the bloood flow) or
    -non -occlusive thrombus->healing and resolution ->plaque formation again
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Decribe the clinical presentation of Angina

A
  • chest pain that radiate to the jaw, shoulder ,back or arm
    relieved by rest and made worse by exertion or emotional stress.
    and last <20 minutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the prognosis of IHD

A
  • Good prognosis
  • it is a primaty care disease
    prognosis depends on :
  • left ventricular function
  • number of coronary arteries with siignificant stenosis
  • Extrent of jeopardized myocardium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is the diagnosis of IHD made ?

A
  1. History : risk factors , precipitatinf factors such as anemia ,thyrotoxicosis and tachyarrythmias . HPT,Diabetes
  2. Examination : often little on examination , need to look for macrovascular disease ->diminished peripheral pulses ,bruits etc . Evidence of Ischaemic changes to the heart ->enlarged heart ,signs of HF,S3/S4
  3. Investigations :
    - Bloods -> Glucose ,cholesterol and renal function if required
    - ECG:abnormal resting ECG( pathological Q wave and T wave invertion )
    - left ventricular dysfunction , LVH on ECG

RISK STRATIFICATION :
- CLINICAL->HPT ,Diabetes
- ECG : abnormal resting ECG
-LV DYSFUNCTION

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

what are the primary objective of Angina management ?

A

1.To prevent MI
2. Reduce symptoms in order to improve qualityy of life .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the mnemonic for angina pectoris management ?

A

A-Aspirin and Anti-anginals
B- Beta blockers and BP
C- Cholesterol and Cigarettes
D-Diet and Diabetes
E- Education and Excercise
F- Follow up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Explain platelet plug formation/pathways of platelet activation

A

Hemostasis - stopping bleeding /clot formation
2 phases ->primary hemostasis (formation of platelet plug) and secondary hemostasis( coagulation )
PRIMARY HEMOSTASIS:
- Platelet plug forms at the side of an injured blood vessel
1. Endothelial injury -
- nerves,smooth muscle cells detect injury
-trigger reflexive contraction of vessel(vascular spasm)->decreased blood loss
- Secretion of nitric oxide,prostaglandins stop,secretion of endothelin begins->causing further contraction .
2. Exposure
- damage to endothelial cells exposes collagen
- Damaged cells release Von Willebrand factor (binds to collagen )
3.Adhension
- GP1B surface proteins on platelets bind to Von Willebrand factor .
4. Activation
- Platelet changes shape (forms arms to grab other platelets),releases more von Wilebrand factor,serotonin,calcium,ADP,thromboxane A2(positive feedback loop)->causes platelet recruitment and aggregation
- ADP,thromboxane A2 result in GPIIB/IIIA expression.
5. Aggregation
- GPIIB/IIIA binds to fibrinogen ,links platelets->platelet plug( but weak plug)

COAGULATION CASCADE :
lot of steps but leads to fibrin->intertwines with the platelet plug ->fribin clot (strong blood clot)

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

WHAT IS THE MAO of Aspirin ?

A
  • Aspirin (75-150 mg/day)- NASAID
    -COX inhibitor
  • binds to COX1 and 2
  • Blocking COX1 ->prevent Arachidonic acid from being converted into Thromboxane A2 (remember TXA2 is responsible for platelet recruitment and aggregation together with ADP)
  • it prevents platelet thromboxane formation and inhibits platlet aggregation
  • and this is important in preventing atherosclerotic plaque formation
  • and helps preserve endothelial function .
17
Q

what are the contraindications for Aspirin ?

A
  • people on anti-coagulants
18
Q

what are the side effect of Aspirit ?

A

COX1: protective factors of the stomach (gastric mucosa,cell turnover )
-therefore ,if it is blocked
- Gastrointestinal ulcerations /peptic ulcers
-Dyspepsia (dificulty digesting )
- Upper abdominal pain
-Bleeding (GI and non GI)

19
Q

Which other anti-platelet to use if aspirin is contraindicated ?

A

Clopidogrel (Thienopyridine group)-> inhibit/ADP P2Yreceptor antagonist -> inhibits the second message cascade inside cells

20
Q

Explain the MOA of Nitrites and why they are given sublingually

A
  • they are potent vasodilators
  • venodilate decreasing preload/venous return
  • the heart does not work as hard
  • less myocardial oxygen required
  • improve sx
    best for acute angina and can be used prophylactically
  • works fast ->spit out when pain subsides ( common side effect ->headache ,can use paracetamol)
21
Q

How is tolerance to nitrates for chronic uses prevented ?

A
  • Giving nitrates to chronic users -> can down regulate the receptors -> tolerance.
  • when giving pt 2 times a day , they must take 1 in the morning and 1 in the aternoon but not 14:00m
  • this will provide a nitrate free period .=8 hours
22
Q

what are the side effects of nitrites ?

A

-Postural hypotension (because it is venodilator )
-Headache
- Flushing

23
Q

what are the contraindication for Nitrates ?

A
  • Hypotension
    -Fixed output state such as mitral and aortic stenosis( because alread their cardiac output is trash and now nitrates can reduce venous return can cause more harm)
  • Previous viagra use ( can cause severe /more hypotension )
24
Q

explain the MAO of beta blockers

A

-Block the beta receptors
- decrease heart rate and myocardial contraction
- Thereby decreasing myocardial oxygen requirements.
-Angina onset is delayed or avoided
- keep resting HR st 55-60/min
- HR can be further decreased in symptomatic patients providing no symptoms of bradycardia
- Should be used as first line if there are no contraindications.
(ALL apear to be equally effective in angina )

25
Q

What are contraindications for beta blocker ?

A
  • Asthma
  • COPD with reversibility
  • CCF?
    -Heart block
  • Bradycardia (<50)
26
Q

What are the side effects of Beta blockers?

A

-Impotence
- Bronchospasm
- Lethargy/decreaed exercise ability
-Bradycardia/heart block
-Cold peripheries

27
Q

what are the benefits and disadvantages of Stent ?

A
  1. Helps keep arteries open -> improves blood flow -> improve sx
  2. DISADVANTAGES :
    - There’s a risk of blood clots forming at the stent site, which can lead to heart attacks or strokes.
28
Q

Explain risk modification for Angina pectoris and follow-up

A
  1. LIPID LOWERING
    - Highly benefits role for statins
    - Reduces risk of MI and the need for revascularisation
    - Diet must not be overlooked
    2.SMOKING CESSATION
    - Decreases risk of cardiac event by 45%
    3.HYPERTENSION
    - Beneficial effects on cardiac mortality confirmed in many trials
    - Poorly controlled HPT aggreavates angina
    - Rational prescribing (B blocker) facilitates control of both .
    4.DIABETES
    - Strict control prevents microvascular complications as well as accelerated atherosclerosis.
    5.OBESITY
    - Is commonly associated with angina
    - contributes to other risk factors e.g HPT,Diabetes,hypercholesterolaemia .
    -reduction improves these risks and reduces O2 demand .
    6.EXERCISE
    - there is good trial data to support exercise
    - BP lowering ,Lipid improvement as well .
29
Q

what aspects to focus on during follow-up

A
  • Has the activity decreased
  • changes in anginal symptoms
    is the therapy tolerated ?
  • Are the modifiable risks treated?
  • Has co-morbid illness developed ?
30
Q

What can you refer for ?

A
  1. Failure of medical therapy
  2. for Diagnosi
  3. MI
  4. CCF symptoms or signs
  5. Dizziness or syncopal signs
  6. Poor quality of life
  7. A very positive stress test
31
Q

What is the benefit of giving nitrates sublingually ?

A

1.Rapid Absorption: Sublingual administration allows for quick absorption of the medication into the bloodstream through the mucous membranes under the tongue. This provides rapid relief from acute angina symptoms.
2. Improved Bioavailability: The sublingual route enhances the bioavailability of nitrates, ensuring that a higher proportion of the drug reaches the bloodstream and is available to exert its therapeutic effect.
3.Effective Dose Management:-> can spit it out when the pain subsides
4.Bypass the first pass effect

pharmacology (12 decks)

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