Ischaemic heart disease Flashcards
what is the differential diagnosis for chest pain
- Angina ->MI/cardiac ischaemia
- Asthma
-pleuretic chest pain -> pericarditis - Aortic dissection
-Pulmonary embolism
-Gastroesophageal reflex disease - Musculoskeletal pain
-Acute pneumonia - Biliary colic
- Esophageal spasm
what are the risk factors
- Obesity
- Age : male greater than 40 ,Postmenopause women
- Family history
- Previous MI
- Hypertension
- Diabetes
- Smoking
8.Metabolic syndrome
( Western diet and lifestyle are a problem )
what is metabolic syndrome ,explain ?
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.
Define Angina
Clinical syndrome characterised by discomfort in the chest ,jaw,shoulders ,back or arm .
- usually last less than 20 minutes .
What are the aggravating factors for angina ?
- exertion
- emotional distress
what makes angina better ?
Relieved by rest
what is the most common cause of Angina ?
Most common cause is Atherosclerosis
Which population has high incidence of IHD?
- the incidence is increasing in all population groups
- Large increase in number of young women
Explain formation of artheroscllerotic plaque
- 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
Decribe the clinical presentation of Angina
- 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
Describe the prognosis of IHD
- 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 is the diagnosis of IHD made ?
- History : risk factors , precipitatinf factors such as anemia ,thyrotoxicosis and tachyarrythmias . HPT,Diabetes
- 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
- 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
what are the primary objective of Angina management ?
1.To prevent MI
2. Reduce symptoms in order to improve qualityy of life .
what is the mnemonic for angina pectoris management ?
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
Explain platelet plug formation/pathways of platelet activation
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)
WHAT IS THE MAO of Aspirin ?
- 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 .
what are the contraindications for Aspirin ?
- people on anti-coagulants
what are the side effect of Aspirit ?
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)
Which other anti-platelet to use if aspirin is contraindicated ?
Clopidogrel (Thienopyridine group)-> inhibit/ADP P2Yreceptor antagonist -> inhibits the second message cascade inside cells
Explain the MOA of Nitrites and why they are given sublingually
- 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)
How is tolerance to nitrates for chronic uses prevented ?
- 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
what are the side effects of nitrites ?
-Postural hypotension (because it is venodilator )
-Headache
- Flushing
what are the contraindication for Nitrates ?
- 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 )
explain the MAO of beta blockers
-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 )
