Brainscape's Knowledge GenomeTM

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


See full index

MP323 > L11 - L17 > Flashcards

L11 - L17 Flashcards

1
Q

Cholesterol & LDL’s

  • LDL Pathways
A
  • LDL removed by receptors goes to liver to be utilised or excreted
  • when LDL exceed receptor availability it is taken away by “scavenger pathway” by monocytes and macrophages leading to a high blood cholesterol level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

LDL Scavenger Pathway

  • when LDL level exceeds receptor capacity
A
  1. LDL enters arteries promoting accumulation of monocytes and inflammatory cells causing plaque build up
  2. LDL cholesterol is oxidised as macrophages are newly bound to them. these become foam cells
  3. macrophages recruit smooth muscle cells to site which forms a fibrous cap over plaque
  4. lipids release from foam cells & further ulceration leads to proliferation of atheroma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Platelet Function

  • why antiplatelets needed
A

endothelial blood vessel damage =

  • loss of endothelium antithrombotic properties (adenosine triphosphate & NO)
  • increased procoagulant functions like tissue factor and factor Xa
  • platelets stick to breaks in the endothelium & change conformational to allow fibrinogen binding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Antiplatelets

  • aspirin mechanism of action
A
  1. thromboxane A2 is platelet agonist produced by COX-1
  2. aspirin blocks production of thromboxane A2 by inhibiting COX-1, irreversibly binding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Antiplatelet

  • Clopidogrel (irreversible)
A
  1. ADP platelet agonist produced by platelets
  2. clopidogrel irreversibly inhibits ADP P2Y12 receptor to prevent ADP activating platelets

Ticagrelor
- same receptor but reversibly binds

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

Ischemia

  • definition & symtpoms
A
  • lack of blood supply to heart
  • coronary artery block causes less blood to heart

symptoms - angina, chest pains

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

ACS

  • Angina
  • Causes: HF, severe anaemia, HTN lv hypertrophy
A

Stable - angina on physical exertion, fixed plaques

Unstable - angina on minimal exertion or rest. can be confused for MI, check troponin

Prinzmetals - coronary artery spasm, causes temp ischemia

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

Angina Management

  • treatment
A

Treatment
1 - BB 1st line (if intolerable then rate limiting CCB)
- add CCB if symptoms poorly controlled by BB

  1. sublingual GTN tablets or spray
    - morning and afternoon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cardiac Monitoring

  • Holter Monitor
A

portable cardiac monitoring device to detect silent ischemia

  • records ST segments to check for ST depression of 1-2mm or more
  • this is the telltale sign of ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Angina Severity Classifications

A

Class 1 - angina during prolonged activity

Class 2 - Angina during vigorous activity

Class 3 -symptoms with everyday activity

Class 4 - inability to perform any task without angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Angina ECG & Treatment

A
  • Not seen on ECG because it only causes temporary changes to reading

Treatment:
- lifestyle : no smoking, limit alcohol, diet and exercise
- antiplatelet
- beta blockers (1st Line)
- if intolerant , give rate limiting CCB
- GTN Nitrates (symptom relief)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Angina Treatment

  • Beta Blockers (1st line)
  • treatment
A

Bisoprolol 5–10 mg once a day

  1. acts on B2 receptor , preventing NA binding , stopping vasoconstriction and inc. BP
  2. decreases oxygen demand of heart by lowering rate (less NA) & force of contraction (less sodium entry means less Ca2+ entry)
    - less demand = less ischemia

blocks NA/A binding to Beta-adrenoceptor stopping activation of adenyl cyclase which inc. cAMP to activate PKA. PKA would have increased contractility etc.

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

Treating Angina

  • CCB
    (Verapamil 80-160mg 3 times daily)
A
  • if BB isn’t able to be given , give rate limiting CCB
  1. Blocks calcium entry into L-type calcium channels
  2. reducing heart contractions & lowering oxygen requirement of myocardium muscle
  • ischemia increases Ca influx, inc. contraction from membrane depolarization. CCB prevent this
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Angina Treatment

  • Potassium Channel Activator (Nicorandil)
    10-20mg twice daily titrated up to 40mg if required
A
  • Nicorandil activates K+ ATP channels on SMC to hyperpolarise the membrane, decreasing Ca2+ entry

Nicorandil is a nitrate and a PCA
- at low conc. it dilates coronary arteries
- at high conc. it is PCA

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

Surgical Angina Treatment

  1. Stenting
  2. Angioplasty
  3. Bypass Surgery
A

Stenting - coronary intervention to widen the artery and allow better perfusion

Angioplasty - balloon inserted with tube running through to allow blood flow

Bypass Surgery
- bypass from veins bringing blood to heart, around the blockage, back into arteries

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

STEMI vs. NSTEMI

A

STEMI
- complete occlusion of minor coronary artery or partial occlusion of major coronary artery
- causes partial thickness damage of heart muscle

NSTEMI
- occurs by complete occlusion of major coronary artery previously affected by atherosclerosis
- causes full thickness damage to heart muscle

17
Q

Damage During MI EVENT

  • stages
A

1- irreversible damage can occur within 20-40min after blood flow interruption

2- large amounts of tissue can be saved if flow is restored within 6hrs of coronary occlusion

3- infarction of tissue will lead to cellular changes like disproportionate thinning

18
Q

Diagnosing MI

  • troponin test - released from damaged muscle
  • myoglobin test - present in skeletal muscle not specific to MI
A

Troponin

  • requires rise and gradual fall of troponin
  • or rapid rise & fall of creatinine kinase MB
  • chest pains, SoB and Q-wave plumet

Myoglobin
- released within 1-2hrs of MI , peaking at 13-15hrs

19
Q

Electrical Conduction of Heart

  • SA & AV nodes
  • PQRST
A

P - Wave (initial spike)
- firing of SA node and depolarisation of atria (contraction)

PR interval
- electrical conduction through atria AND AV delay

PR segment
- 0.05 second delay of impulse at AV node

QRS (spike)
- ventricular depolarisation, contraction forcing blood out of heart to body

ST Segment (should be flat)
- the beginning of ventricular repolarization

T Wave
- ventricles repolarize back to base electrical state

20
Q

Electrical Conduction During MI

  • T-waves
  • ST elevation
  • Q depression
A
  1. T waves become tall & narrow at start of MI
    - then become inverted further on
  2. when ST segment raises = NSTEMI
  3. as a result, baseline voltage prior to QRS is depressed
  • during STEMI, ST segment stays at 0 but seems elevated because baseline voltage is below 0
21
Q

ACS Management

  • MONA Therapy
  • during/after MI
A

M - morphine 5-10mg IV slow injection for pain & metoclopramide to counteract sickness

O - oxygen 94-98%

N - nitrates as infusion to dilate blood vessels since sublingual GTN wont work in MI

A - aspirin 300mg stat (if already on antiplatelet therapy give 75mg)

Extras
- Fondaparinux 2.5mg SC to prevent +laque build up
- Ticagrelor 180mg stat

22
Q

Secondary Prevention after MI

A

Dual Anti-Platelet
- Aspirin 75mg
- Ticagrelor 90mg BD

  • Beta Blocker (1yr to lifelong)
  • ACE-I ramapir;
  • High dose statin (atorvastatin 40-80mg)
23
Q

STEMI Immediate Management

A
  1. PCI within first 2hrs
  2. Ticagrelor 180mg loading
  3. aspirin 300mg
  4. thrombolyse with tenectaplase
  5. give BB bisoprolol
24
Q

Heart Failure

  • SoB ,Tiredness, odema
A
  • reduced cardiac output and/or elevated intracardiac pressures. output cant meet metabolic needs
  • Heart Disease : structure abnormality (valves/chambers/muscle)

Systolic HF: heart can’t eject blood properly
Diastolic HF: Heart cant fill with blood properly

25
Q

HF Treatment

  • ACE-I
  • ARB
A

ACE-I
- 1st enalapril 20mg BD
- ramipril if they have MI before HF
- GIVE WITH BETA BLOCKER bisoprolol 2.5mg if patient is stable

ARB (valsartan)
- never use with ACE-I
- give if patient experiences s/e with ACE-I

26
Q

HF Treatment

  • Beta Blocker
  • Aldosterone Antagonist
  • Diuretic
A

Beta Blocker
- Only given to patients with Stable HF
- given with ACE-I
- GIVE FUROSEMIDE FIRST

Aldosterone Antagonist
- eplerenone if EJF is <40%
- for adv HF (NYHC class III - IV)

27
Q

Pharmacokinetic Interactions

  • ADME process affected
A

Adsorption
- doxy cant be given with iron/calcium/zinc
- iron can bind to drug reducing adsorption

Distribution
- weakest pharmacokinetic interactions
- phenytoin displaced from target site by aspirin

Metabolism
- any drug affecting CYP450

Excretion
- lithium is narrow ther. index. if given with diuretic it will inc. conc. causing lithium toxicity

28
Q

Pharmacodynamic Drug Interactions

  • adding second drug causes interaction
A

Synergistic
- drugs enhance each others effect
- good in HTN, bad in Heart Blockage (BB + rl CCB)

Antagonistic
- giving agonist and antagonist at the same time

Metabolic
- digoxin has narrow therapeutic index. with low K+ levels it will sensitise heart to digoxin causing s/e

29
Q

Heart Failure Aetiology

chronic - long-term symptoms
acute - emergency situation rapid HF

A
  1. increased resistance causes HTN and heart muscle hypertrophy , increasing oxygen need
  2. ischemia prevents oxygen supply to heart preventing it from doing its job
  3. Left side failure most common. blood backed up from left atrium into pulmonary veins
    - causes pulmonary oedema
  4. RHS failure much more rare
30
Q

Starlings Law

  • higher preload = greater contraction force
A
  • if fibres are overstretched then contraction is reduced
  • high HR means higher CO. unless excessive HR because of inadequate filling time for heart. so stroke volume decreases
31
Q

Bodies Response to Heart Failure
- Increase Cardiac Output

  1. Sympathetic innervation - NA release
  2. Myocardial Hypertrophy - inc. CO
  3. Hormonal Response - RAAS system
A
  1. inc. sympathetic innervation. NA increases contractility and HR.
    - this causes peripheral vasoconstriction, inc. afterload
  2. Myocardial Hypertrophy - thickening of heart walls, increasing muscle mass and contraction strength
  3. Hormonal Response from reduced Cardiac Output
    - detected by baroreceptors in JG apparatus
    - stimulates kidney renin release, stimulating Ang conversion to AngI
    - causes aldosterone release
    - increases fluid volume, peripheral constriction & BP
32
Q

Diagnosing Heart Failure

  • Chest X-ray
  • ECG
A

Chest X-Ray
- shows heart structure to see if it is enlarged

ECG
- estimate ejection fraction from heart activity

33
Q

Other Drugs in Heart Failure

  • SGLT-2 Inhibitors (dapaglifozin)
  • Exacerbating Drugs
A

SGLT-2 inhibitors
- causes urination, decreasing sodium & glucose in blood
- takes H2O with it to decrease blood pressure
- inc. risk of UTI bc inc. glucose attracts bacteria

Exacerbating Drugs
- NSAID’s, COX2 inhibitors, rate-limiting CCB, corticosteroids

34
Q

Diuretics Use

A

Thiazide
- Bendroflumethiazide 2.5mg OD
- works on distal convoluted tubule, inhibiting Na/Cl channel to stop ion reabsorption

Loop Diuretic
- Furosemide IV, given during stroke/HF
- inhibits Na/K/2Cl channel to stop ion reabsorption. works on proximal convoluted tubule

S/E
- increased urination, don’t take in evening
- angioedema ankle swelling
- causes hypokalaemia

MP323 (4 decks)

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