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CBL Year 2 > Chest Pain > Flashcards

Chest Pain Flashcards

1
Q

What is the angle of Louis? Where is it? What is its clinical significance

A

sternal angle
between t4-t5
marks the point at which the costal cartilages of the second rib articulate with the sternum. This is particularly useful when counting ribs to identify landmarks as rib one is often impalpable.

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2
Q

What systems can cause chest pain

A

cvs
respiratory
msk
gastro

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3
Q

What is pleuritic chest pain

A

chest pain on inspiration

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4
Q

Pathologies to think about in chest pain (CVS) important

A

MI
Aortic dissection
pericarditis
angina (stable and unstable)

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5
Q

Pathologies to think about in chest pain (resp) important

A

PE

Pneumothorax

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6
Q

Pathologies to think about in chest pain (msk) important

A

costochondritis

muscle strain / pull

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7
Q

pathologies to think about in chest pain (gastro) important

A

peptic ulcer
indigestion
GERD

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8
Q

athletes ecg

A

can be abnormal but benign - Can have t wave inversions and st elevations

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9
Q

how to calculate hr in ecg

A

look at rhythm strip (lead II)

divide the number of large boxes (5 mm or 0.2 seconds) between two successive QRS complexes into 300.

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10
Q

typical evolution of the ECG changes seen in an ST-elevation myocardial infarction, starting with hyper-acute T-waves and ending with pathological Q-waves

A 
Normal
hyper acute t waves
ST segment elevation
improvement with ST elevation with repurfusion 
T wave inversion
pathological q waves
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11
Q

typical ECG changes in stable angina

A

usually normal between attacks. During an attack there may be a transient ST segment depression, symmetrical T wave inversion or tall, pointed, upright T wave may appear. If the angina is provoked by exertion, an exercise stress ECG should be performed.

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12
Q

typical ECG changes in ACS (acute coronary syndrome)

A

Although the ECG may be completely normal in a patient with myocardial ischemia and evolving infarction, classic ECG changes occur in STEMI. 14 Within minutes, there is J-point elevation, and tall, peaked, “hyperacute” T waves develop; ST-segment elevation and reciprocal-lead ST-segment depression also occur.1

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13
Q

ECG changes in first degree heart block

A

here is delay, without interruption, in conduction from atria to ventricles
‘Marked’ first degree heart block is present if PR interval > 300ms

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14
Q

ECG changes second degree heart block Mobitz type II

A

A form of 2nd degree AV block in which there is intermittent non-conducted P waves without progressive prolongation of the PR interval

(PR intervals are consistent but some P waves do not conduct) - you get a normal looking P and QRS and then a random p sometimes without a QRS

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15
Q

ECG changes second degree heart block Mobitz type I

A

increasing delay of AV nodal conduction until a P wave fails to conduct through the AV node. This is seen as progressive PR interval prolongation with each beat until a P wave is not conducted. There is an irregular R-R interval.

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16
Q

ECG findings in atrial fibrillation

A

Irregularly irregular rhythm
No P waves
Absence of an isoelectric baseline
Variable ventricular rate
QRS complexes usually < 120ms, unless pre-existing bundle branch block, accessory pathway, or rate-related aberrant conduction
Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude > 0.5mm)
Fibrillatory waves may mimic P waves leading to misdiagnosis

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17
Q

ECG changes suggestive of PE (including S1 Q3 T3)

A

A large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together indicate acute right heart strain

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18
Q

Normal BP

A

120/80

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19
Q

pre hypertension bp

A

systolic: 120–139 mm Hg diastolic: 80–89 mm Hg

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20
Q

hypertension bp

A

systolic: 140 mm Hg or higher diastolic: 90 mm Hg or higher

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21
Q

hypotension bp

A

systolic blood pressure to less than 90 mm Hg or mean arterial pressure of less than 65 mm Hg. It may be relative to a decrease in diastolic blood pressure to less than 40 mm Hg.

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22
Q

define accelerated hypertension

A

defined as a recent significant increase over baseline BP that is associated with target organ damage. This is usually seen as vascular damage on funduscopic examination, such as flame-shaped hemorrhages or soft exudates, but without papilledema.

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23
Q

retinal changes in accelerated hypertension

A

retinal vascular damage caused by hypertension. Signs usually develop late in the disease. Funduscopic examination shows arteriolar constriction, arteriovenous nicking, vascular wall changes, flame-shaped hemorrhages, cotton-wool spots, yellow hard exudates, and optic disk edema.

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24
Q

Complications of hypertension (serious)

A

stroke
retinopathy (damage to retina vasculature)
MI
Aortic dissection
abdominal aortic dissection
left ventricular hypertrophy and nephropathy

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25
Q

recognise Left ventricular hypertrophy on ECG

A

Voltage Criteria

Limb Leads

R wave in lead I + S wave in lead III > 25 mm
R wave in aVL > 11 mm
R wave in aVF > 20 mm
S wave in aVR > 14 mm

Precordial Leads

R wave in V4, V5 or V6 > 26 mm
R wave in V5 or V6 plus S wave in V1 > 35 mm
Largest R wave plus largest S wave in precordial leads > 45 mm
Non Voltage Criteria

Increased R wave peak time > 50 ms in leads V5 or V6
ST segment depression and T wave inversion in the left-sided leads: AKA the left ventricular ‘strain’ pattern

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26
Q

aortic dissection symptoms

A

Sudden severe chest or upper back pain, often described as a tearing or ripping sensation, that spreads to the neck or down the back.
Sudden severe stomach pain.
Loss of consciousness.
Shortness of breath.

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27
Q

abdominal aortic aneurysm rupture symptoms

A

sudden, severe pain in the tummy or lower back. dizziness. sweaty, pale and clammy skin.

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28
Q

physiology of left coronary blood flow

A

left coronary artery (LCA) arises from the left posterior aortic sinus and quickly bifurcates into the left circumflex artery (LCX) and left anterior descending artery (LAD), which supply blood to the left atrium and left ventricle

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29
Q

physiology of right coronary blood flow

A

right coronary artery (RCA), arising from the anterior aortic sinus, supplies blood to the right atrium, right ventricle, sinoatrial node, atrioventricular (AV) node, and select portions of the left ventricle.

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30
Q

define atherosclerosis

A

thickening or hardening of the arteries. It is caused by a buildup of plaque in the inner lining of an artery. Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin. As it builds up in the arteries, the artery walls become thickened and stiff.

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31
Q

four stages of atherosclerosis

A

1) endothelial tissue injury: damage can occur from smoking, diabetes, abnormal level of cholesterol and other lipid, and force (hypertension)
2) Lipoprotein deposition: lipoprotein molecules can gain entry where they are then modified by oxidation (via free radicals or oxidizing enzymes) or glycation (in diabetes). This modified lipoprotein, or LDL, is inflammatory and able to be ingested by macrophages, creating “foam cells” and causing a “fatty streak” in the arterial wall.
3) inflammatory reaction: The modified LDL is antigenic and attracts inflammatory cells into the arterial wall. Also, after endothelial injury, inflammatory mediators are released further, increasing leukocyte recruitment.
4) smooth muscle cell cap formation: Smooth muscle cells migrate to the surface of the plaque, creating a “fibrous cap.” When this cap is thick, the plaque is stable; however, thin capped atherosclerotic plaques are thought to be more prone to rupture or erosion, causing thrombosis.

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32
Q

concept of ischaemic heart disease

A

term given to heart problems caused by narrowed heart arteries. When arteries are narrowed, less blood and oxygen reaches the heart muscle. This is also called coronary artery disease and coronary heart disease.

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33
Q

Compare and contrast stable angina with acute coronary syndromes.

A

Stable angina is a chest discomfort due to myocardial ischemia that is predictably reproducible at a certain level of exertion or emotional stress. The spectrum of ACS includes unstable angina (UA), non–ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI).

Stable angina - brought on by exertion
ACS - more blockage - brought on by anything!

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34
Q

invasive and un-invasive treatments for MI

A

These aims can be achieved medically using intravenous (i.v.) thrombolysis or invasively either with intracoronary (i.c.) thrombolysis, percutaneous transluminal coronary angioplasty (PTCA), or bypass surgery.

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35
Q

what is thrombolysis

A

also called fibrinolytic therapy, is the breakdown of blood clots formed in blood vessels, using medication. It is used in ST elevation myocardial infarction, stroke, and in cases of severe venous thromboembolism.

the “clot-busting” drug will be delivered through a peripheral intravenous (IV) line, usually through a visible vein in your arm.

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36
Q

Potential complications of MI

A 
arrhythmias
 ventricular wall aneurysm
ventricular wall rupture
 mitral valve prolapse
Dressler’s syndrome 
 thromboembolic complications.
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37
Q

what is Dressler’s syndrome

A

is a type of inflammation of the sac surrounding the heart (pericarditis). Dressler syndrome is believed to be an immune system response after damage to heart tissue or to the sac surrounding the heart (pericardium)

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38
Q

what percentage of people are right coronary artery dominant ?co-dominant? left posterior descending?

A

RCA - 70%
co - 20%
left - 10%

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39
Q

atherosclerotic constitutional risk factors

A

age
gender (earlier age and greater frequency in males compared to females)
genetics

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40
Q

atherosclerotic modifiable risk factors

A

hypertension (> risk of IHD by 60%)
hyperlipidaemia/hypercholesteramia
smoking
diabetes

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41
Q

describe stable angina (likely symptoms)

A 
pain over sternum radiating to left shoulder/ arm, jaw, tongue, teeth
pain duration from seconds to hours
sharp, sticking, stabbing, knifelike
obstruction >60-70%
 relieved by rest
ECG normal or ST segment depression
no cardiac biomarkers (troponin, CRP)
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42
Q

What is a CABG

A

coronary artery bypass graft

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43
Q

what are lipids

A

organic biomolecules which are soluble in non-polar solvents and much less soluble in water
they themselves are non-polar

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44
Q

major lipids in the plasma are

A

fatty acids
TAG - triacylglyerols/triglycerides
cholesterol
phospholipids

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45
Q

discuss triaclyglycerols

A

form of storage of energy (more efficient than glycogen)
formed in liver and adipose tissue
metabolism of them is regulated via triglyceride lipase

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46
Q

discuss cholesterol (few facts)

A

is a component of membranes
bile acids - synthesised in the liver and stored in gallbladder
involved in vitamin d synthesis
involved in steroid synthesis (aldosterone, cortisol and sex hormones)

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47
Q

what is HMG CoA reductase

A

stage in cholesterol synthesis where statins come in

statin is the enzyme inhibitor to stop the synthesis of cholesterol

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48
Q

what do lipoproteins consist of

A

consist of a non-polar core and a surface layer of phospholipids, cholesterol and apolipoproteins

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49
Q

what do apolipoproteins do

A

let body work out which lipoproteins are which

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50
Q

are chylomicrons TAG rich or cholesterol rich

A

TAG rich

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51
Q

are LDL TAG rich or cholesterol rich

A

cholesterol rich

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52
Q

5 lipoproteins

A 
chlymicrons
VLDL
IDL
LDL
HDL
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53
Q

chylomicrons description

A

major transport of dietary fat (exogenous)
90% TAG
TAG removed from them by lipoprotein lipase
also transports cholesterol and fat-soluble vitamins

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54
Q

How does the body get rid of chlyomicrons

A

by the liver

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55
Q

VLDL description

A

-very low density lipoprotein
principal transport form of endogenous TAG
formed in the liver
TAG removed by LPL, similar to chylomicrons - making IDL (intermediate density lipoprotein)
more TAG removed with hepatic TAG lipase to form LDL

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56
Q

LDL description

A

-low density lipoprotein
formed from VLDL via IDL
10% TAG 50% cholesterol
binds to LDL receptors on cell membranes, then are broken down releasing cholesterol
uptake of LDL in the arterial wall contributes to atherosclerosis
LDL = bad cholesterol

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57
Q

HDL description

A

high density lipoprotein
synthesised in liver (and gut) - initially as nascent hdl (disc shaped)
carry cholesterol from adipose tissue to the liver and to tissues for steroid hormone synthesis
HDL = good cholesterol, want high proportion of this on blood tests

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58
Q

3 lipid disorders

A

familial hypercholesterolaemia
type III hyperlipidaemia
hypertriglyceridaemia

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59
Q

describe familial hypercholesterolaemia

gene? raised what? mutations affecting what?

A

autosomal dominant
raised cholesterol - usually TAG level is normal
several mutations affecting the LDL receptor pathway
genetic testing is available in UK

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60
Q

signs of familial hypercholesterolaemia

A 
tendon xanthomata (swelling of knuckles, knees or achilles tendon)
xanthelasmata (small clumps of cholesterol near inner corner of eye)
corneal arcus ( pale white ring around iris)
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61
Q

define pathgnomonic

A

(of a sign or symptom) specifically characteristic or indicative of a particular disease or condition.

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62
Q

management of familial hypercholesterolaemia

A

refer to lipid clinic
cascade testing (to identify relatives with it)
start high intensity statin treatment
include diet and lifestyle advice

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63
Q

describe type III hyperlipoproteinaemia

gene, polymorphism of? what are increased? signs? treatment?

A 
autosomal recessive 
polymorphism of APOE2
cholesterol and TAG are increased
signs: palmar xanthomata ( in creases of palms) and eruptive xanthomata on knees and elbows
generally responsive to diets or statins
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64
Q

causes of primary hypertriglyceridaemia

A

familial combined hyperlipidaemia

polygenic hypertriglcyeridaemia

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65
Q

causes of secondary hypertriglyceridaemia

A

uncontrolled diabetes
hypothyroidism
alcohol related liver disease

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66
Q

most common side effect of statins

A

muscle pain

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67
Q

what does the drug ezetimibe do

A

decreases absorption of cholesterol from the gut
not licensed for first line use - but can be used in combination with statins for patients with familial hypercholesteramia

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68
Q

describe primary prevention of lipid lowering therapy

A

lifestyle modification, address other CVS risks

if risk assessment indicates then start atorvastatin 20mg when >10% risk of developingCVD in 10 years

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69
Q

describe secondary prevention of lipid lowering therapy

A

start atorvastatin 80mg unless lower dose is indicated

do not delay treatment to manage modifiable risk factors

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70
Q

why is myoglobin used as a marker for myocardial necrosis

A

its released earlier from damaged cells than other cardiac markers allowing for earlier detection of acute MI

71
Q

troponin as a cardiac marker

A

type of protein found in the heart
only found in the blood when the heart muscle is damaged
indicator of damage but not an indicator of the mechanism to which its damaged

72
Q

potassium effect on heart

A

keeps heart beating at the right pace

helps to control electrical signals in the myocardium

73
Q

effects of hypokalaemia and hyperkaleamia on the heart

A

causes arrhythmias

74
Q

what is myositis

A

name for a group of rare conditions. The main symptoms are weak, painful or aching muscles. This usually gets worse, slowly over time. You may also trip or fall a lot, and be very tired after walking or standing.
can be caused by statins

75
Q

9 potentially modifiable risk factors for CVD

A 
smoking
poor diet
hypercholesteramia
hypertension
insufficient physical activity
obesity
diabetes
stress
excess alcohol consumption
76
Q

assessment tool for CVD

A

QRISK3 - use an online calculator

77
Q

Diagnostic criteria for MI

A

rise and/or fall in cardiac biomarkers & one of following:
symptoms of ischaemia
new significant ST changes or new LBBB
development of pathological Q wave on ECG
imaging evidence of new loss of viable myocardium
identification of intracoronary thrombus by angiography

78
Q

ECG changes in hyperkalaemia

A

tented t waves, reduced P wave amplitude

79
Q

causes of hyperkalaemia

A

acute kidney injury
chronic kidney disease
drugs - (potassium-sparing diuretics, ACE Inhibitors, NSAIDS
mineralocorticoid deficiency (Addison disease)

80
Q

hypokalaemia and the heart

A

increases the gradient across the cardiac cell membrane -increases the action potential and therefore reducing cardiac excitability
may cause arrhythmia’s such as AF

81
Q

ecg changes in hypokalaemia

A

reduced t waves
st depression
prolonged PR interval

82
Q

causes of hypokalaemia

A

gastrointestinal loss - vomiting or diarrhoea
endocrine conditions - increased mineralocorticoid activity (conn’s disease, Cushing syndrome)
diuretics - non potassium sparing
insulin treatment with no potassium supplementation

83
Q

causes for secondary hypertension

A 
chronic kidney disease
renovascular hypertension (renal artery stenosis)
phaeochromocytoma (excess adrenaline)
Conn's syndrome (excess aldosterone)
Cushing syndrome (excess cortisol) 
Acromegaly (excess GH)
Coarction of the aorta
pregnancy
84
Q

lab investigations for hypertension

A 
plasma creatinine
plasma potassium
urinalysis for protein
plasma renin/aldosterone
dexamethasone suppression test
urinary catecholamines
85
Q

how does chronic kidney disease cause secondary hypertension

A

because of fluid retention

86
Q

how does phaeochromocytoma cause secondary hypertension

A

produces too much adrenaline and noradrenaline

because of stimulation of cardiac beta adrenoreceptors

87
Q

how does conn’s or cushings syndrome cause secondary hypertension

A

excess aldosterone causes sodium retention

88
Q

6 complications of hypertension

A
  1. stroke
  2. heart failure
  3. kidney disease
  4. eye disease
  5. diabetes
  6. pre-eclampsia
89
Q

what is considered normal blood pressure?

A

systolic of 120-129

diastolic of <80-84

90
Q

what is considered high normal blood pressure?

A

130-139 systolic

85-89 diastolic

91
Q

blood pressure reading of hypertension

A 
grade 1 (mild): systolic 140-159 and diastolic 90-99
grade 2 (moderate): systolic 160-179 and diastolic 100-109
grade 3 (Severe): >180 systolic and >110 diastolic
92
Q

primary hypertension

A

90-95% of cases - termed “essential” or “idiopathic”

93
Q

secondary hypertension

some examples of what cause it

A

about 10% of cases

  • renal or renovascular disease
  • endocrine disease: phaeochomocytoma (tumour of adrenal medulla), Cushings syndrome (excess cortisol), Conn’s syndrome (excess aldosterone), Acromegaly (excess growth hormone), hypo/hyper thyroidism, pregnancy, coarctation of aorta, iatrogenic (contraception/HRT)

Secondary high blood pressure (secondary hypertension) is high blood pressure that’s caused by another medical condition

94
Q

does hypertension cause hypertrophy

A

yes

95
Q

What determines blood pressure

A

MAP=CO x TPR

mean arterial pressure = cardiac output x total peripheral resistance

96
Q

what is the physiological role and source of Nitric Oxide (Vascular SM relaxation mediators)

A

physiological role: paracrine mediator

source: endothelium

97
Q

what is the physiological role and source of Atrial Natriuretic Peptide (ANP) (Vascular SM relaxation mediators)

A

physiological role: reduce BP

source: atrial myocardium, brain

98
Q

what is the physiological role and source of Vasoactive intestinal Peptide (VIP)
(Vascular SM relaxation mediators)

A

physiological role: digestive secretion and relax smooth muscle
Source: neurons

99
Q

What is the physiological role and source of histamine

Vascular SM relaxation mediators

A

physiological role: increase blood flow

source: mast cells

100
Q

what is the physiological role and source of adrenaline

Vascular SM relaxation mediators

A

physiological role: increase flow to skeletal muscle, heart and liver
source: adrenal medulla

101
Q

what is the physiological role and source of Ach (via NO and decreased NA)
(Vascular SM relaxation mediators)

A

physiological role: erection

Source: parasympathetic nerves

102
Q

what is the physiological role and source of bradykinin

Vascular SM relaxation mediators

A

physiological role: increases local blood flow via NO

source: tissues

103
Q

what is the physiological role and source of adenosine

Vascular SM relaxation mediators

A

physiological role: increases blood flow to match metabolism

source: hypoxic cells

104
Q

What is the physiological role and source of prostanoids

Vascular SM relaxation mediators

A

physiological role: relaxation and/or contraction in various tissues
source: autocrine/paracrine

105
Q

ACD algorithm for drugs for hypertension

A

Younger than 55years then give A which is ACE inhibitors as first line
over 55yrs or black patients of any age give C (Ca channel blockers) or D (Diuretics) as first line

Second line: give A+C or A+D

Third line: A+C+D

Fourth line: Add either: further diuretic therapy or alpha-blocker or beta-blocker or consider seeking specialist advice

106
Q

Brief description of ACE inhibitors as used for regulation of BP
(including two commonly used ones, and some side effects)

A

Long term control of BP involves renin angiotensin aldosterone system (RAAS)
angiotensin is a vasoconstrictor

catopril and enalapril are prototypic drugs

Side effects: Rash, hyperkalaemia, taste disturbances, first dose hypotension

(Angiotensin-converting enzyme (ACE) inhibitors are medications that help relax the veins and arteries to lower blood pressure. ACE inhibitors prevent an enzyme in the body from producing angiotensin II, a substance that narrows blood vessels)

107
Q

describe calcium channel blockers in regulating BP

A

lower BP
prevent calcium from entering cells of heart and arteries
calcium causes heart and arteries to contract more frequently
by blocking calcium, calcium channel blockers allow blood vessels to relax and open

Dihydropyridines - Nifedipine, Amlodipine

108
Q

Side effects of calcium channel blockers in regulating BP

A

peripheral oedema

dizziness

109
Q

3 classes of diuretics and some examples and strength

A

loop agents (examples: furosemide, bumetanide) - powerful.. up to 30% filtered Na

Thiazide (example: hydrochlorothiazide) - mild diuretic effect <10% filtered Na

K sparing (Examples: Amiloride, Spironolactone) - weak diuretics <5% filtered Na

110
Q

Describe thiazides (diuretics) drugs

A

a drug that increases urine flow
act directly on the kidneys and promote diuresis (urine flow) by inhibiting the sodium/chloride cotransporter located in the distal convoluted tubule of a nephron (functional unit of a kidney)

They decrease sodium reabsorption which increases fluid loss in urine, which in turn decreases extracellular fluid and plasma volume

it reduces cardiac output and lowers blood pressure

111
Q

side effects of thiazide (diuretic) drugs

and what can it reduce the efficacy of

A

electrolyte disturbances
decrease glucose tolerance
can reduce efficacy of anticoags and uricosurics -(substances that increase the excretion of uric acid in the urine, thus reducing the concentration of uric acid in blood plasma.)

can increase LDL and cholesterol

112
Q

beta blockers effect on the heart

A

(also known as beta adrenergic blocking agents)
they reduce blood pressure
block effects of hormone adrenaline
cause heart to beat more slowly and with less force, also help to widen veins and arteries to improve blood flow

113
Q

examples of beta blockers

A

Bisoprolol
Atenonol
Propranolol

114
Q

When are beta blockers used (or not)

A

not used to treat ONLY high blood pressure, only used when diuretics haven’t worked etc.

used to prevent, treat or improve symptoms of:
Arrhythmia 
Heart failure
Angina
Heart attacks
Migraine
certain types of tremors
115
Q

three common side effects of beta blockers

A

cold feet/hands
weight gain
fatigue

116
Q

how do direct renin inhibitors work

A

block the enzyme renin from triggering a process that helps regulate blood pressure (the angiotensin-aldosterone system)
so blood vessels relax and widen, making it easier for blood to flow through the vessels

117
Q

Causes of heart failure

A

volume overload: valve regurgitation
pressure overload: systemic hypertension, outflow obstruction
loss of muscle: post MI, chronic ischaemia, connective tissue diseases, infection, poisons
restricted filling: pericardial diseases, restrictive cardiomyopathy, tachyarrhythmia
Chronic heart failure

118
Q

define pathophysiology

A

the disordered physiological processes associated with disease or injury

119
Q

pathophysiology of heart failure

A 
inadequate tissue perfusion
volume overload
oedema
enlarged ventricles
spherical shape
reduced efficacy
120
Q

what does RAP stand for (chest pain case)

A

right atrial pressure

121
Q

what drugs for HF improve the symptoms

A

nitrates (acute treatment to quickly reduce RAP - right atrial pressure)
potent diuretics (loop agents to reduce RAP)
ACE inhibitors
Digoxin

(Digoxin is a type of drug called a cardiac glycoside. Their function is to slow your heart rate down and improve the filling of your ventricles (two of the chambers of the heart) with blood. For people with atrial fibrillation, where the heart beats irregularly, a different volume of blood is pumped out each time.)

122
Q

Nitrates and HF

A

they dilate the blood vessels of the heart to reduce stress on heart

they have a direct relaxant effect on vascular smooth muscle

example: mononitrate, isosorbide dinitrate

123
Q

what is Digitalis drug?

A

made from plant foxglove that stimulates heart muscle

124
Q

digitalis drug actions

A

2 up 2 down rule
for heart

increased force
increased excitability
decreased A-V conduction
decreased rate

125
Q

when to use digitalis

A

indicated when heart failure with atrial flutter/fibrillation
more likely to be given to older sedentary patients
long half life means careful titration of patient does is indicated

126
Q

what are receptor sympathomimetics

A

agents which in general mimic responses due to stimulation of sympathetic nerves. These agents are able to directly activate adrenergic receptors or to indirectly activate them by increasing noradrenaline and adrenaline (mediators of the sympathoadrenal system) levels.

127
Q

what is a pulmonary embolism

A

thrombus within the pulmonary arterial circulation

usually arises from embolisation of proximal DVT from lower limb through R heart

128
Q

virchows triad

A

hypercoagulability
endothelial injury
venous stasis

129
Q

what does CTEPH stand for

A

chronic thromboembolic pulmonary hypertension

130
Q

Describe CTEPH

A

chronic thromboembolic pulmonary hypertension
chronic breathlessness, hypoxia and right sided heart failure
caused by obstruction of major pulmonary arteries
clots are replaced by fibrous tissue
lifelong anticoags are recommended

131
Q

symptoms of a PE

A

breathlessness (Dyspnoea)
chest pain ( can be pleuritic or non pleuritic)
haemoptysis
syncope or pre-syncope (loss of consciousness or feeling faint)
fever
unilateral leg swelling (if associated with a DVT)
palpitations
generally low grade fever

132
Q

clinical signs of a PE

A

tachycardia
tachypnoea
hypotension (its a severe PE as it effects L heart CO)
hypoxia
right heart strain
unremarkable respiratory exam
rarely pleural rub (late and rare feature as part of lung has died)

133
Q

5 aims of clinical assessment and investigations of a PE

A
  1. does the patient have a pe?
  2. severity of pe (high, intermediate or low mortality risk)
  3. why has patient had a clot (risk factors for VTE or underlying cause)
  4. any cautions or contraindications to anticoagulants?
  5. other important considerations (suitability for outpatient management)?
134
Q

What scoring system do you use to assess likelihood of PE (think MDCalc)

A

Wells score for PE

135
Q

Clinical investigations of suspected PE

A

D -Dimer: VTE very unlikely if wells score is unlikely and negative D-Dimer

Arterial blood gas (if done): may be normal but could also be hypoxia, hypocapnia and respiratory alkalosis

Other blood tests of: FBC, renal, liver, clotting, troponin, CRP and Ca2+

136
Q

PE manifestation on a ECG

A

S1Q3T3

Deep S wave in lead I ( the first downward deflection of the QRS complex that occurs after the R wave.)
Q wave in lead III
inverted T wave in lead III

137
Q

what scan is usually used to confirm diagnosis of PE

A

CTPA

(CT pulmonary angiogram) performed with contrast material

138
Q

CXR to diagnose PE

A 
usually shows normal CXR
rarely can show:
-reduced vascularity in peripheral lung
-enlargement of central pulmonary artery 
-pleural based area of increased opacity
-wedge shaped infarct
139
Q

when would you use VQ SPECT or planar scan to diagnose PE

A

may be considered if CXR is normal and young patient (esp women of childbearing age) or contraindication to CT (e.g. contrast allergy or severe renal impairment)

140
Q

What to do if suspected PE with wells score of more than 4 points but CTPA negative

A

DVT suspected so consider proximal leg vein US

or DVT not suspected so stop any anticoags and think about other diagnoses

141
Q

criteria for haemodynamic instability

A
  • cardiac arrest
  • systolic BP <90mmHg
  • Vasopressors required to achieve a BP>90mmHg despite an adequate filling status, in combination with end organ hypoperfusion
  • systolic BP drop of >40mmHg for >15min, not caused by new onset arrhythmia, hypovolaemia or sepsis
142
Q

What scoring system do you use to assess mortality risk of PE

A 
sPESI 
-Simplified Pulmonary Embolism Severity Index 
-Includes:
Age (<80(0),>80(+1))
history of cancer: no(0), yes (+1)
history of chronic cardiopulmonary disease: no(0), yes(+1)
heart rate bpm: <110(0), >110(+1)
Systolic BP mmHg: >100 (0), <100 (+1) 
O2sats: >90%(0), <90%(+1)
143
Q

What to do with a patient who has an acute PE, is on anticoagulants but is haemodynamically unstable

A

reperfusion treatment and haemodyamic support

144
Q

Preferred anticoagulants for PE

A

rivaroxaban and Apixaban (can be initiated without heparin)

145
Q

When is outpatient management of a PE not suitable

A
  • HR>110, systolic BP <100, requirement for inotropes, critical care, thrombolysis or embolectomy
  • SaO2 <94%
  • Evidence of R heart dysfunction
  • Active bleeding or risk of major bleeding
  • On anticoagulants at time of PE
  • Severe pain (requiring opiates)
  • Other co-morbidities requiring hospital admission
  • Chronic kidney disease
146
Q

Talk about anticoagulant dose and duration for a VTE

A

initial treatment for acute PE: 3-6 months (therapeutic dose)
after that decision is who stays on them long term and who doesn’t: balance risk of long term bleeding and recurrence

147
Q

difference between a therapeutic dose and a prophylactic dose

A

therapeutic: quantity which is required to elicit the desired therapeutic response in the individual in the treatment of disease or ailment.
prophylactic: A preventive measure. The word comes from the Greek for “an advance guard,” an apt term for a measure taken to fend off a disease or another unwanted consequence.

148
Q

patient with a provoked PE: how long should you keep them on anticoagulants

A

3-6 months

149
Q

patient with an unprovoked PE or persistent risks: how long should you keep them on anticoagulants

A

consider long term

150
Q

How many days before an operation should you stop warfarin

A

5 days before

151
Q

how many days before an operation should you stop DOACs

A

2 days before

152
Q

low bleeding risk operation examples

A

dental extraction
joint injection
cataract surgery
low risk endoscopies

153
Q

medium and high bleeding risk operation examples

A

medium - most surgery

high - neurosurgery

154
Q

how does a PE cause RVD (right ventricular dysfunction)

A

a PE results in a rapid increase in pulmonary vascular resistance which leads to pulmonary hypertension (PH) that only reverses with the lysis of the vascular blockage or the failure of the RV contractile function

155
Q

Investigation and management options of Non Cardiac Chest Pain (NCCP)

A

careful history and examination
ECG
blood tests including cardiac biomarkers
CXR

156
Q

Causes on non-cardiac chest pain (Generally)

A 
Lung pathology
MSK chest pain
Abdominal pathology
systemic inflammatory disorders
medically unexplained chest pain
157
Q

structures that would give rise to MSK chest pain

A 
skin and subcutaneous tissue
ribs
tendons and ligaments
intercostal muscles
diaphragm 
nerves
158
Q

characteristics of MSK chest pain

A 
worse with movement
reproducibility
chest wall tenderness
pleuritic
little or no physiological compromise
159
Q

Causes of MSK chest pain

A 
strains and sprains (coughing, vomiting, trauma)
Costochondritis
Tietze Syndrome
Fibromyalgia
Rheumatological disease
160
Q

Treatment options for MSK causes of chest pain

A

anti inflammatories are the main stay of treatment

advice and reassurance

161
Q

what is costochondritis

A

inflammation where your ribs join your breastbone. It causes sharp pain in the middle of your chest.
often gets better within a few weeks
not sure what causes it: can be from excessive coughing, chest injury or strain due to exercise

162
Q

what is Tietze syndrome

A

rare, inflammatory disorder characterized by chest pain and swelling of the cartilage of one or more of the upper ribs (costochondral junction), specifically where the ribs attach to the breastbone (sternum). Onset of pain may be gradual or sudden and may spread to affect the arms and/or shoulders.

163
Q

what is fibromyalgia

A

Fibromyalgia is a condition that causes widespread pain and extreme tiredness.
Symptoms of fibromyalgia vary from person to person. The main symptom is pain all over your body.
There’s no cure for fibromyalgia, but treatments like painkillers, talking therapies and exercise programmes may help ease some of your symptoms.
It’s not clear what causes fibromyalgia. It can start after a stressful event like an injury, illness or the death of a loved one.

164
Q

abdominal pathology causing chest pain

A 
peptic ulcer disease
perforated viscus
choelcystitis
pancreatitis
biliary colic
oesophageal spasm
165
Q

what is peptic ulcer disease

A

Peptic ulcers are open sores that develop on the inside lining of your stomach and the upper portion of your small intestine. The most common symptom of a peptic ulcer is stomach pain. Peptic ulcers include: Gastric ulcers that occur on the inside of the stomach.

166
Q

Causes of peptic ulcer disease

A

Helicobacter pylori infection

  • secretes urease to create an alkaline environment
  • commonest cause of PUD

non-steroidal anti-inflammatory

  • protective mucus secretion is stimulated by prostaglandins
  • NSAIDs, corticosteroids and aspirin interfere with Prostaglandin synthesis

stress

lifestyle

rare syndromes

167
Q

symptoms of peptic ulcer disease

A

epigastric pain
-classically upper abdominal and associated with mealtimes

bloating
water brash (when your body makes too much saliva, causing it to mix with your stomach acid and back up into your throat.)
nausea
loss of appetite

168
Q

what happens in haemorrhage of a peptic ulcer

A

haematemesis (vomiting blood)
melaena
syncope
breathlessness

169
Q

what happens in perforation of a peptic ulcer

A

full-thickness ulceration through the GI wall

  • digestive secretions, food and gas leak into abdominal cavity
  • chemical and bacterial peritonitis ensues

severe, sharp unremitting abdominal pain
-diaphragmatic pain can cause shoulder/chest pain

managed with emergency surgery

170
Q

what if familial mediterranean fever

A

inherited disorder of pyrin
-found in granulocytes, mediates inflammatory cytokine release

causes attacks of painful inflammation of various organs

  • accompanied by fever
  • first attack usually by age 20
171
Q

what kind of body attacks (inflammation?) do you get with familial mediterranean fever

A 
classically affects abdomen - peritonitis
joint attacks - synovitis
skin - erysipeloid eruptions
pleuritis
pericarditis
172
Q

management of familial mediterranean fever (FMF)

A

acute attacks

  • self-limiting
  • treatment is supportive - analgesia, antipyretics(reduces fever), fluids

Prophylaxis
colchicine - reduces attack frequency and amyloid deposition

amyloid (an abnormal protein that is produced in your bone marrow and can be deposited in any tissue or organ. Amyloidosis frequently affects the heart, kidneys, liver, spleen, nervous system and digestive tract. )

173
Q

Acute chest syndrome in a sickle crisis

A 
vaso-occlusive crisis of the pulmonary vasculature
second most common crisis type
accounts for 25% deaths in sickle cell disease
features include:
-pleuritic chest pain
-dyspnoea
-fever
-cough +/- sputum, haemoptysis
174
Q

clues pointing to non-cardiac aetiology on presentation of chest pain

A 
pleuritic pain
chest wall tenderness
"non-anginal" chest pain - not related to exertion or onset at rest
little or no effect on anti-anginals
younger age
psychiatric co-morbidities

CBL Year 2 (14 decks)

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