Week 2 Flashcards

1
Q

symptoms of angina (5)

A

chest pain
referred pain
dyspnoea
sweating
fatigue
syncope

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2
Q

mech of dyspnoea in cardiac issues (MI, HF, ischaemia) 4 steps

A

1.reduced cardiac ouput
2. increased pulmonary pressure
3. interstitial oedema and pulmonary congestion
4. gas exchange impairment

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3
Q

what are the nerves involved in referred pain in MI

A

cardiac visceral spinal afferents

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4
Q

reason for referred pain

A

the cardiac visceral spinal afferents converge with sensory nerves from chest and upper limbs at the same spinal nerves hence referred pain

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4
Q

what are the key spinal nerves from which referred pain is derived from

A

c3-T5

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5
Q

aortic dissection pain 2 characteristics

A

tearing pain
radiates to back and shoulder

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6
Q

pericarditis 2 characteristics

A

sharp
worse upon deep breathing

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7
Q

pulmonary embolism 3 characteristics

A

pleuritic pain: sharp, stabbing
worse uppon inspiration
radiation to back and shoulder

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8
Q

pneumothorax pain 2 charateristics

A

pleuritic pain: sharp, stabbing
worse upon inspiration

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9
Q

GORD pain 2 characteristics

A

burning central pain
worse after eating and lying down

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10
Q

ECG findings for unstable angina and NSTEMI (2)

A

ST depression, T wave inversion

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11
Q

what other conditions cause high troponin 7

A

pericarditis
myocarditis
physical activity
stroke
sepsis
trauma
pulmonary embolism

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12
Q

what are the two key troponins

A

I and T

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13
Q

TIMI score (7 criteria)

A

risk assessment for unstable angina and NSTEMI

age>65
Aspirin
Prior stenosis
ST depression
Cardiac markers
>3risk factors
Angina

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14
Q

ED presentation for STEMI process 5

A

insert cannula
aspirin
analgesic
ECG every 10min
establish reperfusion method

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15
Q

discharge after ACS 6

A

dual antiplatelet (aspirin+ticagrelor)
ACE inhibitor
Beta blocker
High intensity statin
Cardiac rehab
Other risk factor management

16
Q

type 1 MI

A

due to plaque rupture or erosion

17
Q

type 2 MI

A

due to oxygen supply demand mismatch

18
Q

type 3 mi

A

sudden cardiac death without elevated biomarkers

19
Q

type 4 MI

A

death during PCI

20
Q

type 5 MI

A

death during cardiac surgery

21
Q

causes of type 2 (think groups then examples of each)

A

Oxygen delivery: RF, PE, pneumothorax
Heart rate: tacchycardia
BP: severe hypertension, hypotension
Coronary: vasospasm, endothelial dysfunction, dissection

22
Q

causes of vasospasm 3

A

smoking
drugs
endothelial dysfunction

23
Q

symptoms of coronary artery spasm

A

same as mi: dyspnoea, tachycardia, syncope, referred pain, chest pain

24
Q

benefits of fibre in reducing coronary artery risk 2

A
  1. absorb cholesterol allowing more excretion than absorption
  2. reduce rate of sugar absorption important in diabetes management which is major risk factor of CAD
25
Q

benefits of plant sterols and stanols

A

similar structure to cholesterol hence compete for absorption, reducing cholesterol absorption

26
Q

DASH diet

A

dietary approaches to stopping hypertension

includes low salts

27
Q

signs of PAD 2 generic

A

asymptomatic
intermittent claudication

28
Q

severe signs of PAD progression

A

palor
pulselessness
cold
parasthesia
paralysis
pain
beurger’s sign
gangrene
ulcerations
charcots foot

29
Q

symptoms of stroke 6

A

hemiparesis
confusion aka dysarthia
dysphasia
syncope
unilateral vision loss
hemi-negligence

30
Q

where does cerebrovascular atherosclerosis most commonly occur

A

in carotids, specifically the bifurcation between common to internals

31
Q

PAD management

A

pharmacological: dual antiplatelet, statins, ACE (to control BP)
Bypass
Stenting

32
Q

CBV management

A

Gold standard: Carotid artery endoarterectomy if stenosis >50%

carotid stenting

pharmacological: statins, dual antiplatelet, ACE

33
Q

ethics of tolerance

A

Acceptance of other beliefs even if they do not align with one’s as long as they do not cause harm

34
Q

AFIB signs on ECg

A

irregular irregular rate and rhythm
absence of p waves

35
Q
A