ICP Flashcards

1
Q

what vertebrae levels are the important jerks

A

L3,L4 - knee jerk

S1, S2 - ankle jerk

other jerks included in neurological examination are

Bicep - C5

supinator - C6 /brachioradialis muscle

triceps - C7

plantar response /babinski reflex

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2
Q

whats koilonychia and leukonychia

A

Koilonychia = spoon shaped nails which is a sign of iron deficiency anaemia

Leukonychia = white spots on the nails due to low albumin levels so found in chronic liver failure

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3
Q

Scncope definition and 2 types

A

Syncope refers to transient loss of consciousness. There are two main types of cardiac syncope and the history may go a long way to help determine the diagnosis.

Vasovagal Syncope (fainting) and variations

Stokes-Adams attacks

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4
Q

vasovagal syncope - description

A

o loss of consciousness and muscle strength characterised by a fast onset, short duration, and spontaneous complete recovery. It is caused by a decrease in blood flow to the brain, typically from low blood pressure. There is frequently a prodrome which may include feeling warm, lightheaded, blurred vision, nausea and an unpleasant gastric sensation accompanied occasionally by borborygmi and eructation.
o Common descriptions are those of pallor, sweating, and dilated veins which may cause a grey colour. Recovery of consciousness is sudden and complete with no sequelae although normal motor function may take a few minutes.
o Vasovagal Syncope may also be associated with a short episode of muscle twitching. When consciousness and muscle strength are not completely lost, it is called presyncope. It is recommended that presyncope be treated the same as syncope

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5
Q

vasovagal syncope - history/ descriptions

A

 Precipitating factors (emotion, sight of blood, pain)
 Prodromal symptoms (nausea, blurred vision)
 Colour change (pallor, grey, and sweatiness)
 Recovery (spontaneous, sudden, complete)
 There should be an absence of confusion or drowsiness
 Pallor and sweating indicate release of catecholamines to overcome hypotension
 Vasovagal syncope may run in families
 Collateral history from a witness is very valuable and should be sought in every case

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6
Q

strokes-adams attacks - description

A

o Typically an attack occurs without warning, leading to sudden loss of consciousness. During an attack, a patient may be pale with hypoperfusion. Abnormal movements may be present, typically consisting of twitching after 15–20 seconds of unconsciousness. (These movements, which are not seizures, occur because of brainstem hypoxia and not due to cortical discharge as is the case for epileptiform seizures). Breathing typically continues normally throughout the attack, and, upon recovery, the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into the systemic circulation, which has become dilated due to hypoxia.
o As with any syncopal episode that results from a cardiac dysrhythmia, the fainting does not depend on the patient’s position. If it occurs during sleep, the presenting symptom may simply be feeling hot and flushed on waking.

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7
Q

strokes adams attacks - history/ symptoms

A

o History
 A prodrome may precede Vasovagal Syncope
 A prodrome is absent in Stokes-Adams attacks
 Pallor by a flush as consciousness returns is typical
 A cold sweat is less of a feature of Stokes-Adams attacks
 Recovery is sudden and complete without sequelae
 May occur with tachycardia as well as bradycardia

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8
Q

what causes strokes adam attacks after exercise

A

o Syncope during exercise suggests structural heart disease
o Syncope related to exercise should always be thoroughly evaluated
o The causes are often reversible and would include:
 Cardiac failure and cardiomyopathy
 Outflow tract obstruction (aortic stenosis and HCM)
 Aberrant origin of the RCA
 Occasionally VVS after severe exertion (benign)

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9
Q

simple ectopic beats

A

 Ectopic beats are common. Many people without any cardiac disease experience ectopic beats. Many asymptomatic people will have ectopic beats on routine ambulatory ECG monitoring.
 In some people they are very intrusive and cause symptoms.
 They are often described as “missed beats” when in fact they are premature additional beats. Because they are premature cardiac filling is incomplete and so the beat may be impalpable at the wrist, hence the “missed beat” sensation.
 They commonly occur at rest, for example lying in bed, sitting and after meals. They may occur in runs and last for a variable amount of time. They frequently superess with activity.
 They are more frequent with any intercurrent illness, stress, fatigue and anxiety.

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10
Q

sinus tachycardia

A

 Sinus tachycardia is common
 Catecholamine hormones (adrenaline and noradrenaline will make the heart beat harder and faster
 Increased circulating concentrations of these hormones occur with anxiety, stress, panic disorder
 Sinus tachycardia may occur with thyrotoxicosis (increased sensitivity to catecholamines) and anaemia
 While the onset of tachycardia may be sudden the sensation of palpitation eases off gradually

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11
Q

cardiac arrhythmia

A

 A cardiac arrhythmia occurs independent to external influences
 They occur secondary to an intra-cardiac circuit or due to an automatic focus discharging
 They are sudden in onset
 They terminate abruptly
 They usually have a rapid rate (which is constant apart from AF)
 They may be regular (SVT or VT) or irregular (AF)
 There may be associated symptoms
 There may be precipitating and relieving factors (Valsalva Maneuver)
 They may be followed by polyuria
 Considerations
• Younger patients consider sinus tachycardia or SVT
• Older patients suspect paroxysmal atrial fibrillation if irregularity of rhythm is described during tachycardia
• Patients with heart disease (particularly previous myocardial infarction or cardiomyopathy) especially if there is a history of syncope or pre-syncope following the onset of tachycardia consider ventricular tachycardia
• Remember to ask for family history of Sudden Cardiac Death

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12
Q

atrial fibrillation

A

• Atrial fibrillation is the commonest cardiac arrhythmia. It may be permanent, persistent or paroxysmal. It may occur in the young or the older patient. The key feature of the history is that the cardiac rhythm is irregular.
• In younger patients it may be related to :
o Training
o Alcohol
o Thyrotoxicosis
• In older patients it may be related to :
o Obesity
o Sinoatrial disease (common)
o Hypertension
o Sleep apnoea syndrome
• While mitral stenosis due to rheumatic fever remains the classic cardiac disease to cause atrial fibrillaton any cardiac disease that increases left atrial pressure may be associated with atrial fibrillation. Cardiac failure, myocardial infarction, cardiomyopathy and valve disease
• One of the major complications off atrial fibrillation is embolic stroke and systemic embolism. This can be prevented by anticoagulation treatment. There is a score that can be calculated from the history.

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13
Q

types of chest pain - how to differentiate

A
  • There are many causes for chest pain
  • All structures in the chest may cause pain
  • Chest wall pain (muscles, ribs, sinews, cartilage) - feels muscular
  • Pain radiating from the spine and nerves - short lived and severe
  • The lungs and pleura (pleuritic pain) - worse with respiration
  • The oesophagus - heartburn worse after hot drinks or meals or lying flat and relieved by antacids or milk
  • The heart - pericardium worse when leaning forwards and backwards
  • The aorta - may be between shoulder blades and have a tearing quality
  • CAD is increasingly commonly detected (increasing use of CT) and many individuals will have coronary disease and have no symptoms
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14
Q

angina

A

• It may be caused by coronary artery disease
• It may be due to cardiomyopathy
• It may be due to aortic stenosis
• It is precipitated by effort and relieved promptly by rest
• Prompt relief by using the GTN (Glyceryl trinitrate) is characteristic
• It may present in the chest, and radiate to arms, jaw and teeth
• Breathlessness and chest tightness are not always angina
• Angina is believed to be due to myocardial ischaemia. This occurs when myocardial oxygen demand exceeds myocardial oxygen delivery. Exercise or effort increases oxygen demand.
• Myocardial ischaemia can be demonstrated on the ECG recording as ST segment depression. Myocardial ischaemia will increase with continuing exercise and resolve promptly with rest
• Exercise increases heart rate and blood pressure (increases myocardial work and myocardial oxygen demand) and rest reduces heart rate and blood pressure. GTN causes immediate vasodilatation and will lower blood pressure. True angina resolves very quickly within a minute or two. Chest tightness that resolves over the course of many minutes is unlikely angina
• Angina is more easily precipitated after a meal. This is because eating increases myocardial work. There is an increase blood flow (cardiac output) to the gut.
• Heart rate increases just as it would with exercise. Blood pressure falls due to splanchnic vessel dilatation. Peripheral blood vessels (systemic) constrict and this also contributes to the increasing in myocardial work.
• There is good reason to ask if the angina or discomfort is more easily precipitated after a meal
• Angina is more troublesome or more easily precipitated in cold weather. This is because exposure to cold increases peripheral resistance due to vasoconstriction and blood pressure.
This means that angina develops with less effort in cold weather because the person is starting with increased cutaneous vasoconstriction. This is why your hands go white in the cold.
This is why we ask patients if the angina is more easily precipitated in cold weather.

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15
Q

breathlessness

A
  • Breathlessness due to the heart is thought to be related to an increase the left atrial pressure. This increasing in left atrial pressure is transmitted back to the pulmonary capillaries. This changes the trans-capillary pressure gradient and fluid exudes into the alveoli causing pulmonary oedema. The reduction in capacity for gas exchange due to the oedema causes breathlessness.
  • The most important determinant of the left atrial pressure is Starling’s Law of the heart. This states that the heart will contract more, the more it is stretched. The more cardiac filling the more blood it will eject. This will occur until the filling pressure reaches the critical point that affects the trans-pulmonary capillary pressure gradient. In a diseased myocardium the curve is much flatter.
  • Breathlessness (dyspnoea) is an important symptom that may indicate cardiac disease
  • It is also an important symptom for respiratory disease
  • Breathlessness may occur with anaemia
  • Breathlessness may occur with obesity
  • Breathlessness may occur with hyperventilation
  • Cardiac dyspnoea occurs in any situation where there is an increase in left atrial pressure
  • Exercise, lying flat, sleep and transfusion of blood and fluids will all increase filling pressures
  • Typically cardiac dyspnoea occurs with effort (muscle contraction increases venous return)
  • Typically cardiac dyspnoea occurs when lying flat due to increased venous return : orthopnoea
  • Typically cardiac dyspnoea causes the patient to wake suddenly from sleep and sit up : paroxysmal nocturnal dyspnoea
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16
Q

cardio exam - position

A

lying down with bed at 45 degrees

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17
Q

cardio exam - hands

A
  • Tobacco staining
  • Tendon xanthomata
    o Build up of cholesterol on extensor tendons
    o Familial hypercholesterolemia
  • Pallor
    o anaemia
  • Signs of endocarditis
  • Clubbing
    o CVD, endocarditis
  • Peripheral perfusion
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18
Q

capillary refill time

A
  • Apply pressure to nail; bed then release

- Blood should return in 2 seconds if perfusion good

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19
Q

radial pulse

A

feel at lateral edge of risk using 3 fingers

  • Rate
    o Count no. pulses in 15 seconds and x by 4 to estimate pulse rate in bpm
    o Compare on each side – if difference could be peripheral vascular disease, or aortic coarctation or dissection
  • Rhythm
  • Synchrony

collapsing pulse a sign of aortic regurgitation (pulse vol. exaggerated when arm extended vertically bc of gravity dependant fall in diastolic pressure)

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20
Q

brachial pulse

A
  • For pulse volume and character
  • Support arm around the elbow
  • feel pulse with thumb medial to biceps tendon
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21
Q

jugular venous pulse

A
  • Waveform and height/ pressure
  • Reflects the pressure in the right atrium
  • Lateral to carotid artery
  • Best identified looking across neck using oblique light
  • Normally 2 waves – presystolic caused by atrial contraction and systolic in time with arterial pulse
  • Not normally visible in health when patient at 45 degrees - lower headrest to bring JVP into view
  • Lower headrest to differentiate JVP from carotid pulse (as carotid doesn’t vary with position)
22
Q

abdominal jugular test

A
  • Place hand on the abdomen and press down

- increases intraabdominal pressure, Increases venous return to heart and temp. rise in JVP pressure

23
Q

carotid arterial pulse

A
  • Deep to anterior border of SCM
  • Often visible
  • Use thumb to palpate
    o Assess volume and character
24
Q

face exam

A
  • Xanthelasma
  • Corneal arcus
  • Jaundice
  • Pallor
  • Central cyanosis
    o Blue discoloration of mucus membranes
25
Q

chest scars

A
  • Scars
    o Common in midline – cardiac surgery
    o Above clavicle - pacemaker surgery
    o In line with ribs – lung surgery
26
Q

chest exam - apex beat

A
  • Apex beat
    o In 5th intercostal space
    o If difficult roll patient onto left side
    o In female lift breast up
    o If forceful = LV hyperbole, if displaced = LV dilitation
27
Q

chest exam - thrills and heave

A
  • Thrills and heaves
    o For heave Place hand over sternum if heave present hand moves up and down with heart
    o For thrill you can feel vibration with fingers over sternum and clavicle and apex
28
Q

chest exam - auscultation, main areas to check and

A

o At apex, lower left sternal border, pulmonary area and aortic area correspond with where to hear the 4 main valves
o Listen with bell and diaphragm at each site
o Bell used for low pitched sounds (mitral stenosis), diaphragm high pitched (aortic stenosis)
o Timing or heart sounds important to figure out if murmurs are systolic or diastolic
o Note character of 1st and 2nd heart sound
 Splitting and added sounds (eg 3rd heart sound)
o Use carotid pulse to assist timing
o Can listen at base of neck for aortic stenosis using diaphragm

29
Q

chest exam - turning patient to left side and sitting forward - what for and how

A

Turn patient to there left side
- Tell them to take deep breath in and hold
- This tests for mitral stenosis and aortic regurgitation
- Listen at the apex with the bell
Patient sit forward
- Listen for aortic regurgitation at the lower left sternal border with diaphragm
- Get patient to breath in deep
While still sitting forward
- Listen at the back at the lung bases for crackles of pulmonary oedema
- Press over sacrum to check for fluid

30
Q

abdomen exam cardio

A
  • Inspect scars
  • visible pulsations
  • extensions suggestive of ascites bc this present in right sided cardiac failure
  • hepatomegaly in right sided cardiac failure
  • splenomegaly in chronic endocarditis
  • pulpate in midline for abdominal aortic aneurysm
  • listen for Bruits over abdominal aorta and both renal arteries
31
Q

leg exam cardio

A
  • scars of vascular surgery and vein harvesting for vascular surgery
  • dilated or varicose veins
    o hemosiderin pigmentation
    o varicose eczema
    o ulcers
  • arterial insufficiency results in
    o pallor
    o hair loss
    o ulceration
    o blac/gangrenous dustal tissues
  • check temperature of each leg from foot upwards
  • check for pitting oedema
32
Q

femoral pulse cardio

A

Femoral Pulse
- below inguinal ligament, halfway between superior anterior iliac spine and pubic tubercle
- note pulse volume and character
- pulsate femoral and radial pulse at same time on same side
o radial femoral delay feature of aortic coarctation
- listen for a Bruits over the femoral artery

33
Q

knee examination cardio

A
  • flex at 30 degrees
  • thumbs at the front and fingertips at the back to feel popliteal pulse
  • posterior tibial pulse best felt 2cm below and posterior to the medial malleolus
  • dorsalis pedis pulse palpated using 3 fingers
    o located lateral to extensor tendon of great toe
34
Q

investigations of MI

A

Bloods: FBC, UEs, CRP, lipids, Cardiac enzymes (Cardiac troponin levels increase within 3-12 hours from the onset of chest pain, peaking at 24-48 hours. )

Serial ECGs and continuous ECG monitoring in a coronary care unit (CCU).

CXR: to assess the patient’s heart size and the presence or absence of heart failure and pulmonary oedema. This may also assist in differential diagnosis.

Pulse oximetry and blood gases: monitor oxygen saturation.

Echocardiography can define the extent of the infarction and assess overall ventricular function and can identify complications, such as acute mitral regurgitation, left ventricular rupture or pericardial effusion.

Myocardial perfusion scintigraphy using single photon emission computed tomography (SPECT) sometimes used

35
Q

pre-hospital treatment of MI

A

Pain relief with GTN sublingual/spray and/or an intravenous opioid 2.5-5 mg diamorphine or 5-10 mg morphine intravenously with an antiemetic

Aspirin 300 mg orally

IV access/ pre hospital thrombolysis more common in more rural setting

36
Q

hospital treatment of MI

A

Patency of the occluded artery can be restored by percutaneous coronary intervention (PCI) or by giving a thrombolytic drug. PCI is the preferred method.

Long-term low-dose aspirin reduces overall mortality, non-fatal re-infarction, non-fatal stroke and vascular death.

Clopidogrel, in combination with low-dose aspirin, is recommended for AMI with ST-segment elevation.

Beta-blockers:When started within hours of infarction, beta-blockers reduce mortality, non-fatal cardiac arrest and non-fatal re-infarction

Angiotensin-converting enzyme (ACE) inhibitors:These reduce mortality whether or not patients have clinical heart failure or left ventricular dysfunction. They also reduce the risk of non-fatal heart failure.

Cholesterol-lowering agents:Ideally, initiate therapy with a statin as soon as possible for all patients with evidence of cardiovascular disease (CVD) unless contra-indicated.

37
Q

whats the most common cause of heart failure in the uk

A

coronary heart disease and hypertension

38
Q

signs of heart failure

A

Tachycardia at rest, low systolic blood pressure (BP), a displaced apex (LV dilatation) or RV heave (pulmonary hypertension), a narrow pulse pressure or pulsus alternans (alternating large and small pulse pressures) and a raised JVP.

There may be a gallop rhythm due to presence of or murmurs of mitral or aortic valve disease.

Bilateral basal end-inspiratory crackles ± wheeze (‘cardiac asthma’).

Tachypnoea.

Pleural effusions.

Tender hepatomegaly with ascites.

Often extensive peripheral oedema. There may be swollen ankles, sacral oedema or ascites

39
Q

investigations into heart failure

A
NT-proBNP
ECG
Echo
Bloods
CXR

Consider staging: NYHA I-IV

40
Q

management of heart failure

A

Prognosis is poor on the whole, with approximately 50% of people with heart failure dying within five years of diagnosis

Community-based heart failure nurses provide an important adjunct to self-care, as well as a bridge to secondary care.

Smoking, diet, fluid intake, alcohol, exercise

Drugs: diuretics, ACE-I, b-blocker, morphine (end stage)
Palliative care

41
Q

Peripheral vascular disease risk factors and signs

A

Risk Factors: Smoking, Diabetes mellitus, Hypertension, Hyperlipidaemia, Physical inactivity, Obesity

The most common symptom is muscle pain in the lower limbs on exercise (intermittent claudication)

Walking impairment - eg, fatigue, aching, cramping or pain in the buttock, thigh, calf or foot, particularly when symptoms are quickly relieved at rest. Pain comes on more rapidly when walking uphill than on the flat

Ischaemic rest pain

42
Q

examination/ investigation of PVD

A

Examination of the lower limbs should include auscultation of the femoral arteries at the groin level.

The affected leg may be pale and cold, with a loss of hair and with skin changes.

Inspection of the feet, noting the colour, temperature and integrity of the skin, and the presence of ulcerations. There may be poorly healing wounds of the extremities. Patients with severe PAD or critical lower-limb ischaemia may have ulceration or gangrene.

Palpation of the femoral, popliteal, dorsalis pedis and posterior tibial pulses.

Examination usually reveals weak or absent pulses
The main method to confirm the diagnosis is Doppler ultrasonography (ABPI)

Bloods

43
Q

management of PVD

A

Most patients’ symptoms improve with optimal medical treatment and invasive intervention is often not required. Approximately 20% will deteriorate and develop critical limb ischaemia.

STOP SMOKING

A supervised exercise programme has been shown to be a very important part of management and should be offered to all patients with intermittent claudication

Medication: statins and antiplatelet drugs

Surgery: NICE states that angioplasty should be offered when risk factor modification has been discussed, supervised exercise has failed to improve symptoms and imaging shows angioplasty is suitable for the patient

44
Q

headache red flag symtpoms

A

New onset of, or change in, headache in patients who are aged over 50 years.
Headache in patients who are aged under 5 years.
Thunderclap: rapid time to peak headache intensity (seconds to five minutes) - same-day specialist assessment required.
Headache waking the patient up (NB: migraine is the most frequent cause of morning headache).
Headache precipitated by physical exertion or Valsalva manoeuvre (eg, coughing, laughing, straining).
Headache onset with exertion or sex.
First or worst headache of the patient’s life.
Headache that changes with posture.

45
Q

seizure pattern

A

Prodromal aura / altered consciousness
Classically rigidity followed by clonic seizure but not all seizures follow this pattern
Tongue biting and incontinence may occur
Slow recovery, confusion, transient neurological symptoms

46
Q

seizure causes

A

Primary epilepsy

Mass lesions, stroke

47
Q

how to examine the crania; nerves

A
  • 2nd-optic-visual acuity with Snellen chart, inspection of pupils, pupillary responses with pen torch(direct and consensual response), assessment of visual fields
  • 3rd, 4th and 6th cranial nerves-inspection for ptosis, squints, assessment of eye movement, observation for nystagmus
  • 5th –sensory-test light touch in the 3 distributions of the 5th nerve
  • 7th-assess motor function-raise eyebrows, screw up eyes, show teeth, puff out cheeks
  • 9th, 10th 11th-observe speech, cough, examine movement of soft palate, turn head against resistance, shrug shoulders
  • 12th-observe tongue, poke tongue out and move tongue from side to side
48
Q

epilepsy general info and types

A
  • About 1 in 30 people in the UK develop epilepsy
  • Most commonly starts in childhood and in people aged over 60
  • A seizure is a short episode of symptoms caused by a burst of abnormal electrical activity in the brain
    Classification:
  • Focal
  • Generalised
  • Unclassified
49
Q

focal seizure symptoms

A
  • Focal: aura; automatism, lip-smacking, plucking at clothes, hair (motor); transient paraesthesiae (sensory); odd epigastric sensation, nausea, abnormal taste or smell (autonomic); unreality, déjà vu, fear (psychiatric)
50
Q

triggers for epilepsy

A

-inadequate sleep, alcohol abuse or medications such as antidepressants (which lower the seizure threshold); menstrual cycle.

51
Q

epilepsy management

A

Lifestyle: safety, triggers, driving
Medication (anti-epileptic drug AED)
- Treatment with AED therapy is generally recommended after a second epileptic seizure
VNS (vagus nerve stimulation) is indicated for use as an adjunctive therapy in reducing the frequency of seizures in adults who are refractory to anti-epileptic medication but who are not suitable for resective surgery
Surgery is increasingly used as treatment for refractory focal epilepsy