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Medicine PJE > CR Cardio-related issues > Flashcards

CR Cardio-related issues Flashcards

1
Q

Atrial Fibrillation ECG diagnosis

A

absence P waves

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2
Q

Concentric and Eccentric hypertrophy

A

o Concentric
 Due to increased afterload = aortic stenosis
• Afterload = the stress in the wall of the left ventricle during ejection
 Wall thickness increases, compliance reduced (stiffness)

o Eccentric
 Volume overload that leads to dilation of chamber (e.g. Regurg.)
 Elevates oxygen demand, lowers efficacy

concentric can lead to eccentric (reduced compliance = volume overload)

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3
Q

Rheumatic Heart Disease

A

Mainly affects the aortic and mitral valves

Underlying mechanism is believed to be production of antibodies against person’s own tissues after strep A infection

Valves become thickened (fibrosis) = become narrow and incompetent.

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4
Q

Aortic Stenosis Summary

A

Causes: Age, Congenital Bicuspid valve (CBV)

Symptoms: LV failure, breathlessness (pleural effusion due to increased LAP), angina (more O2 demand), Syncope (flow can’t readily increase)

Signs: SLOW RISING CAROTID PULSE, S4 heart sound (forceful contraction of atria that cannot contract any further), severe pressure gradient LVP>LAP

Treatment: TAVI surgery

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5
Q

Aortic Regurg Summary

A

Causes:
Aortic Valve Leaflet Disease
Aortic Root Dilating Disease

Symptoms: Dyspnoea (pleural effusion due to increased LAP), angina (more O2 demand), eccentric hypertrophy

Signs: RAPIDLY RISING CAROTID PULSE, end-diastolic murmur (aortic backflow), ejection murmur (turbulent ejection from overloaded LV)

Treatment: Surgery

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6
Q

Mitral Prolapse summary

A

Cause:
Marfan syndrome, Ehler’s danlos (connective tissue disorders)
Myxomatous degeneration (pathological weakening of chordae tendinae)

Symptoms: asymptomatic NOTE: during systole valve prolapses back into LA = MR

Signs: Mid-systolic click (MR), late murmur (regurg.)

No treatment necessary

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7
Q

Mitral Stenosis Summary

A

Causes: Rheumatic fever

Symptoms: Increased LAP, Atrial fib. (loss of conduction tissue

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8
Q

Mitral Regurg. Summary

A

MOST COMMON

Causes:
Mitral Valve Leaflet D
Subvalvular Disease
Functional MR (LV dilation)

Symptoms: Increased LAP, Atrial fib. (loss of conduction tissue

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9
Q

Causes of Aortic Valve Leaflet Disease

A

Calcific disease, CBV, rheumatic, infective endocarditis

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10
Q

Causes of Aortic Root Dilating Disease

A

Marfan syndrome, aortic dissection, ankylosing spondylitis

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11
Q

Causes of Subvalvular Disease in mitral regurg.

A

Chordal rupture, Papillary muscle dysfunction or muscle rupture

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12
Q

Hypertension grades

A

Grade 1 = Ambulatory blood pressure monitoring (ABPM) = 135/85

Grade 2 = ABPM is = 150/95

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13
Q

Treatment for Isolated Systolic Hypertension

A

Lower sodium and richer fruit and vegetable diet

ISH serious in elderly

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14
Q

Postural Hypertension Clinical Definition

A

A decrease in standing > 20 mmHg or DBP >10 mmHg when associated with dizziness/fainting

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15
Q

Why does • Systolic pressure generally increase with age

A

o Elastin gradually replaced by collagen because of free radical damage

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16
Q

Classes of Hypertension

A

Primary = 90-95% of cases. (idiopathic)

Secondary = about 5% - clear underlying cause
Renal/renovascular disease
Cushing’s syndrome (adrenal cortical tumour)
Conn’s syndrome (hypersecretion of aldosterone)
Coarctation of the aorta.
Iatrogenic.
o Hormonal and oral contraceptive.
o NSAIDs
Thyroid (either hyper/hypo) or parathyroid disease

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17
Q

Blood Pressure is Controlled by

A
  1. Baroreceptors in carotid artery (neuronal system).

2. The renin-angiotensin-aldosterone system (RAAS).

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18
Q

Hyponatremia symptoms

A

Is serious as it affects action potential production and can cause brain swelling.

Mild: Loss of energy, fatigue, Confusion, muscle weakness

Severe: Nausea, vomiting, headache, seizures coma.

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19
Q

Obesity and Hypertension

A

•Obesity = increases renal renin release, angiotensin formation and sodium retention.

High levels of leptin (due to increased number of fat cells) increase sympathetic vasoconstriction

Hypokalaemia = increases plasma renin, angiotensin II

Exercise and lose weight (best therapy)

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20
Q

Approach to Hypertensive Treatment

A

Step 1:
People under 55 should receive and ACE-blocker (Ramipril) OR a ARB (Losartan) (angiotensin II receptor blocker)
• Do not combine ACE inhibitor and ARB

People over 55 = calcium channel blockers (Consider for Afro-Caribbean’s)
• If not suitable = thiazide-like diuretic (decrease intra-vascular volume).

If diuretic treatment = offer thiazide-like diuretic such as:
• Chlortalidone or indapamide

Step 2:
• CCB + ACE inhibitor or an ARB
• If CCB not suitable = thiazide-like diuretic + ACE/ARB
• For black people = consider ARB > ACE + CCB.

Step 3: Treatment with three drugs if required.
Step 4: If no change (resistant hypertension) consider adding a fourth antihypertensive drug.

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21
Q

Metabolic syndrome triad

A

obesity, hypertension, diabetes

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22
Q

Most common type of cardiac defect

A

Ventricular Septal Defect (Acyanotic)

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23
Q

Stages of Atherosclerosis Development

A

1) Endothelial damage that makes vessel dysfunctional and alters permeability
2) Uptake of modified LDL particles, adhesion and infiltration of monocytes that become macrophages —> foam cells
3) As a response to injury, smooth muscle proliferates and moves into intima to form fibrous cap

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24
Q

Vasodilators

A

NO

PGI2 (Prostaglandin I2/prostacyclin)

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25
Q

LDL uptake in Atherosclerosis

A

LDL receptor normally recognises apolipoprotein B100

Modified LDL is not recognised by receptor (AB100) and are taken up by macrophages
No negative feedback = uptake is unlimited causing accumulation.

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26
Q

What causes proliferation of smooth muscle into intima in atherosclerosis

A

Platelet derived Growth factor released from macrophages

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27
Q

Atherosclerosis treatment

A

Statins -HMG CoA inhibitor (reduces intracellular cholesterol synthesis)

  • Increase in LDL liver receptors
  • Reduced plasma cholesterol

Polypill - contains a statin, 3 b.p. lowering drugs, folic acid and aspirin
(2012 onwards without aspirin)

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28
Q

Causes of Angina

A

DECREASED myocardial O2 supply:

  • Coronary artery disease
  • Severe Anaemia

INCREASED myocardial O2 demand:

  • Left ventricular hypertrophy
  • Right ventricular hypertrophy
  • Rapid tachyarrhythmia.
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29
Q

Angina ECG features

A

Diagnostic Features:
Planar or down-sloping ST depression

Prognostic features:

  • Poor exercise tolerance
  • Early ST depression
  • Slight ST depression (ischaemia), poor exercise tolerance
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30
Q

Angina treatment

A

Increase O2 delivery (coronary flow):

  • Nitrates
  • CaBs
  • Nicorandil
  • Revascularise

Reduce O2 demand:
Reduce heart rate:
- BB
- Ivabradine

Reduce LV wall tension:

  • BB
  • Nitrates
  • Nicorandil
  • CaBs
  • Ranolazine

Reduce contractility:

  • BB
  • CaBs
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31
Q

Angina Second degree prevention

A

Aspirin to all patients

Statins to all patients

ACE-I if any other indications (HT/DM)

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32
Q

Total body iron

A

3-5g

2g in circulating Hb

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33
Q

Absorption of iron

A

Duodenum

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34
Q

Role of Transferrin

A

Takes up fe2+ (can carry 2)

Clinical measurement for suspected iron deficiency

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35
Q

Role of ferritin

A

stores iron, releases when needed (buffer against iron deficiency and overload)

small amounts in serum = iron carrier

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36
Q

What can serum ferritin be used for

A

Diagnostic test for iron deficiency anaemia.

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37
Q

Definition of Anaemia (measurements)

A

<13.5 g/dl (male)

<11.5 g/dl (female)

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38
Q

Anaemia signs and symptoms

A 
Symptoms:
Tiredness
Fainting
Shortness of Breath
Worsening Angina
Palpitations
Signs:
Pallor (unhealthy pale appearance)
Rapid heart rate
Bounding pulse
Systolic flow murmur
Cardiac failure 
Retinal haemorrhages
39
Q

What is classed as Iron Deficiency

A

10ml loss/day

40
Q

Types of microcytic anaemia

A

Iron Deficiency Anaemia
Thalassaemia (alpha and beta)
4 missing genes = alpha
2 missing genes = beta

41
Q

Types of normocytic anaemia

A

Chronic Disease

Haemolytic Anaemia:

Abnormal breakdown in spleen/liver

  • Hereditary spherocytosis (Autosomal dominant)
  • Sickle cell disease
  • Thalassaemia (microcytic)
  • Anti-body induced
  • Rhesus mismatched transfusion

Abnormal breakdown in blood:

  • ABO mismatched transfusion
  • Snake bites
  • Infections
  • Malaria
42
Q

Types of macrocytic anaemia

A

Vitamin B12 (Cobalamin) Deficiency

  • Pernicious Anaemia (autoimmune again parietal cells)
  • Surgical gastroectomy
  • Chron’s disease

Folate (Vitamin B9) Deficiency

43
Q

Vitamin B12 absorption

A

Absorbed in ileum after binding to intrinsic factor (from parietal cells in gastric musoca)

44
Q

Diagnosis of Vitamin B12 Deficiency

A

increased serum methylmalonic acid

45
Q

Symptoms of Vitamin B12 Deficiency

A

Insidious = stores of B12 can be almost 3 years, so symptoms are gradual but could be fatal.

Anaemia

Glossitis = inflammation of the tongue

Mild Jaundice = due to RBCS breakdown

Neurological Symptoms

46
Q

Virchow’s Triad

A

Reduced blood flow (stasis)
Vessel wall disorder.
Hypercoagulability

47
Q

Deep vein thrombosis Diagnosis

A

Dependant on Wells Score

If above 2 = compression ultrasound

If below/CUS is negative = D-dimer

48
Q

Pulmonary embolism Diagnosis

A

ECG = sinus tachycardia, T wave inversion on anterior leads (V3, V4)

Arterial blood gases = hypoxia, low CO2

CXR = small pleural effusion, peripheral wedge shaped density above diaphragm

49
Q

Treatment of VTE, DVT, PE

A

Start heparin if likely diagnosis
Continue if diagnosed
Stop heparin after min. 5 days
Continue Warfarin

50
Q

Direct acting oral anti-coagulants (DOAC)

A 
Dabigatran = acts on thrombin
Rivaroxaban = acts on Factor Xa 
Apixaban = acts on Factor Xa
Edoxoban = acts on Factor Xa
51
Q

Low Molecular Weight Heparin (LMWH)

A

Anti-Xa and Anti-thrombin
Safer than unfractioned heparin
Half-life about 4 hours

Side Effects:
Osteoporosis
Major bleeding
Heparin induced thrombocytopenia.

52
Q

Why is Unfractioned Heparin used over LMWH

A

when rapid reversibility is required

53
Q

Fondaparinux

A

Synthetic pentasaccharide

54
Q

Warfarin

A

Vitamin K antagonist (factors II, VII, IX, X, protein C&S)

Delayed onset of action

Side Effects:
major bleeding risk
TERATOGENETIC

55
Q

Aspirin

A

Irreversibly inhibits COX (mainly COX1) and thromboxane synthase (potent platelet stimulator)

Contraindications:
Children <16 (fulminant liver failure)
Caution in patients with existing bleeding disorder and Patients with hypertension
Given in all cases of suspected STEMI

Side Effects:
Commonly overdosed causes:
Respiratory alkalosis
Severe metabolic acidosis

Can initiate asthma, cause bleeding, Gastritis, tinnitus, renal impairment.

56
Q

Beta Blockers

A

Stop the effects of the sympathetic nerve stimulation or circulating catecholamines the beta-adrenoceptors

Beta 1 = mainly in the heart, also kidney.
o Heart: In the SA node reduces H.R, in myocardium decreased cardiac contractility.
o Kidney = inhibits release of renin, reduces activity of RAAS system.

Beta 2 = lung, peripheral blood vessels, skeletal muscle,
o NS = inhibits release of neurotransmitters, decreases SNS

Contraindications:
Pregnancy (IUGR, neonatal hypoglycaemia, bradycardia)
Breast Feeding

Side Effects:
Bronchospasm
Bradycardia
Hypotension
Erectile Dysfunction

Example: Propanolol

57
Q

Statins

A

Inhibits action of HMG-coA reductase, by preventing conversion of HMG-CoA to mevalonic acid, increases LDL receptors expressed outside cell

Non-cholesterol effects:
o Decreased Inflammation
o Increased Apoptosis.
o Gene Regulation

Side Effects:
Increases likelihood of developing diabetes.
Sleep disturbance
(Rare) hepatitis and jaundice. 
Muscle toxicity
58
Q

ACE inhibitors

A

Inhibits plasma ACE competitively, leads to vasodilation.

Side Effects:
Dry irritant cough (accumulation of bradykinin)
Angioedema, impairment of renal function

Examples:
Captopril
Ramipril

59
Q

Clopidogrel

A

P2Y12a inhibitor, Further inhibits platelet aggregation

60
Q

Acute Myocardial Infarction Symptoms

A
  • Chest Pain
  • S4 (atrial contraction during diastole = ejection of blood into ventricles that cannot expand any further).
  • Low grade fever

Autonomic disturbance (stimulated by low CO).

  • Tachycardia
  • Sweating
  • Vomiting
61
Q

STEMI Reperfusion Therapy

A
  1. Aspirin and ticagrelor (platelet aggregation inhibitor)
  2. Heparin (anticoagulant)
  3. PPCI (primary percutaneous coronary intervention = coronary angioplasty)
62
Q

NSTEMI Emergency Treatment

A
  1. Aspirin and ticagrelor
    a. P2Y12
  2. GPIIb/IIIA inhibitor.
  3. Fondaparinux (factor Xa inhibitor)
  4. Anti-ischaemic drugs (BB, nitrates)
  5. Angiography (PCI if required)
63
Q

Secondary Prevention of Myocardial Infarction

A

Lifestyle
Drugs = aspirin, ticagrelor, statins, beta blockers, ACE-I
Devices = implantable cardioverter defibrillator (ICD)
- secondary VF (>24 hours after onset of infarct) or LV ejection fraction is <35%

64
Q

Types of Stroke

A

ISCHAEMIC (blood clot in cerebral artery ) - 85% of all strokes

HAEMORRHAGIC (Intracerebral haemorrhage)

LACUNAR (Occlusion of deep brain structure) - no cortical signs

65
Q

Location of Stroke

A

Branches of MCA - highly tortuous (turbulent flow)

Branches form lenticulo-striate arteries - Leave MCA at nearly 90 degrees

66
Q

Tonsillar Herniation

A

rise in ICP can cause cerebellum to extrude through foramen magnum - • Compression of lower brainstem and upper cervical cord.

67
Q

How is K+ removed in the brain

A

K+ released into extracellular space and removed by glial cells (buffer electrolyte changes).

68
Q

Excess Glutamate

A

NMDA and AMPA receptors

Excess stim. –> excess influx of Ca2+ ions into nerve cells
Excess Ca2+ = increase metabolic demand = uses more oxygen –> Hypoxic = absence of O2 = free radicals
Leads to apoptosis/cell death

69
Q

Penumbra region

A

Hypoxic neurons near hypoxic brain region which can survive

70
Q

Penumbra region Treatment

A

1) Restore Blood Flow:
Tissue plasma activators.
o Statins improve cerebral blood flow
Increase NO production.

  1. Combat Excitoxicity = NMDA antagonists, AMP antagonists
  2. Combat Free Radical Damage = antioxidants, free radical scavenger enzymes (superoxide dismutase), cool down the brain
71
Q

Shock criteria

A 
Likely if Mean Arterial Pressure is <60 mm Hg 
Other clinical signs of hypo perfusion:
	Tachycardia
	Tachypnoea
	Mental confusion.
72
Q

What mediates Constriction of arterioles

A

Mediated by sympNS
• Noradrenaline (alpha receptors on arterioles)
• Angiotensin 2 (hormonal control)

Mediated by local control:
• Endothelin: released from lining epithelium (can constrict/dilate)
• Nitric Oxide: vasodilator
• Prostacyclin: vasodilator produced by endothelial cells.

73
Q

Prostacyclin

A

from prostaglandins (arachidonic acid):
o Inhibits platelet activation
o Reduces calcium entry into smooth muscle cells.
o Opposite to thromboxane.

74
Q

Stages of Shock

A

Compensation:
Baroreceptors detect fall in BP = increase heart rate –> increased CO to restore BP

Decompensation:
arterioles cannot maintain constriction; blood preload reduction is too great.
Organs are not perfused and start to fail.

75
Q

Classes of Shock

A

Obstructive Shock: Physical obstruction to the vessels entering or leaving the heart
o Pulmonary embolism.
o (Tension) Pneumothorax.
o Cardiac tamponade.

Distributive Shock: Loss of vasoconstriction in one or more end organs
Classical Symptoms:
o Fever (may be absent in elderly/immunosuppressed).
o Chills
o Fatigue
o Vomiting

Cardiogenic Shock: Due to failure of heart to pump effectively 
Symptoms of acute cardiac ischemia:
	Chest pain
	Shortness of breath
	Nausea
	Vomiting

Hypovolemic Shock: Normally due to haemorrhage
Classical Signs (note = history is vital).
o Low blood pressure
o High heart rate
o Confusion/anxiety
o Slow capillary refill

76
Q

How much blood loss is life-threatening

A

Acute loss of 40% (>2 litres)

77
Q

Classes of Hypovolemic Shock

A

Class 1 = loss of <15%. Fully compensated (patient = tired)

Class 2 = loss of 15-30%. Tachycardia, tachypnoea, decrease in pulse pressure, delayed cap refill etc…
• Rest + normal access to water/food = fully compensated.

Class 3 = loss of <30%. Most patients’ = blood transfusion or plasma volume expanders. May have end-organ damage.

Class 4 = loss of > 40%. May be unconscious. This is life threatening. Blood transfusion should be given immediately

78
Q

Septic Shock Management

A

Hypovolemia = restore blood volume with i.v. colloids and crystalloids

Vasopressor drugs (dopamine, noradrenaline, ADH).

79
Q

How many genes code for alpha and beta globin

A

Alpha = 4 genes (chromosome 16)

Beta = 5 genes (chromosome 11)

80
Q

Two different forms of Fetal Haemoglobin

A

Hb Gower-1 = produced in the embryonic yolk sac
o First 6 weeks
o Zeta 2 Epsilon 2
o Variants may occur in early weeks

Fetal Haemoglobin F = zeta gene switched off after 6 weeks.
o Made in liver and spleen
 Lower affinity for O2 than Hb Gower-1 but still higher than maternal Hb.
o Alpha 2 Gamma 2

81
Q

Alpha Thalassemia and types

A

Deleted/faulty alpha gene on chromosome 16

One Alpha Gene Defective = Alpha thalassemia minima
- No clinical symptoms

Two Alpha Genes Defective = Alpha thalassemia minor
o Mild microcytic anaemia
o Often mistaken as IDA

Three Alpha Genes Defective = Haemoglobin H disease
o Two unstable haemoglobins present: Haemoglobin Barts (gamma 4) Haemoglobin H (beta 4)
o Have higher oxygen affinity = poor release of O2 in tissues

Four Alpha Genes Defective:
• Fetus cannot live outside the uterus
• Hydrops fetalis = fluid accumulation

82
Q

Beta Thalassemia

A

Autosomal recessive, Point mutation on chromosome 11

Beta thalassaemia minor (β+)  one allele defect
Beta thalassaemia major (βo)  both allele defect.

Pathological Effects
• Excess alpha globin produced. These can transfer O2 but are unstable, precipitate on RBC membrane.
o Intra-medullary (in bone marrow) destruction of developing RBCs
o Erythroid hyperplasia.
o Ineffective erythropoiesis.
• Results in severe hypochromic microcytic anaemia

83
Q

Excess haemolysis

A

Free iron may be released into the blood:

  • Fenton reaction = iron + hydrogen peroxide (from mitochondria) = hydroxyl radicals.
  • Radicals damage all biological tissues –> diabetes, glandular dysfunction, cirrhosis
84
Q

Excess haemolysis Treatment

A 
Desferoxamine 
•	Toxicity with higher doses 
Deferiprone
•	Oral 
•	Neutropenia
•	Danger in pregnancy. 
Deferasirox 
•	Oral
•	Gi bleeding
85
Q

SICKLE CELL DISEASE Genetics

A

Mutation: glutamic acid to valine
o Codon 6 of beta globin chain.
o Produces βS chain.
Haemoglobin S produced (α2βS2)
Deoxygenated blood = haemoglobin S may precipitate or crystallize.
o RBCs have decreases survival time –> anaemia.
o Occlude capillaries –> lead to ischemia and infarction

86
Q

Haemoglobin C

Haemoglobin E

A 
Haemoglobin C - abnormal beta subunit
Reduced plasticity/flexibility of RBCs.
Excess red cell destruction:
Heterozygous = no anaemia.
Homozygous = mild haemolytic anaemia

Haemoglobin E - single point mutation in beta subunit
Inherited from both parents.
Mild beta thalassemia a few months after birth.

87
Q

Signs and Symptoms of Heart Failure

A

Symptoms:
Fatigue
Dyspnoea
Oedema

Signs:
Cool Skin (blood is redistributed to more vital organs)
Peripheral cyanosis 
Basal crackles
Increased JVP
Ankle swelling
Ascites = fluid in abdominal cavity
Tachycardia
Sweating
S3 = rapid filling in diastole. 
Alternating pulse
88
Q

Chest-X Ray of Heart Failure

A 
A.	Alveolar oedema
B.	Kerley B-lines.
C.	Cardiomegaly.
D.	Blood flow perfusion to upper lobes.
E.	Effusion
89
Q

Complications of Heart Failure

A

Intravascular thrombosis due to stasis = pulmonary and systemic embolisms

Infection = chest infection (because of oedema) or ulcerated cellulitic legs

Valvular dysfunction = enlargement of LV or RV.

Multi-organ failure = liver or renal failure

Cardiac arrhythmias.

90
Q

Brain Natriuretic Peptide (BNP)

A

Secreted by myocardial cells in response to increased LAP

  • Promotes natriuesis (excretion of sodium and therefore water) and vasodilation
  • Inhibits ADH and aldosterone release

Levels >100 pg/ml = heart disease as likely cause of dyspnoea and fluid retention

91
Q

Diastolic failure

A

ventricle is not able to fill properly = concentric hypertrophy

92
Q

Systolic failure

A

heart cannot contract properly = eccentric hypertrophy

93
Q

Systolic Failure Medication

A

ACE Inhibitors
ARBs (if ACE’s not tolerated)
Beta-Blockers (all grades of failure)
Spironolactone (potassium sparing drug)

Medicine PJE (7 decks)

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