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CR2 > CR - Week 1 > Flashcards

CR - Week 1 Flashcards

1
Q

How is the heart innervated?

A

Cardiac plexus, anterior to the carina, containing parasympathetic, sympathetic, adn general visceral afferents

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2
Q

What is the parasympathetic pathway of the heart

A

Passes through the reticular formation in the medulla through the cardio-inhibitory centre and starts from the dorsal motor nucleus. It travels via the vagus nerve to the SA and AV node

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3
Q

How is referred cardiac pain caused?

A

Ischaemia

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4
Q

What and how can there nbe coronary artery variations?

A

Dominance, depends on the origin of yje posterior descending artery
- Right and left (left = longer circumflex)

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5
Q

What is teh relationship between atrial fibrillation and atrial enlargement?

A

Larger atrium = increased fibrillation risk, atrial fibrillation is as a result of ectopic firing

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6
Q

Why is there a risk of stroke in atrial enlargement?

A

in a large atrium, blood pools causing passive ventricle filling.

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7
Q

What happens in a bundle branch block?

A

Impulse conduction ceases, so depolarisation cannot happen so is altered. The impulse travels through myocytes, slowing impulse speed, prolonging the QRS complex. This can lead to a loss of ventricular synchrony and a wide QRS complex

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8
Q

What is cardiac remodeling

A

Structural changes as a result of a difference in preload and afterload

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9
Q

What does cardiac remodelling lead to?

A

An increase in myocardial mass and increased collagen synthesis due to increased (myocyte) size

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10
Q

What are some physiological reasons for cardiac modelling?

A

pregnancy and atheletes

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11
Q

What are the two types of hypertrophy?

A

Concentric and eccentric

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12
Q

What are the causes of pathological ventricular hypertrophy?

A
  • response to pathological stress
  • Pressure overload
  • Volume overload (hypervolemia)
  • cardiac injury
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13
Q

What does ventricular hypertrophy lead to?

A

New sarcomeres, increased myocyte size, collagen synthesis, insufficient angiogenesis, increaserd fibrous tissue, myocyte apoptosis

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14
Q

What is preload and afterload?

A 
Preload = end diastolic pressure
Afterload = aortic resistance
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15
Q

What happens in concentric hypertrophy?

A

Increased afterload, increased wall thickness and this can lead to eccentric hypertrophy

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16
Q

What happens in eccentric hypertrophy?

A

Chamber dilation, elevates oxygen demand, lowers mechanical efficacy
- from concentric due to increased afterload increasing EDV so more push back

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17
Q

What is valvular disease?

A

Valve inflammation

- fibrosis and calcification, stenosis and regurgitation

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18
Q

What are the effects of aortic stenosis?

A

hypertrophied myocardium reducing compliance and decreasing coronary blood flow reserve

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19
Q

What is aortic regurgitation?

A

diastolic murmer, rheumatic, associated with aortic stenosis. Complex but absent sound and elevates pre and afterload

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20
Q

What is mitral regurgitation?

A
  • may show evidence of left atrial enlargement adn left ventricular eccentric hypertrophy
  • most common valvular diease
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21
Q

What is mitral stenosis?

A
  • Rheumatic

- ventricular filling reduced - reduced cardiac output

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22
Q

Where does cardiogenic pulmonary oedema occur?

A

Lung Hilum, kerley B lines visible

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23
Q

What is the difference between pulmonary oedema abd pleural effusion?

A
  • Oedema = fluid in the alveoli adn vasculature

- effusion = fluid saturated in pleural space

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24
Q

What is the conduction system of the heart?

A
  1. Stimulus orinates in SA node and travels across the walls of the atria, causing them to contract
  2. stimulus arrives at the AV node, and travels along AV bundle
  3. stimulus descends to heart apex through bundle branches
  4. after stimulus reaches purkinje fibres, the ventricles contract
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25
Q

What does lead 2 do?

A

Generate rhythm strip, where PR interval is measured

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26
Q

What are the features of a 12 lead ECG?

A
  • 120-200ms PR interval
  • less than 120ms QRS
  • Absent s wave in v6
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27
Q

What is rhythm?

A

ECG originates in the SA node, RR interval and normal P wave = sinus rhythm or otherwise, not sinus

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28
Q

What is sinus arrhythmia?

A

Heart rate varies in phase with breathing

- increases in inspiration

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29
Q

What do regular P waves but irregular RR intervals mean?

A

Heart block, QRS complexes don’t have to follow

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30
Q

What does a wide QRS indicate?

A

Slow/desynchronised ventricular depolarisation

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31
Q

When does valve closure happen?

A

at the beginning ventricular contraction, blood regurgitation

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32
Q

what does hypokalaemia produce?

A

Small, inverted T wave, T wave is due to the difference in repolarisation

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33
Q

what is sinus bradycardia?

A

less than 60 bpm,

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34
Q

What is sinus tachycaria?

A

SNS overactivity originating from the SA node. 120bpm

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35
Q

What is junctional rhythm?

A

Damage to the SA node, block in the induction pathway. AV node acts as a pacemaker
- missing/inverted P wave

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36
Q

What are the 4 types of supraventricular tachycardia?

A
  • atrial fibrilation
  • atrial flutter
  • AV nodal reentrant tachycardia
  • wolff parkinson white syndrome
    =P waves absent/buried in preceding T wave
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37
Q

what is atrial fibrilation caused by?

A
  • Ischaemia -> atrial tissue damage

- low stroke volume

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38
Q

What is the difference between atrial flutter and atrial fibrillation?

A

In atrial flutter there is only 1 excitatory focus (not SAN, high rate)
In fibrillation, node excitees itself at a high rate at seperate atrial pacemakers

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39
Q

What is AV nodal reentrant tachycardia?

A

Reentry circuit around AV node, not SA node

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40
Q

What is Wolff parkinson white syndrome?

A

extra electrical pathway between atria and ventricles, may cause paroxsysms of tachycardia or atrial fibrillation

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41
Q

What is ventricular tachycardia?

A

poor cardiac output, rhythm is triggered by abnormal tissue in ventricles

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42
Q

What is ventricular fibrillation?

A

All disorganised, little to no cardiac output, immediate treatment is defibrillation

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43
Q

What do you look at in a heart block?

A
  • primary sinus bradycardia, long PR

- If QRS is missing or irregular (pathological)

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44
Q

What is mobitz type 1 second degree heart block

A

ALSO CALLED WENKENBACH

- increased PR interval, eventually no QRS adn missed ventricular beat

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45
Q

What is Mobitz type 2 heart block?

A

regular P waves., ventricles fail to respond to atrial impulses. Irregular ventricular rate

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46
Q

What is 3rd degree heart block?

A

present but unsynchronised Pwaves, slow escape rhythm. Maintained but limited cardiac output,

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47
Q

What is bundle branch block

A

Wide QRS, notch on it too.

Asynchronous activation of ventricular muscle in ventricles due to delay or blockage in purkinje fibres

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48
Q

what is ST elevation?

A

Myocardial infarction, due to failure of ventricular action potentials to propagate into some part of ventricuar muscle; visible on 2 leads for acute MI diagnosis

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49
Q

When do you get an inverted T wave?

A

hypokalaemia, hypothyroidism

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50
Q

What is ST depression?

A

reciprocal response to ST elevation, on its own it indicates ischaemia/hypokalaemia

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51
Q

Which leads are negative?

A

aVR is negative, others are positive

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52
Q

What is the difference between primary and secondary haemostasis?

A 
Primary = platelet plug formation
secondary = fibrin clot formation
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53
Q

What is haemostasis?

A

Cessation of bleeding at a vascular injury site by thrombus formation, consists of a platelet plug and a fibrin clot

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54
Q

Where do platelets come from?

A

megakaryocytes, formed from myeloid stem cells in bone marrow

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55
Q

How is platelet production regulated?

A

Thrombopoietin, high platelet count = thrombocytosis and low is thrombocytopenia, normal is 150-400

56
Q

How does local vasoconstriction occur in primary haemostasis?

A

intact endothelial lining releases nitric oxide adn prostacyclin, relaxing smooth muscle. When endothelium is damaged, NO and prostacyclin release stops and endothelin is released from damaged cells and acts on ETa as a vasoconstrictor. There is sympathetic nerve fibre damage - release of local noradrenalin constricts

57
Q

What triggers secondary haemostasis?

A

Blood clot formation, triggered by exposure to the blood of the tissue underlying endothelium, leads to the start of platelet plug formation and the start of the coagulation cascade

58
Q

What protein is foind in blood plasma?

A

von williband factor

59
Q

What receptors are used to bind VWF to platelets?

A

glycoprotein 1b receptors, express glycoprotein 2b and 3a

60
Q

What happens at the start of platelet plug formation?

A

VWF binds to exposed damaged collagen, platelets bind to VWF GP1b receptors, collagen and platelet bridge formed

61
Q

waht are the three components of the coagulation cascade?

A

intrinsic, extrinsic, common

62
Q

What is released from damaged blood vessels and what does it do?

A

Tissue factor 3, reacts with factor 7 to convert to factor 7a which reacts with calcium and factor 10 to factor 10a

63
Q

Why is factor 10a important?

A

10a and calcium2+ converts a small amount of prothrombin to thrombin, which is the initiation phase of the coagulation cascade(+ve feedback)

64
Q

What is the platelet release reaction?

A

Platelets release ADP, 5HT, thromboxane A2

65
Q

How are platelets activated?

A

Thrombin binds platelets with fibrinogen and then are activated

66
Q

What is bleeding time?

A

Time taken to form an effective platelet plug and stop initial haemorrhage

67
Q

Why is aspirin an anticoagulant?

A

Blocks cyclooxygenase enzyme, preventing prostaglandin H2 formation and therefore preventing thromboxane a2

68
Q

How is the platelet plug stabalised?

A

thrombin, catalysed by conversion of fibrinogen to fibrin (coagulation cascade)

69
Q

What can sepsis do (in coagulation)?

A

Disseminated intramuscular coagulation - clots form in intact blood vessels because fibrin blocks blood vessels

70
Q

What do you find in platelets?

A

Polyphosphate anions that are released from activated platelets

71
Q

What triggers the start of the intrinsic pathway?

A

platelets converting factor 12 to 12a

72
Q

What does factor 12 do?

A

activate kallikrein like bradykinin which triggers the extravasation of blood vessels

73
Q

What tests are used to test for coagulation disorders?

A

bleeding time - platelet function
prothrombin time - extrinsic and common pathway
activated partial thromboplastin time - intrinsic and common

74
Q

What is normal INR?

A

0.8-1.2

75
Q

What is the effect of factor 13a?

A

unstable clots, prolonged bleeding without it. Important in wound healing, and pregnancy

76
Q

What is haemophilia A caused by?

A

deficiency in factor 8, due to less feedback stimulation of thrombin and less thrombin in clots

77
Q

What is haemophilia B caused by?

A

factor 9 deficiency, leads to a reduced positive feedback loop

78
Q

how are clots removed?

A

Plasmin breaks down fibrin and lyses clot, plasmin circulates as inactive plasminogen. Convrt prevented by alpha 2 antiplasmin release. When release ceases, T issue plasminogen activator released converting plamasminogen to plasmin.

79
Q

What is D-dimer?

A

Fragment of lysed protein circulating blood and are high in proteins with spontaneous clots, D- dimer measurements is a useful tool to measure clots

80
Q

What does vitamin K do?

A

modifies factor 7, 9, 10 to increase calcium binding,

81
Q

When do you use vitamin K as a treatment?

A

Warfarin overdose

82
Q

What are two anticogulants?

A
  • Heparin = natural, must be injected

- Warfarin = difficult to predict effects, INR must be monitored

83
Q

What are some directly acting anticoagulants?

A

DABIGATRAN

10a inhibitors = rivaroxaban, apixaban, edoxaban

84
Q

what is the value for macrocytic anaemia

A

less than 96 fl,

85
Q

Why is b12 important?

A

DNA replication, myelin synthesis, nerve metabolism, fatty acid synthesis
- lower availibility of reduced gluthathione in cobalamin deficiency exposing cells to oxidative stress

86
Q

Where is B12 found?

A

meat proteins stored in liver

87
Q

what happens in a B12 deficiency?

A

severe and irreversible nervous system damage, also affects metabolism

88
Q

how is the b12/intrinsic factor complex absorbed?

A

pinocytosis into a vesicle in an enterocyte in ileal wall

89
Q

How can you assess B12 levels?

A

indirectly via serum methylmalanoic acid - can be false positive

90
Q

What can b12 be used as a cofactor for?

A

tetrahydrofolate synthesis by methionine synthase

91
Q

What histologically can you tell macrocytic anaemia?

A

hypersegmented nuclei in neutrophils -> maybe due to free haemoglobin present

92
Q

what are the factors of pernicious anaemia?

A

anaemia, atrophic glossitis, mild jaundice, neurological symptoms

93
Q

What can you see in haemolytic anaemia?

A

pallor, anaemia, jaundice, Gallstones, splenomegaly, healthy bilirubin is below 17, above 34-51 is jaundice

94
Q

what are the main reasons for haemolytic anaemia?

A

damaged cell membrane, abnormal haemoglobin, deficiency in intracellular enzyme

95
Q

What happens in hereditary spherocytosis?

A

defect, RBC becomes spherical and very fragile. It is autosomal dominant. Low haemoglobin, high serum bilirubin

96
Q

what is an enzyme defect in RBC?

A

glucose 6 phosphate dehydrogenase deficiency, X linked

97
Q

Which triggers carriers of G6PD?

A
  • Broad beans
  • bacterial/viral infection
  • oxidative stress drugs eg dapsone contrimoxazole, primaquine
98
Q

what happens in autoimmune haemolytic anaemia?

A

IgG reacts with red cell membrane antigens, labelling it for destruction. They are removed then by the spleen

99
Q

What are the causes of haemolytic anaemia?

A

idiopathic.

- secondary: blood transfusion, drugs, connective tissue and systemic erythmatous

100
Q

How much iron does the average diet contain?

A

15mg, 3-5g in the total body

101
Q

how is iron mainly carried and transported?

A

DMT 1

- divalent metal transporter 1

102
Q

What does ferric reductase do?

A

converts and reduces Fe3+, allowing it to be transported into the cell

103
Q

what are the normal ferritin levels?

A

20-250 micrograms in men, 20-160 micrograms

104
Q

What is ferritin?

A

hollow polyprotein - 24 apoferritin subunits, many atoms stored in its inactive form
- small amounts are secreted into the serum - iron carrier

105
Q

why is plasma ferritin important?

A

indirect marker of total amount of iron stored in the body

- low serum ferritin is an important diagnostic tool for deficency

106
Q

How is iron transported out of the enterocyte?

A
  • ferroportin molecules in the basolateral membrane

- outer side is bound by transferrin molecules in the plasma

107
Q

What is hepcidin, what does it do?

A
  • protein made in liver that regulates iron metabolism
  • inhibits iron transport inrp blood, binds to ferroportin. breaks down the transporter protein, presenting iron from being exported, reducing absorption
108
Q

What happens in hepcidin levels in chronic disease?

A

rises; chronic disease anaemia

109
Q

What are transferrins?

A

iron binding glycoproteins carrying iron around the body vs the blood. Each transferrin molecule carries 2 atoms in the ferric form

110
Q

How is iron stored as ferritin?

A

transferrins are loaded with iron binding to transferrin receptors on the surface of a cell needing iron.
Then transported into a cell via endocytosis and stored in a vesicle .
Low pH allows transferrin to release iron, ions are reduced to ferrous form.
Transported out by DMT1 and are stored in ferritin molecules for future use.
Transferrin released to be reused as empty endosome adn transferrin receptor is transported to cell surface

111
Q

How does erythropoesis occur in adults?

A

Red marrow, bone marrow is also known as myeloid tissue

112
Q

when does red blood cell formation occur in the foetus?

A
  • Yolk sac at 3rd week
  • liver at 6 weeks
  • bone marrow at 3 months onwards
113
Q

Describe the process of erythropoiesis

A

-Haematopoietic stem cell or haemocytoblast
- differentiates into a cell called a common myeloid progenitor
- proerythroblasts. The proerythroblast then undergoes a series of transformations where its nucleus progressively shrinks
- erythroblast
- normoblast
- reticulocyte
RBC

114
Q

what is a proerythroblast?

A

A common myeloid progenitor that can differentiate and commit to form RBCs

115
Q

what is the development pathway for an erythrocyte?

A

most reticulocytes stay in the marrow but some may be released into the blood, they are less efficient than erythrocytes

116
Q

what is diapedesis?

A

new erythrocytes squeeze through pores in the capillary membrane to enter blood

117
Q

How is erythropoiesis controlled?

A

Erythropoietin produced in interstitial cells in kidney around proximal tubule

118
Q

Why does the kidney control erythropoietin?

A

Tightly regulated GFR so O2 levels are not altered by changes of blood pressure or excersize, instead by renal flow and arterial haemoglobin

119
Q

What does EPO do?

A

Increases the speed of erythroblast maturation, increasing proerythroblast formation

120
Q

How do RBCs make ATP?

A

Anaerobic glycolysis, glucose enters via GLUT1 transporter, driven by NAD, pyruvate reacts with NADH to form lactate and NAD+. 2 ATP per glucose

121
Q

What is erythrocyte sedimentation rate?

A

indirectly measures degree of inflammation in the body, increases with age due to increased fibrinogen levels

122
Q

How does the spleen recycle redblood cells?

A

rigid senescent cells - transported in narrow sinus’, unable to make ATP. Cells swell and will be larger, prosthetic haem groups removed and broken apart. haems iron atoms are collected by transferrin carrying iron in the blood to the liver -> bone marrow

123
Q

What is Bilivirdin?

A

Opened porphyrin ring, reduced to bilirubin by bilivirdin reductase

124
Q

What is (un)conjugated bilirubin?

A

bilirubin that binds with albumin, the complex is released in blood. comjugated bilirubin is when you have unconjugated bilirubin that has binded with glucironic acid by hepatocytes to become glucuronic acid

125
Q

What happens to conjugated bilirubin?

A

Passes from the liver in bile to small intestine, bacteria converted into urobilinogen. Most urobilinogen leaves the body in faeces or after sterobilin conversion

126
Q

When can you see elevted urobilinogen in plasma?

A

Haemolytic anaemia

127
Q

What are the anaemia values?

A

Adult Male <13.5 g/dl Hb Adult Female <11.5 g/dl Hb Child 6–14 years <12 g/dl Hb
Infant 6 months–6 years <11 g/dl Hb

128
Q

what is iron deficency anaemia?

A

10ml blood loss per day, MCH less than 27 pg

129
Q

Describe iron bioavailability in adults

A

haem iron is highest in meat, easily imported by enterocytes. Proton pumo inhibitors can reduce stomach acid and decrease iron absorption, increased when iron is in form of haem, hypoxia, pregnancy and low iron in diet.

130
Q

How are blood groups determined?

A

Red blood cell surfaces, the carbohydrate lipid bilayer acts as an antigen. Genes determine the structure and sugar residues from one type adn protein (ABO)

131
Q

What are autoantibodies and alloantibodies?

A
  • antibodies reacting with antigens on a persons own RBCs (auto)
  • antobodies produced after exposure to foreign red blood cell antigens = allo
132
Q

Explain the ABO blood group system.

A

The expression of A and/or B polysaccharide antigens is determined by the presence of certain enzymes
•Naturally occurring antibodies
• Anti-a
• Anti-b
• Primarily I gM Antibodies but some I gG
Antibodies

A - has anti -B in plasma
B - has anti -A in plasma
O - has anti -A and anti -B in plasma
AB - has no ABO antibody in plasma

• Blood of g rou p A will b e ag g lu t in at ed b y an t i-a
• Blood of g rou p B will b e ag g lu t in at ed b y an t i-b
• Blood of g rou p AB will b e ag g lu t in at ed b y an t i-a
an d an t i-b
• Blood of g rou p O will n ot b e ag g lu t in at ed b y an ti-
a or an t i-b

133
Q

What is the difference between genotype and phenotype

A

phenotype amd genotype table

  • phenotype = cell membrane antigens
  • genotype = DNA encoded
134
Q

what is the rhesus blood group system?

A

3 protein pairs inherited as a triplet, c,d e.

D = immunogenic and determines positive or negative rhesus factor

135
Q

Wat are the rhesus factor genotypes?

A

CcDe

- anti C, anti c, anti D, anti e but not anti E

136
Q

what are the rhesus criteria for blood transfusions?

A

avoid RhD+ve to RhD-ve

Especially child bearing age

137
Q

whta happens if a foetus os rhesus positive but the mother is negative?

A

haemolytic disease of the foetus and newborn

CR2 (1 decks)

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