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2 - CR/MET > CR physiology > Flashcards

CR physiology Flashcards

1
Q

Types of antibodies against ABO antigens

A

IgM

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2
Q

What is mixed in forward blood grouping?

A

Patients blood with known antibodies

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3
Q

What is mixed in reverse blood grouping?

A

Patients blood with known blood cells

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4
Q

Types of antibodies against Rhesus antigens

A

IgG

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5
Q

Most clinically important Rhesus antigen?

A

D

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6
Q

When does HDN occur?

A

Rh- negative most carrying second Rh+ child

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7
Q

What type of alleles are A and B?

A

Codominant

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8
Q

Which are the most common blood groups seen in Caucasians?

A

A and O

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9
Q

What is the most common blood groups seen in Asians?

A

B

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10
Q

Rhesus - innate or immune antibodies?

A

Immune

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11
Q

When can Rh sensitisation occur?

A

Transfusion
Pregnancy
Transplant

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12
Q

Which is more common - Rh+ or Rh-?

A

Rh+

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13
Q

How is HDN prevented?

A

Anti-D injection to all Rh- mothers

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14
Q

Treatment of acute transfusion reaction?

A

Stop transfusion
Saline for hypotension
Frusemide to maintain renal perfusion
DIC treatment

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15
Q

What does a direct Coombes test test for?

A

Autoimmune antibodies to own RBCs

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16
Q

What does an indirect Coombes test test for?

A

Detects unbound antibodies present in patients plasma
Used to look for rare antibodies
Used in cross matching

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17
Q

Step 1 antihypertensive treatment

A

<55 = ACEI

>55 or black = CCB

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18
Q

Step 2 antihypertensive treatment

A

ACEI + CCB

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19
Q

Step 3 antihypertensive treatment

A

ACEI + CCB + thiazide

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20
Q

Step 4 antihypertensive treatment

A

Above + further diuretics or alpha/beta blocker

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21
Q

Side effects of CCBs

A

Flushing, oedema

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22
Q

Side effects of ACEIs

A

Cough, hypotension

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23
Q

Side effects of ARBs

A

Hypotension

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24
Q

Side effects of Thiazides

A

Low K+, impotence

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25
Q

Side effects of beta blockers

A

Bronchospasm, lethargy

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26
Q

MI immediate treatment

A

Oxygen
Aspirin
Opiates
Thrombolysis/PCI

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27
Q

Secondary MI prevention

A

Beta blockers
ACEIs
Statins
Lifestyle

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28
Q

Polypil contents

A

Aspirin (75mg)
Statin
3 BP lowering drugs
Folate

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29
Q

1 small square on ECG

A

= 0.04s

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30
Q

1 big square on ECG

A

= 0.2s

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31
Q

P wave duration

A

<0.08

<2 small squares

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32
Q

PR interval duration

A

<0.2s

<5 small squares

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33
Q

QRS complex interval

A

<0.12s

<3 small squares

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34
Q

First degree heart block

A

Regular

PR intervals >0.2s

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35
Q

Second degree heart block type 1

A

Each successive PR interval gets longer until a QRS complex is dropped

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36
Q

Second degree heart block type 2

A

QRS complexes randomly dropped

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37
Q

Third degree heart block

A

No synchrony between atrial and ventricular rhythms

Often bradycardic

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38
Q

AF

A

Irregular rhythm

Rate = 100-160

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39
Q

Atrial flutter

A

Regular rhythm
F waves instead of P waves
Rate = 110
F wave rate = 300

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40
Q

Junctional rhythm

A

AVN takes over as pacemaker
Rate = 40-60
P wave may be seen and may be inverted

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41
Q

SVT

A

Rate = 140-200
Regular rhythm
Due to AF, AF or Wollf-Parksinson-White syndrome
P waves often absent

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42
Q

AV nodal re-entrant tachycardia

A

Regular
P waves often seen after QRS complex
Reentry circuit within to just next to the AVN

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43
Q

Pathology of WPW syndrome

A

Extra electrical pathway connecting atria and ventricles
Shortened PR interval
Delta wave

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44
Q

Bundle branch block

A

Prolonged QRS
Notched R waves in V1 in RBBB
Notched R waves in V6 in LBBB

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45
Q

Causes of LAD

A

LVH

Inferior MI

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46
Q

Causes of RAD

A 
RVH 
LV atrophy 
Lateral MI 
COPD, tall, thin
Dextrocardia
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47
Q

Sites of RBC production in foetus

A

3-6 weeks = yolk sac
6 weeks - 3 months = liver and spleen
3 months onwards = bone marrow

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48
Q

Which bones become the final haematopoietic bones?

A

Vertebrae, sternum, ribs, cranial bones, ilium

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49
Q

Appearance of proerthyroblast

A

Large cell with large nucleus
Basophilic cytoplasm
Perinuclear halo
Nucleoli

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50
Q

Appearance of early erythroblast

= basophilic normoblast

A

Still dark blue cytoplasm
Less cytoplasm
Loss of perinuclear halo

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51
Q

Appearance of intermediate erythroblast

= polychromatophillic normoblast

A

Nucleus getting smaller

Reduced blue staining of cytoplasm

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52
Q

Appearance of late erythroblast

= orthochromic normoblast

A

Cytoplasm almost completely pink

Nucleus even smaller

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53
Q

Appearance of a reticulocyte

A

Expulsion of nucleus
Slightly bigger than mature RBC
Blue hue remains to cytoplasm

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54
Q

When does a reticulocyte become an erythrocyte?

A

After 1 day in circulation

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55
Q

Erythrocyte diameter

A

7.8um

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56
Q

Normal erythrocyte levels

A

= 5.2x10 6 /uL in males

= 4.7x10 6 /uL in females

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57
Q

Where is EPO produced?

A

Kidney fibroblasts

Type I glomus cells of carotid body

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58
Q

What does increased ESR show?

A

Infection of the blood

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59
Q

What structures are formed when ESR is high?

A

Rouleaux

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60
Q

GLUT transporters in RBCs

A

GLUT1

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61
Q

What enzyme breaks open haemoglobin?

A

Haemoxygenase

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62
Q

What is biliverdin?

A

Openen pophyrin ring without iron

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63
Q

What converts biliverdin –> bilirubin?

A

Biliverdin reductase

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64
Q

Where does biliverdin –> bilirubin take place?

A

Within macrophages

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65
Q

What conjugated bilirubin?

A

Glucoronic acid

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66
Q

What does bacteria convert bilirubin to?

A

Urobilinogen

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67
Q

What is urobiliogen further oxidised to?

A

Stercobilin

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68
Q

Average VO2 max

A

250ml/min

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69
Q

Local dilatory factors released by muscle

A

NO, adenosine, phosphates, carbon dioxide, H+, K+

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70
Q

Pulmonary ventilation at rest

A

8L/min

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71
Q

Pulmonary ventilation in peak levels of exercise

A

100L/min

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72
Q

Which way does oxygen dissociation curve shift in exercise?

A

To the right

Improves oxygen delivery to tissues

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73
Q

What causes this Bohr shift?

A

Increased CO2 and H+

Increased local temperature

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74
Q

Platelet diameter

A

1-4um

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75
Q

Normal platelet range in blood

A

140-400x10 9 /L

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76
Q

Lifespan of platelets

A

8-14 days

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77
Q

How are platelets removed?

A

By the reticuloendothelial system

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78
Q

What does GpIb bind to?

A

vWF

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79
Q

What does GpIIB/IIIA bind to?

A

vWF and fibrinogen

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80
Q

What do alpha granules release?

A

Proteins –> vWF, fibrinogen, TPAI-1

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81
Q

What do delta granules release?

A

ADP

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82
Q

What disorder = lack of GpIb?

A

Bernard Soulier syndrome

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83
Q

What disorder = lack of GpIIb/IIIa?

A

Glanzmann’s syndrome

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84
Q

What factors do platelets release that cause attractions and aggregation?

A

Serotonin, ADP, TXA2

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85
Q

Treatment of mild VWF disease?

A

DDAVP

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86
Q

Extrinsic pro-tenase complex

A

TF + VIIa

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87
Q

Intrinsic pro-tenase complex

A

VIIIa + IXa

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88
Q

Which enzymes does thrombin enhance the activity of?

A

5,8,9,11,13

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89
Q

Haemophilia A

A

Factor 8 deficient

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90
Q

Haemophilia B

A

Factor 9 deficient

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91
Q

Haemophilia A treatment

A

DDAVP, factor VIII

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92
Q

Haemophilia B treatment

A

factor IX

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93
Q

Where are common bleeding sites?

A

Soft tissue
Joints
Operative sites
Cranium

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94
Q

What does antithrombin inhibit?

A

2, 7, 9, 10, 11, 12

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95
Q

What does protein C inhibit?

A

5 and 8

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96
Q

What are vitamin K dependant?

A

2, 7, 9, 10, protein C, protein S

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97
Q

What does tPA activate

A

Plasminogen –> plasmin

Fibrin –> fibrinogen

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98
Q

What does fibrin breakdown produce?

A

D-dimer

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99
Q

What is the reaction that produces NO?

A

L-arginine + oxygen

–> NO + citrulline

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100
Q

Where is NOS I found?

A

In the brain

Calcium dependant

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101
Q

Where is NOS II found?

A

Most nucleated cells

Particularly in macrophages

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102
Q

What activates NOS II?

A

Inflammatory cytokines

Calcium independant

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103
Q

Where is NOS III found?

A

Vascular endothelial cells

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104
Q

How is NOS III activated?

A

Sheer stress from blood friction opens calcium channels
Calcium activated calmodulin
Calmodulin activates eNOS
With cofactors –> biopterin H4, FMN, FAD
Can also be stimulated by ACh –> calcium entry

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105
Q

Nitric oxide action

A

Diffuses from endothelium –> smooth muscle cells
Activates guanylate cyclase
Converts GTP –> cGMP
Causes vascular smooth muscle relaxation

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106
Q

How is NO produced in exercise when there is a lack of oxygen?

A

Exercise converts nitrate to nitrous acid

Reduced –> NO

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107
Q

What happens to eNOS in atherosclerosis

A

Endothelium damaged so cannot produce NO by eNOS
Coronary vessels cannot dilate in exercise
–> angina and acidosis

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108
Q

How does NO improve oxygen delivery?

A

NO enters blood
Binds to haemoglobin to displace oxygen
Forms nitrosohaemoglobin

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109
Q

How does acid base balance alter blood brain flow?

A

Increased in acidosis

Decreased in alkalosis

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110
Q

Where can clots commonly form?

A

Auricles of the atria

Deep veins of the calf

111
Q

When does hypoxic ventilation drive begin?

A

PO2 <60mmHg

112
Q

When do we initially suffer the effects of altitude?

A

Over 2000m

113
Q

Where is the death zone?

A

7500m and above

114
Q

How is a metabolic acidosis generated by the kidney?

A

Decreased H+ ATPase activity in DCT

Increased bicarbonate excretion

115
Q

How is an increased erythrocyte number generated?

A

Increased EPO secretion

116
Q

How is pulmonary vascular resistance decreased?

A

Collateral circulations

Increased NO synthesis

117
Q

What is the action of Diamox

A

= acetazolamide
Carbon anhydrase inhibitor
Prevents bicarbonate reabsorption in the PCT
Speeds up acclimatisation
High doses can also block carbon dioxide transport by Hb to decrease respiratory loss

118
Q

Treatment of high altitude cerebral oedema

A 
Oxygen 
Descent 
Diamox 
Dexamethasone
Hyperbaric chamber
119
Q

Treatment of high altitude pulmonary oedema

A 
Oxygen 
Sit upright 
Descent 
Hyperbaric chamber 
Nifedipine (CCB) --> reduces PAH 
Viagra (sildenafil) --> slows down cGMP breakdown
120
Q

Causes of respiratory acidosis

A 
Hypoventilation 
Narcotics + alcohol 
COPD, asthma
Scoliosis 
Severe obesity 
Neuromuscular damage
121
Q

Treatment of respiratory acidosis

A

Underlying cause
Bronchodilators
CPAP/BiPAP
Oxygen

122
Q

Signs and symptoms of respiratory acidosis

A

Those of low CNS pH
Headache, drowsiness, anxiety, fatigue, memory loss, muscle weakness
Slowed breathing, gait disturbance, blunted tendon reflexes, tremor, papilloedema, tachycardia, hypotension

123
Q

Maximum bicarbonate levels that can be reached

A

45mmol/L

124
Q

Minimum bicarbonate levels that can be reached

A

12mmol/L

125
Q

Respiratory alkalosis causes

A 
Hyperventilation 
Anxiety, pain 
Pregnancy
Sepsis and fever
Altitude 
Salicyclates and progesterone 
CVA
126
Q

Symptoms of respiratory alkalosis

A

Dizziness, confusion, cramps and tingling in hands and mouth, blurred vision, spasms, seizures, irregular HR, tetany

127
Q

Diagnostic FEV1/FVC ratios

A 
<75% = obstructive 
>75% = restrictive
128
Q

Peak flow in asthma

A

Diurnal variation

129
Q

Reversibility testing

A

400mg salbutamol by inhaler
2.5mg salbutamol by nebuliser
30mg/day steroids for 2 weeks

Peak flow must improve by >15% and >200ml

130
Q

When is total lung carbon monoxide increased?

A

Increased cardiac output, polycythaemia, alveolar haemorrhage

131
Q

When is total lung carbon monoxide decreased?

A

Decreased perfusion, decreased ventilation, V/Q mismatch, anaemia

132
Q

Causes of reduced lung surface area

A

Lobectomy, pneumonectomy, airway obstruction, increased dead space, emphysema

133
Q

Causes of hypovolaemic shock

A

Haemorrhage

Cholera

134
Q

Causes of cardiogenic shock

A

MI, valve disease, myocarditis, heart failure

135
Q

Causes of obstructive shock

A

PE

Cardiac tamponade

136
Q

Causes of distributive shock

A

Sepsis

Anaphylaxis

137
Q

How are mast cells activated

A

Cross linking with IgE
Via complement C3a and C5a
Via nerves –> substance P
Via direct contact with pathogen

138
Q

What do mast cells release?

A

Histamine
Leukotrienes
Prostaglandins

139
Q

What does histamine do?

A

Increases capillary permeability
Vasodilation
Itching

140
Q

What do leukotrienes do?

A

Increase capillary permeability

Cause chemotaxis

141
Q

What do prostaglandins do?

A

Arteriolar dilation
Pain
Fever

142
Q

What is angioedema

A 
Swelling of subcutaneous tissues
Face
Lips 
Hands and feet 
Pharynx 
Larynx
143
Q

What drugs commonly trigger anaphylaxis?

A 
Beta lactase 
Aspirin 
NSAIDs
Insulins 
Anaesthetics
144
Q

Anaphylaxis treatment

A 
500mg adrenaline in 0.5ml 
Epipen = 300mg adrenaline in 0.3ml 
High flow oxygen 
Saline 
Antihistamines (chlorpheniramine) 
Corticosteroids (hydrocortisone)
145
Q

Total body iron

A

3-5g

146
Q

Where is iron absorbed?

A

Duodenum

147
Q

How is iron absorbed?

A

As Fe2+

Ferric reductase can reduce Fe3+ to 2+

148
Q

Transferrin

A

Iron binding plasma protein
Carries two Fe3+ ions
Binds to transferring receptor and is endocytose
Releases iron

149
Q

Ferritin

A

Intracellular iron store
Buffer
Cytoplasmic
Diagnostic for iron deficiency

150
Q

Anaemia Hb levels

A

Adult male <13.5g/dl
Adult female <11.5g/dl
6-14 <12g/dl
6m-6yrs <11g/dl

151
Q

Anaemia cell sizes

A 
<76fl = microcytic 
76-96fl = normocytic 
>96fl = macrocytic
152
Q

Causes of microcytic anaemia

A

Iron deficiency

Thalamssaemia

153
Q

Causes of normocytic anaemia

A

Chronic disease
Acute blood loss
Cancer
Haemolysis –> sickle cell

154
Q

Causes of macrocytic anaemia

A

B12/folate deficiency

Alcoholic liver disease

155
Q

Factors enhancing iron absorption

A 
Iron in meat 
Fe2+ iron 
Pregnancy 
Acid pH 
Hypoxia 
Iron deficiency
156
Q

Factors reducing iron absorption

A 
Iron in vegetables
Fe3+ iron
Alkaline pH 
Iron overload 
Inflammatory disorders
157
Q

Vitamin B12

A 
Water soluble
Found in meat, eggs, animal protein
Not destroyed by cooking 
Can be stored 
Absorbed in ileum bound to IF
158
Q

Signs of pernicious anaemia

A

Insidious onset
Glossitis
Mild jaundice
Neurological symptoms

159
Q

Treatment of pernicious anaemia

A

IM B12 every 3 months

160
Q

Folate

A 
Water soluble vitamin 
Found in liver, greens, yeast 
Destroyed by cooking
Very little can be stored
Absorbed in the duodenum and jejunum
161
Q

Features of haemolytic anaemia

A

Jaundice

Raised LDH

162
Q

Extravascular haemolysis

A 
Sickle cell disease
Thalassaemia 
Antibody induced 
Rhesus mismatched transfusion 
Hereditary spherocytosis
163
Q

Intravascular haemolysis

A

ABO mismatched transfusion
Mechanical trauma
Snake bites
Infection

164
Q

Extra vs intravascular haemolysis

A 
Extra = spherocytes present
Intra = haemoglobin in blood, very high LDH, haemoglobinuria
165
Q

Triggers to G6PD deficiency

A

Fava beans
Infection
Drugs

166
Q

Autoimmune haemolytic anaemia

A

IgG antibodies against membrane components

Extravascular haemolysis

167
Q

Diagnosing angina

A

HISTORY
Exercise ECG
Functional imaging

168
Q

Common sites of atheromas

A 
Arterial branch points 
-Carotid
-Aortic 
-Iliac 
Renal arteries 
Coronary arteries
169
Q

Endothelial factors

A 
Vasodilators --> NO, prostacyclin
Vasoconstrictors --> AgII, endothelin 
Pro-fibrinolysis --> tPA
Anti-fibrinolysis --> TPAI-1
Anti-inflammatory --> NO
Pro-inflammatory --> E-selectin
Cell adhesion --> VCAM, ICAM, IL-8
170
Q

LDL modification

A

Oxidation by ROS

Glycation by DM

171
Q

Actions of oxidised LDL

A

Inflammatory mediator production

Cell adhesion molecule production

172
Q

How does modified LDL lead to lipid accumulation?

A 
Does not bind to normal LDL receptor 
Binds to scavenger receptor 
This has no negative feedback 
--> massive lipid accumulation 
--> foam cell
173
Q

What causes smooth muscle proliferation and migration?

A

Growth factors from endothelial cells and macrophages

E.g. PDGR

174
Q

Which cells form foam cells?

A

Macrophages

Smooth muscle cells

175
Q

What does a stable plaque cause?

A

Stable angina pectoris

176
Q

What does an unstable plaque cause?

A

Thrombus formation

MI

177
Q

What does the LDL receptor recognise

A

Lipoprotein B100

178
Q

What happens when a plaque ruptures

A

Haemorrhage
Release of tissue factor
Collegen exposure

179
Q

Lipid blood levels

A

TC <200mg/dl
LDL <130mg/dl
HDL >40mg/dl

180
Q

Where are alpha genes found?

A

Chromosome 16

181
Q

Where are beta genes found?

A

Chromosome 11

182
Q

Forms of alpha gene

A

2 alpha genes

1 zeta gene

183
Q

Forms of beta gene

A 
Epsilon 
Gamma G 
Gamma A 
Delta 
Beta
184
Q

What is Hb Gower 1?

A

Produced in the yolk sac up to 6 weeks

Zeta 2 epsilon 2

185
Q

What is HbF?

A

Produced after 6 weeks in utero from the liver and spleen

Alpha 2 gamma 2

186
Q

What happens when 3 alpha genes are missing?

A

Haemoglobin H disease
Haemoglobin H (beta 4) and haemoglobin Barts (gamma 4) are formed
These have a higher affinity for oxygen
–> poor tissue perfusion

187
Q

What happens when 4 alpha genes are missing

A

All haemoglobin is haemoglobin Barts (gamma 4)
Baby cannot survive
–> hydrops foetalis

188
Q

Manifestations of beta thalassaemia major

A 
Hypochromic, microcytic anaemia
Bone marrow expansion 
Splenomegaly 
Extra medullary erythropoietic masses 
Failure to thrive 
CCF
189
Q

What is the problem caused by iron overload?

A

Fenton reaction
Ferrous irons react with hydrogen peroxide
Forms destructive hydroxyl radical
–> cirrhosis, diabetes, glandular dysfunction

190
Q

Iron chelating agents

A 
Desferrioxiamine = SQ 
Deferiprine = oral
191
Q

Mutation in HbS

A

Glutamic acid –> valine

192
Q

Consequences of HbS

A

Anaemia
More infections
Vaso-occlusive crisis
Chronic tissue damage

193
Q

ECG in heart failure

A

Pathological Q waves
LBBB
Anterior T waves
AF and other arrhythmias

194
Q

BNP

A

Produced by ventricles in response to excessive myocyte stretching
Promotes naturiesis and vasodilation
Inhibits ADH and aldosterone release
>100pg/ml in heart failure

195
Q

Cardiac resynchronisation therapy

A

Must be in sinus rhythm
If QRS prolongation >150ms
If LVEF <35%
If grade III/IV symptoms

196
Q

Implantable cardiac defibrillator

A

Used of AMI >4 weeks previously
LVEF <30%
QRS >120ms

197
Q

Acute heart failure causes

A 
AMI
Tachyarrythmias 
Valve disease --> MS, chordal rupture 
Infection 
Failure to take drugs
198
Q

Immediate AHF treatment

A

IV diuretic
Oxygen
Ventilation

199
Q

Hypotension BP

A

<90/60mmHg

200
Q

Hypertension damage to the eye

A

Arteriolar narrowing

Silver or copper wire arterioles in the centre due to reflected light

201
Q

Causes of secondary hypertension

A 
Renal disease
Pheochromocytoma (chromatin cells) 
Cushing's syndrome 
Conn's syndrome (hyperaldosteroneism) 
Acromegaly 
Hypothyroidism 
CoA
Iatrogenic
202
Q

MI ECG features

A

ST elevation

Pathological Q waves

203
Q

Classification of MI

A 
1 = spontaneous
2 = ischaemic imbalance from spasm, embolism, dissection or hypotension
3 = death from presumed AMI 
4a = from PCI 
4b = from stent 
5 = from CABG
204
Q

Clinical consequences of MI

A 
Chest pain 
4th heart sound
Fever 
Sweating 
Vomiting 
Tachycardia
205
Q

Features of VW disease

A 
Bruising 
Epistaxis 
Gingival haemorrhage 
Post-surgical bleeding
Menorrhagia
206
Q

Clotting times for VW disease

A

High APTT and bleeding time (low VIII)

Normal PT, TT and platelet count

207
Q

Haemorrhage disease of the newborn

A

Prevented by vitamin K at birth

Due to low vitamin K at birth, immature liver and low vitamin K in breast milk

208
Q

How does liver disease cause bleeding problems?

A 
Failure to produce clotting factors 
Failure to absorb or use vitamin K 
Abnormal fibrinogen production 
Portal hypertension --> splenomegaly --> decreased platelet count
--> prolonged PT, APTT, TT
--> high fibrooge degradation products 
--> thrombocyopaenia
209
Q

How does kidney disease cause bleeding problems?

A

Leads to uraemia
Impairs platelet function
–> prolonged bleeding time
–> abnormal platelet aggregation studies

210
Q

Pathology of DIC

A

Due to excessive activation of the haemostatic system

  • -> microvascular thrombus and tissue damage
  • -> depletion of platelets and clotting factors can cause bleeding
211
Q

Causes of DIC

A 
Gram negative sepsis 
Malignancy 
Obstetric disorders
Shock 
Liver disease
Acute transplant rejection 
ABO incompatibility
Snake bite
212
Q

When does massive transfusion syndrome occur?

A

> 5L of blood in 24 hours
50% blood loss in 3 hours
80% of blood replaced

213
Q

Diagnosis of shock

A 
MAP <60mmHg 
Clinical signs of hypo perfusion 
- tachycardia 
- tachypnoea 
- confusion 
- pallor
214
Q

Where do noradrenaline and angiotensin II act in the vascular wall?

A 
Noradrenaline = release outside the arteriole and acts on alpha receptors in smooth muscle 
AgII = carried in plasma and acts on endothelium lining and smooth muscle
215
Q

Action of thromboxanes

A

Vasoconstriction

Platelet aggregation

216
Q

Action of prostacyclins

A

Vasodilation

Inhibit platelet aggregation

217
Q

Immediate shock compensation

A 
Mediated by baroreceptors
Increased SNS outflow 
ADH release 
ANP release inhibited 
--> water retention
218
Q

Long term shock compensation

A 
Kidney mediated 
Increased renin secretion 
Thirst sensation 
Albumin synthesis 
EPO release
219
Q

Hypovolaemic shock classes

A 
1 = <15% = <750ml 
2 = 15-30% = 750-1500ml
3 = 30-40% = 1500-2000ml 
4 = >40% = >2000ml
220
Q

Septic diagnosis

A

Temp >38 and <36
HR >90
RR >20 or paCO2 <32mmHg
WBC >12x10 9/L

221
Q

Septic shock

A

= sepsis with hypotension

222
Q

Pathology of sepsis

A

Bacterial infection leads to excessive host response
LPS stimulates cytokine release
Vasodilation occurs
Reduced SVR and therefore BP

223
Q

What causes TIA

A

Small emboli pinged off from a thrombus

224
Q

Symptoms duration of TIA

A

Typically less than an hour

Must be less than 24 hours

225
Q

Types of ischaemic stroke

A

Thrombotic
Embolic
Lacunar

226
Q

What is a lacunar stroke?

A

Occlusion of arteries supplying deep brain rather than cortex

  • -> motor hemiparesis with dysarthria
  • -> ataxia and hemiparesis
  • -> dysarthria and clumsy hand
227
Q

Consciousness in stroke

A

Loss in hemorrhagic

Usually maintained in ischaemic

228
Q

Lenticulo-striate arteries

A

Branches from MCA

Supply basal ganglia and internal capsule

229
Q

Excito-toxicity

A 
K+ not removed 
Depolarises cells 
Causes excessive NT release
Excess stimulation of NMDA (fast) and AMPA (slow) channels 
Increases metabolic demand of cells 
Leads to free radical formation
230
Q

Stroke treatment

A 
TPAs 
NMDA antagonists (cerestat) 
AMPA antagonists (NBQX) 
Lithium 
Antioxidants 
Superoxidase dimutase enzymes
231
Q

What is found in aortic stenosis?

A 
Ejection systolic murmur 
Soft S2 
Slow rising carotid pulse 
Narrow pulse pressure
S4 and ejection click
232
Q

What causes aortic stenosis?

A

Calcific disease
Congenital bicuspid valve
Rheumatic disease

233
Q

What are the symptoms of aortic stenosis?

A

Dyspnoea
Angina
Syncope
Sudden death

234
Q

What is found in mitral regurgitation?

A 
Pan systolic murmur 
Soft S1
AF 
S3 
RV heave
Right heart failure signs
235
Q

What causes mitral regurgitation

A

Valve prolapse, rheumatic disease, endocarditis
Chordal rupture, papillary muscle dysfunction
LV dilation

236
Q

What are the symptoms of mitral regurgitation?

A

Dyspnoea
Palpitations
Systemic emboli

237
Q

What is found in mitral stenosis?

A 
Mid-diastolic rumble 
Sound S1 with opening snap 
AF 
RV heave 
Right heart failure signs
238
Q

What is seen on mitral stenosis ECG?

A

Bifid P waves

239
Q

What causes mitral stenosis?

A

Rheumatic disease

240
Q

Whats are the symptoms of mitral stenosis?

A

Dyspnoea
Palpitations
Systemic emboli

241
Q

What is found in aortic regurgitation?

A 
Early diastolic murmur with decrescendo 
Rapidly rising carotid pulse 
Collapsing pulse 
Systolic ejection murmur 
Wide pulse pressure 
Very displaced apex beat
242
Q

What causes aortic regurgitation?

A

Calcific disease, congenital bicuspid valve, rheumatic disease, endocarditis
Marfan syndrome, ankylosing spondylitis, aortic dissection, Ehlers danlos

243
Q

What are the symptoms of aortic regurgitation?

A

Often none
Dyspnoea
Angina

244
Q

Definition of mitral prolapse

A

> 2mm systolic prolapse of 1 or both valve leaflets

245
Q

Signs of mitral prolapse

A

Ejection click and late systolic murmur

246
Q

Ddx of DVT

A 
Musculo-tendinous trauma 
Tendinitis 
Ruptured Baker's cyst 
Cellulitis 
Lymphedema 
Haematoma
247
Q

Post thrombotic syndrome

A

Recurrent pain and swelling
Pigmentation and ulceration
More common in proximal DVT

248
Q

PE classic symptoms

A

Dyspnoea
Pleuritic chest pain
Haemoptysis

249
Q

Signs of PE

A

Tachypnoea
Tachycardia
Crepitations
Pleural rub

250
Q

ECG signs of PE

A

Tachycardia
T wave inversions (anterior leads)
S1Q3T3 pattern

251
Q

CXR signs of PE

A

Focal oligaemia
Peripheral wedge shape above diaphragm
Small pleural effusion

252
Q

DDx of PE

A 
Acute coronary syndrome 
Pneumonia 
Bronchitis 
COPD exacerbation 
Asthma attack
253
Q

Diagnosis of PE

A 
CTPA 
V/Q scanning (must have normal CXR) 
Echo 
Pulmonary angiogram 
D-dimer
254
Q

UFH half life

A

60-90 mintes

255
Q

LMWH half life

A

4 hours

256
Q

Fondaparinux half life

A

18 hours

257
Q

Warfarin half life

A

36 hours

258
Q

Causes of thrombophilia

A 
Factor V Leiden 
Prothrombin gene mutation
Protein C deficiency 
Protein S deficiency 
Antithrombin deficiency
259
Q

Pathology of factor V Leiden

A

Cannot be degraded by protein C

260
Q

Antiphospholipid syndrome pathology

A

Autoimmune antiphospholipid antibodies

Increases chance of clot formation

261
Q

Antibodies seen in antiphospholipid syndrome

A

Lupus anticoagulant
Anticardiolipin antibodies
Anti-B2-glycoprotein 1 antibodies

262
Q

Consequences of antiphospholipid syndrome

A

Stroke, TIA
PE
Pregnancy problems –> pre-eclampsia, miscarriage
DVT

263
Q

Asthma treatment ladder

A 
Salbutamol 
\+ inhaled steroid 
\+ LABA
\+ theophylline + leukotriene antagonist + anticholergic 
\+ oral steroid
264
Q

Inputs of the respiratory centre

A 
Baroreceptors 
Central and peripheral chemoreceptors
Hypothalamus 
Progesterone 
Anaemia 
Skeletal muscle afferents 
Occlusion of PA 
Pulmonary stretch receptors 
J receptors
Cortex
265
Q

Outputs of the respiratory centre

A

DRG –> pharyngeal muscles, intercostal muscles, diaphragm

VRG –> expiratory muscles

266
Q

How does pulmonary oedema cause dyspnoea?

A

Stimulates pulmonary J receptors

267
Q

Sitting watching TV

A

1 MET

268
Q

1 flight of stairs without stopping

A

4 METs

269
Q

Walking 2mph

A

2 METs

270
Q

CURB 65

A 
C = confusion 
U = urea >7mmol 
R = respiratory rate >30 
B = SBP <90mmHg 
65 = age >65
271
Q

CURB 65

A 
C = confusion 
U = urea >7mmol 
R = respiratory rate >30 
B = SBP <90mmHg 
65 = age >65
272
Q

How does smoking cause emphysema?

A

Activation of polymorphonuclear leucocytes
Release serine elastase
Smoke also inactivates the inhibitor of elastase, alpha-antitrypsin

273
Q

Causes if type 2 respiratory failure

A 
Brainstem injury 
Metabolic encephalopathy 
Depressant drugs 
Spinal cord lesion 
Neuropathy 
Respiratory muscle damage 
Airway obstruction 
Decreased lung/chest wall compliance
274
Q

Sources of pulse oximetry error

A 
Poor peripheral perfusion
Dark skin 
False nails 
Bright light 
Excessive motion 
Carboxyhaemoglobin

2 - CR/MET (8 decks)

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