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CR physiology Flashcards

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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
Side effects of beta blockers
Bronchospasm, lethargy
26
MI immediate treatment
Oxygen Aspirin Opiates Thrombolysis/PCI
27
Secondary MI prevention
Beta blockers ACEIs Statins Lifestyle
28
Polypil contents
Aspirin (75mg) Statin 3 BP lowering drugs Folate
29
1 small square on ECG
= 0.04s
30
1 big square on ECG
= 0.2s
31
P wave duration
<0.08 | <2 small squares
32
PR interval duration
<0.2s | <5 small squares
33
QRS complex interval
<0.12s | <3 small squares
34
First degree heart block
Regular | PR intervals >0.2s
35
Second degree heart block type 1
Each successive PR interval gets longer until a QRS complex is dropped
36
Second degree heart block type 2
QRS complexes randomly dropped
37
Third degree heart block
No synchrony between atrial and ventricular rhythms | Often bradycardic
38
AF
Irregular rhythm | Rate = 100-160
39
Atrial flutter
Regular rhythm F waves instead of P waves Rate = 110 F wave rate = 300
40
Junctional rhythm
AVN takes over as pacemaker Rate = 40-60 P wave may be seen and may be inverted
41
SVT
Rate = 140-200 Regular rhythm Due to AF, AF or Wollf-Parksinson-White syndrome P waves often absent
42
AV nodal re-entrant tachycardia
Regular P waves often seen after QRS complex Reentry circuit within to just next to the AVN
43
Pathology of WPW syndrome
Extra electrical pathway connecting atria and ventricles Shortened PR interval Delta wave
44
Bundle branch block
Prolonged QRS Notched R waves in V1 in RBBB Notched R waves in V6 in LBBB
45
Causes of LAD
LVH | Inferior MI
46
Causes of RAD
``` RVH LV atrophy Lateral MI COPD, tall, thin Dextrocardia ```
47
Sites of RBC production in foetus
3-6 weeks = yolk sac 6 weeks - 3 months = liver and spleen 3 months onwards = bone marrow
48
Which bones become the final haematopoietic bones?
Vertebrae, sternum, ribs, cranial bones, ilium
49
Appearance of proerthyroblast
Large cell with large nucleus Basophilic cytoplasm Perinuclear halo Nucleoli
50
Appearance of early erythroblast | = basophilic normoblast
Still dark blue cytoplasm Less cytoplasm Loss of perinuclear halo
51
Appearance of intermediate erythroblast | = polychromatophillic normoblast
Nucleus getting smaller | Reduced blue staining of cytoplasm
52
Appearance of late erythroblast | = orthochromic normoblast
Cytoplasm almost completely pink | Nucleus even smaller
53
Appearance of a reticulocyte
Expulsion of nucleus Slightly bigger than mature RBC Blue hue remains to cytoplasm
54
When does a reticulocyte become an erythrocyte?
After 1 day in circulation
55
Erythrocyte diameter
7.8um
56
Normal erythrocyte levels
= 5.2x10 6 /uL in males | = 4.7x10 6 /uL in females
57
Where is EPO produced?
Kidney fibroblasts | Type I glomus cells of carotid body
58
What does increased ESR show?
Infection of the blood
59
What structures are formed when ESR is high?
Rouleaux
60
GLUT transporters in RBCs
GLUT1
61
What enzyme breaks open haemoglobin?
Haemoxygenase
62
What is biliverdin?
Openen pophyrin ring without iron
63
What converts biliverdin --> bilirubin?
Biliverdin reductase
64
Where does biliverdin --> bilirubin take place?
Within macrophages
65
What conjugated bilirubin?
Glucoronic acid
66
What does bacteria convert bilirubin to?
Urobilinogen
67
What is urobiliogen further oxidised to?
Stercobilin
68
Average VO2 max
250ml/min
69
Local dilatory factors released by muscle
NO, adenosine, phosphates, carbon dioxide, H+, K+
70
Pulmonary ventilation at rest
8L/min
71
Pulmonary ventilation in peak levels of exercise
100L/min
72
Which way does oxygen dissociation curve shift in exercise?
To the right | Improves oxygen delivery to tissues
73
What causes this Bohr shift?
Increased CO2 and H+ | Increased local temperature
74
Platelet diameter
1-4um
75
Normal platelet range in blood
140-400x10 9 /L
76
Lifespan of platelets
8-14 days
77
How are platelets removed?
By the reticuloendothelial system
78
What does GpIb bind to?
vWF
79
What does GpIIB/IIIA bind to?
vWF and fibrinogen
80
What do alpha granules release?
Proteins --> vWF, fibrinogen, TPAI-1
81
What do delta granules release?
ADP
82
What disorder = lack of GpIb?
Bernard Soulier syndrome
83
What disorder = lack of GpIIb/IIIa?
Glanzmann's syndrome
84
What factors do platelets release that cause attractions and aggregation?
Serotonin, ADP, TXA2
85
Treatment of mild VWF disease?
DDAVP
86
Extrinsic pro-tenase complex
TF + VIIa
87
Intrinsic pro-tenase complex
VIIIa + IXa
88
Which enzymes does thrombin enhance the activity of?
5,8,9,11,13
89
Haemophilia A
Factor 8 deficient
90
Haemophilia B
Factor 9 deficient
91
Haemophilia A treatment
DDAVP, factor VIII
92
Haemophilia B treatment
factor IX
93
Where are common bleeding sites?
Soft tissue Joints Operative sites Cranium
94
What does antithrombin inhibit?
2, 7, 9, 10, 11, 12
95
What does protein C inhibit?
5 and 8
96
What are vitamin K dependant?
2, 7, 9, 10, protein C, protein S
97
What does tPA activate
Plasminogen --> plasmin | Fibrin --> fibrinogen
98
What does fibrin breakdown produce?
D-dimer
99
What is the reaction that produces NO?
L-arginine + oxygen | --> NO + citrulline
100
Where is NOS I found?
In the brain | Calcium dependant
101
Where is NOS II found?
Most nucleated cells | Particularly in macrophages
102
What activates NOS II?
Inflammatory cytokines | Calcium independant
103
Where is NOS III found?
Vascular endothelial cells
104
How is NOS III activated?
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
105
Nitric oxide action
Diffuses from endothelium --> smooth muscle cells Activates guanylate cyclase Converts GTP --> cGMP Causes vascular smooth muscle relaxation
106
How is NO produced in exercise when there is a lack of oxygen?
Exercise converts nitrate to nitrous acid | Reduced --> NO
107
What happens to eNOS in atherosclerosis
Endothelium damaged so cannot produce NO by eNOS Coronary vessels cannot dilate in exercise --> angina and acidosis
108
How does NO improve oxygen delivery?
NO enters blood Binds to haemoglobin to displace oxygen Forms nitrosohaemoglobin
109
How does acid base balance alter blood brain flow?
Increased in acidosis | Decreased in alkalosis
110
Where can clots commonly form?
Auricles of the atria | Deep veins of the calf
111
When does hypoxic ventilation drive begin?
PO2 <60mmHg
112
When do we initially suffer the effects of altitude?
Over 2000m
113
Where is the death zone?
7500m and above
114
How is a metabolic acidosis generated by the kidney?
Decreased H+ ATPase activity in DCT | Increased bicarbonate excretion
115
How is an increased erythrocyte number generated?
Increased EPO secretion
116
How is pulmonary vascular resistance decreased?
Collateral circulations | Increased NO synthesis
117
What is the action of Diamox
= 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
Treatment of high altitude cerebral oedema
``` Oxygen Descent Diamox Dexamethasone Hyperbaric chamber ```
119
Treatment of high altitude pulmonary oedema
``` Oxygen Sit upright Descent Hyperbaric chamber Nifedipine (CCB) --> reduces PAH Viagra (sildenafil) --> slows down cGMP breakdown ```
120
Causes of respiratory acidosis
``` Hypoventilation Narcotics + alcohol COPD, asthma Scoliosis Severe obesity Neuromuscular damage ```
121
Treatment of respiratory acidosis
Underlying cause Bronchodilators CPAP/BiPAP Oxygen
122
Signs and symptoms of respiratory acidosis
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
Maximum bicarbonate levels that can be reached
45mmol/L
124
Minimum bicarbonate levels that can be reached
12mmol/L
125
Respiratory alkalosis causes
``` Hyperventilation Anxiety, pain Pregnancy Sepsis and fever Altitude Salicyclates and progesterone CVA ```
126
Symptoms of respiratory alkalosis
Dizziness, confusion, cramps and tingling in hands and mouth, blurred vision, spasms, seizures, irregular HR, tetany
127
Diagnostic FEV1/FVC ratios
``` <75% = obstructive >75% = restrictive ```
128
Peak flow in asthma
Diurnal variation
129
Reversibility testing
400mg salbutamol by inhaler 2.5mg salbutamol by nebuliser 30mg/day steroids for 2 weeks Peak flow must improve by >15% and >200ml
130
When is total lung carbon monoxide increased?
Increased cardiac output, polycythaemia, alveolar haemorrhage
131
When is total lung carbon monoxide decreased?
Decreased perfusion, decreased ventilation, V/Q mismatch, anaemia
132
Causes of reduced lung surface area
Lobectomy, pneumonectomy, airway obstruction, increased dead space, emphysema
133
Causes of hypovolaemic shock
Haemorrhage | Cholera
134
Causes of cardiogenic shock
MI, valve disease, myocarditis, heart failure
135
Causes of obstructive shock
PE | Cardiac tamponade
136
Causes of distributive shock
Sepsis | Anaphylaxis
137
How are mast cells activated
Cross linking with IgE Via complement C3a and C5a Via nerves --> substance P Via direct contact with pathogen
138
What do mast cells release?
Histamine Leukotrienes Prostaglandins
139
What does histamine do?
Increases capillary permeability Vasodilation Itching
140
What do leukotrienes do?
Increase capillary permeability | Cause chemotaxis
141
What do prostaglandins do?
Arteriolar dilation Pain Fever
142
What is angioedema
``` Swelling of subcutaneous tissues Face Lips Hands and feet Pharynx Larynx ```
143
What drugs commonly trigger anaphylaxis?
``` Beta lactase Aspirin NSAIDs Insulins Anaesthetics ```
144
Anaphylaxis treatment
``` 500mg adrenaline in 0.5ml Epipen = 300mg adrenaline in 0.3ml High flow oxygen Saline Antihistamines (chlorpheniramine) Corticosteroids (hydrocortisone) ```
145
Total body iron
3-5g
146
Where is iron absorbed?
Duodenum
147
How is iron absorbed?
As Fe2+ | Ferric reductase can reduce Fe3+ to 2+
148
Transferrin
Iron binding plasma protein Carries two Fe3+ ions Binds to transferring receptor and is endocytose Releases iron
149
Ferritin
Intracellular iron store Buffer Cytoplasmic Diagnostic for iron deficiency
150
Anaemia Hb levels
Adult male <13.5g/dl Adult female <11.5g/dl 6-14 <12g/dl 6m-6yrs <11g/dl
151
Anaemia cell sizes
``` <76fl = microcytic 76-96fl = normocytic >96fl = macrocytic ```
152
Causes of microcytic anaemia
Iron deficiency | Thalamssaemia
153
Causes of normocytic anaemia
Chronic disease Acute blood loss Cancer Haemolysis --> sickle cell
154
Causes of macrocytic anaemia
B12/folate deficiency | Alcoholic liver disease
155
Factors enhancing iron absorption
``` Iron in meat Fe2+ iron Pregnancy Acid pH Hypoxia Iron deficiency ```
156
Factors reducing iron absorption
``` Iron in vegetables Fe3+ iron Alkaline pH Iron overload Inflammatory disorders ```
157
Vitamin B12
``` Water soluble Found in meat, eggs, animal protein Not destroyed by cooking Can be stored Absorbed in ileum bound to IF ```
158
Signs of pernicious anaemia
Insidious onset Glossitis Mild jaundice Neurological symptoms
159
Treatment of pernicious anaemia
IM B12 every 3 months
160
Folate
``` Water soluble vitamin Found in liver, greens, yeast Destroyed by cooking Very little can be stored Absorbed in the duodenum and jejunum ```
161
Features of haemolytic anaemia
Jaundice | Raised LDH
162
Extravascular haemolysis
``` Sickle cell disease Thalassaemia Antibody induced Rhesus mismatched transfusion Hereditary spherocytosis ```
163
Intravascular haemolysis
ABO mismatched transfusion Mechanical trauma Snake bites Infection
164
Extra vs intravascular haemolysis
``` Extra = spherocytes present Intra = haemoglobin in blood, very high LDH, haemoglobinuria ```
165
Triggers to G6PD deficiency
Fava beans Infection Drugs
166
Autoimmune haemolytic anaemia
IgG antibodies against membrane components | Extravascular haemolysis
167
Diagnosing angina
HISTORY Exercise ECG Functional imaging
168
Common sites of atheromas
``` Arterial branch points -Carotid -Aortic -Iliac Renal arteries Coronary arteries ```
169
Endothelial factors
``` 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
LDL modification
Oxidation by ROS | Glycation by DM
171
Actions of oxidised LDL
Inflammatory mediator production | Cell adhesion molecule production
172
How does modified LDL lead to lipid accumulation?
``` Does not bind to normal LDL receptor Binds to scavenger receptor This has no negative feedback --> massive lipid accumulation --> foam cell ```
173
What causes smooth muscle proliferation and migration?
Growth factors from endothelial cells and macrophages | E.g. PDGR
174
Which cells form foam cells?
Macrophages | Smooth muscle cells
175
What does a stable plaque cause?
Stable angina pectoris
176
What does an unstable plaque cause?
Thrombus formation | MI
177
What does the LDL receptor recognise
Lipoprotein B100
178
What happens when a plaque ruptures
Haemorrhage Release of tissue factor Collegen exposure
179
Lipid blood levels
TC <200mg/dl LDL <130mg/dl HDL >40mg/dl
180
Where are alpha genes found?
Chromosome 16
181
Where are beta genes found?
Chromosome 11
182
Forms of alpha gene
2 alpha genes | 1 zeta gene
183
Forms of beta gene
``` Epsilon Gamma G Gamma A Delta Beta ```
184
What is Hb Gower 1?
Produced in the yolk sac up to 6 weeks | Zeta 2 epsilon 2
185
What is HbF?
Produced after 6 weeks in utero from the liver and spleen | Alpha 2 gamma 2
186
What happens when 3 alpha genes are missing?
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
What happens when 4 alpha genes are missing
All haemoglobin is haemoglobin Barts (gamma 4) Baby cannot survive --> hydrops foetalis
188
Manifestations of beta thalassaemia major
``` Hypochromic, microcytic anaemia Bone marrow expansion Splenomegaly Extra medullary erythropoietic masses Failure to thrive CCF ```
189
What is the problem caused by iron overload?
Fenton reaction Ferrous irons react with hydrogen peroxide Forms destructive hydroxyl radical --> cirrhosis, diabetes, glandular dysfunction
190
Iron chelating agents
``` Desferrioxiamine = SQ Deferiprine = oral ```
191
Mutation in HbS
Glutamic acid --> valine
192
Consequences of HbS
Anaemia More infections Vaso-occlusive crisis Chronic tissue damage
193
ECG in heart failure
Pathological Q waves LBBB Anterior T waves AF and other arrhythmias
194
BNP
Produced by ventricles in response to excessive myocyte stretching Promotes naturiesis and vasodilation Inhibits ADH and aldosterone release >100pg/ml in heart failure
195
Cardiac resynchronisation therapy
Must be in sinus rhythm If QRS prolongation >150ms If LVEF <35% If grade III/IV symptoms
196
Implantable cardiac defibrillator
Used of AMI >4 weeks previously LVEF <30% QRS >120ms
197
Acute heart failure causes
``` AMI Tachyarrythmias Valve disease --> MS, chordal rupture Infection Failure to take drugs ```
198
Immediate AHF treatment
IV diuretic Oxygen Ventilation
199
Hypotension BP
<90/60mmHg
200
Hypertension damage to the eye
Arteriolar narrowing | Silver or copper wire arterioles in the centre due to reflected light
201
Causes of secondary hypertension
``` Renal disease Pheochromocytoma (chromatin cells) Cushing's syndrome Conn's syndrome (hyperaldosteroneism) Acromegaly Hypothyroidism CoA Iatrogenic ```
202
MI ECG features
ST elevation | Pathological Q waves
203
Classification of MI
``` 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
Clinical consequences of MI
``` Chest pain 4th heart sound Fever Sweating Vomiting Tachycardia ```
205
Features of VW disease
``` Bruising Epistaxis Gingival haemorrhage Post-surgical bleeding Menorrhagia ```
206
Clotting times for VW disease
High APTT and bleeding time (low VIII) | Normal PT, TT and platelet count
207
Haemorrhage disease of the newborn
Prevented by vitamin K at birth | Due to low vitamin K at birth, immature liver and low vitamin K in breast milk
208
How does liver disease cause bleeding problems?
``` 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
How does kidney disease cause bleeding problems?
Leads to uraemia Impairs platelet function --> prolonged bleeding time --> abnormal platelet aggregation studies
210
Pathology of DIC
Due to excessive activation of the haemostatic system - -> microvascular thrombus and tissue damage - -> depletion of platelets and clotting factors can cause bleeding
211
Causes of DIC
``` Gram negative sepsis Malignancy Obstetric disorders Shock Liver disease Acute transplant rejection ABO incompatibility Snake bite ```
212
When does massive transfusion syndrome occur?
>5L of blood in 24 hours 50% blood loss in 3 hours >80% of blood replaced
213
Diagnosis of shock
``` MAP <60mmHg Clinical signs of hypo perfusion - tachycardia - tachypnoea - confusion - pallor ```
214
Where do noradrenaline and angiotensin II act in the vascular wall?
``` 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
Action of thromboxanes
Vasoconstriction | Platelet aggregation
216
Action of prostacyclins
Vasodilation | Inhibit platelet aggregation
217
Immediate shock compensation
``` Mediated by baroreceptors Increased SNS outflow ADH release ANP release inhibited --> water retention ```
218
Long term shock compensation
``` Kidney mediated Increased renin secretion Thirst sensation Albumin synthesis EPO release ```
219
Hypovolaemic shock classes
``` 1 = <15% = <750ml 2 = 15-30% = 750-1500ml 3 = 30-40% = 1500-2000ml 4 = >40% = >2000ml ```
220
Septic diagnosis
Temp >38 and <36 HR >90 RR >20 or paCO2 <32mmHg WBC >12x10 9/L
221
Septic shock
= sepsis with hypotension
222
Pathology of sepsis
Bacterial infection leads to excessive host response LPS stimulates cytokine release Vasodilation occurs Reduced SVR and therefore BP
223
What causes TIA
Small emboli pinged off from a thrombus
224
Symptoms duration of TIA
Typically less than an hour | Must be less than 24 hours
225
Types of ischaemic stroke
Thrombotic Embolic Lacunar
226
What is a lacunar stroke?
Occlusion of arteries supplying deep brain rather than cortex - -> motor hemiparesis with dysarthria - -> ataxia and hemiparesis - -> dysarthria and clumsy hand
227
Consciousness in stroke
Loss in hemorrhagic | Usually maintained in ischaemic
228
Lenticulo-striate arteries
Branches from MCA | Supply basal ganglia and internal capsule
229
Excito-toxicity
``` 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
Stroke treatment
``` TPAs NMDA antagonists (cerestat) AMPA antagonists (NBQX) Lithium Antioxidants Superoxidase dimutase enzymes ```
231
What is found in aortic stenosis?
``` Ejection systolic murmur Soft S2 Slow rising carotid pulse Narrow pulse pressure S4 and ejection click ```
232
What causes aortic stenosis?
Calcific disease Congenital bicuspid valve Rheumatic disease
233
What are the symptoms of aortic stenosis?
Dyspnoea Angina Syncope Sudden death
234
What is found in mitral regurgitation?
``` Pan systolic murmur Soft S1 AF S3 RV heave Right heart failure signs ```
235
What causes mitral regurgitation
Valve prolapse, rheumatic disease, endocarditis Chordal rupture, papillary muscle dysfunction LV dilation
236
What are the symptoms of mitral regurgitation?
Dyspnoea Palpitations Systemic emboli
237
What is found in mitral stenosis?
``` Mid-diastolic rumble Sound S1 with opening snap AF RV heave Right heart failure signs ```
238
What is seen on mitral stenosis ECG?
Bifid P waves
239
What causes mitral stenosis?
Rheumatic disease
240
Whats are the symptoms of mitral stenosis?
Dyspnoea Palpitations Systemic emboli
241
What is found in aortic regurgitation?
``` Early diastolic murmur with decrescendo Rapidly rising carotid pulse Collapsing pulse Systolic ejection murmur Wide pulse pressure Very displaced apex beat ```
242
What causes aortic regurgitation?
Calcific disease, congenital bicuspid valve, rheumatic disease, endocarditis Marfan syndrome, ankylosing spondylitis, aortic dissection, Ehlers danlos
243
What are the symptoms of aortic regurgitation?
Often none Dyspnoea Angina
244
Definition of mitral prolapse
>2mm systolic prolapse of 1 or both valve leaflets
245
Signs of mitral prolapse
Ejection click and late systolic murmur
246
Ddx of DVT
``` Musculo-tendinous trauma Tendinitis Ruptured Baker's cyst Cellulitis Lymphedema Haematoma ```
247
Post thrombotic syndrome
Recurrent pain and swelling Pigmentation and ulceration More common in proximal DVT
248
PE classic symptoms
Dyspnoea Pleuritic chest pain Haemoptysis
249
Signs of PE
Tachypnoea Tachycardia Crepitations Pleural rub
250
ECG signs of PE
Tachycardia T wave inversions (anterior leads) S1Q3T3 pattern
251
CXR signs of PE
Focal oligaemia Peripheral wedge shape above diaphragm Small pleural effusion
252
DDx of PE
``` Acute coronary syndrome Pneumonia Bronchitis COPD exacerbation Asthma attack ```
253
Diagnosis of PE
``` CTPA V/Q scanning (must have normal CXR) Echo Pulmonary angiogram D-dimer ```
254
UFH half life
60-90 mintes
255
LMWH half life
4 hours
256
Fondaparinux half life
18 hours
257
Warfarin half life
36 hours
258
Causes of thrombophilia
``` Factor V Leiden Prothrombin gene mutation Protein C deficiency Protein S deficiency Antithrombin deficiency ```
259
Pathology of factor V Leiden
Cannot be degraded by protein C
260
Antiphospholipid syndrome pathology
Autoimmune antiphospholipid antibodies | Increases chance of clot formation
261
Antibodies seen in antiphospholipid syndrome
Lupus anticoagulant Anticardiolipin antibodies Anti-B2-glycoprotein 1 antibodies
262
Consequences of antiphospholipid syndrome
Stroke, TIA PE Pregnancy problems --> pre-eclampsia, miscarriage DVT
263
Asthma treatment ladder
``` Salbutamol + inhaled steroid + LABA + theophylline + leukotriene antagonist + anticholergic + oral steroid ```
264
Inputs of the respiratory centre
``` Baroreceptors Central and peripheral chemoreceptors Hypothalamus Progesterone Anaemia Skeletal muscle afferents Occlusion of PA Pulmonary stretch receptors J receptors Cortex ```
265
Outputs of the respiratory centre
DRG --> pharyngeal muscles, intercostal muscles, diaphragm | VRG --> expiratory muscles
266
How does pulmonary oedema cause dyspnoea?
Stimulates pulmonary J receptors
267
Sitting watching TV
1 MET
268
1 flight of stairs without stopping
4 METs
269
Walking 2mph
2 METs
270
CURB 65
``` C = confusion U = urea >7mmol R = respiratory rate >30 B = SBP <90mmHg 65 = age >65 ```
271
CURB 65
``` C = confusion U = urea >7mmol R = respiratory rate >30 B = SBP <90mmHg 65 = age >65 ```
272
How does smoking cause emphysema?
Activation of polymorphonuclear leucocytes Release serine elastase Smoke also inactivates the inhibitor of elastase, alpha-antitrypsin
273
Causes if type 2 respiratory failure
``` Brainstem injury Metabolic encephalopathy Depressant drugs Spinal cord lesion Neuropathy Respiratory muscle damage Airway obstruction Decreased lung/chest wall compliance ```
274
Sources of pulse oximetry error
``` Poor peripheral perfusion Dark skin False nails Bright light Excessive motion Carboxyhaemoglobin ```

2 - CR/MET (8 decks)

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