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1
Q 
EG. FLASHCARDS FOR NO LECTURE
EDRF
Effect of NO on smooth muscle 
Colour of nitrous acid 
Nitrous acid - formula
Nitric oxide - formula
Entonox - what is this and it's use?
What is formed when NO is oxidised
How does NO differ from nitrogen dioxide (it is a free radical)HAPE
A

a

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2
Q

Define endothelium

A

Thin (single) layer of simple squamous epithelium

Composed of endothelial cells

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3
Q

Define EDRF

A

Endothelium derived relaxing factor aka. NO

Causes vascular smooth muscle to relax

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4
Q

Function of NO in blood vessels

A

Causes vascular smooth muscle to relax - vasodilation

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5
Q

Appearance of nitrous acid (HNO2)

A

This is colourless (this is NOT NO)

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6
Q

Nitrous oxide vs. nitric oxide - chemical formula

A

Nitrous oxide - N2O

Nitric oxide - NO

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7
Q

Define Entonox

A

Anaesthesia gas

Composed of 50% NO and 50% O2

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8
Q

Use of entonox

A

Pre-hospital care
Childbirth
Emergency medicine

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9
Q

Define free radical

A

Molecule with an unpaired electron in it’s outer valence/reactive shell

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10
Q

Free radicals - oxidising or reducing agents?

A

Free radicals look to take electrons - oxidising agents

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11
Q

Effect of NO being free radical?

A

NO is very unstable (but much more stable than other free radicals)

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12
Q

When is NO stable?

A

In body tissues where the PO2 is lower than 50mmHg

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13
Q

Reaction of NO with hydroxyl (OH) radical

A

NO + OH –> HNO2

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14
Q

Enzyme that synthesises NO?

A

Nitric oxide synthase (NOS)

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15
Q

Function of NOS

A

L-arginine + 1/2 O2 –> citrulline + NO (+ H+ + e-)

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16
Q

Three isoforms of NOS

A

1 - bNOS - brain
2 - iNOS - induced (not calcium dependent)
3 - eNOS - endothelial

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17
Q

Location of bNOS

A

Central and peripheral neuronal cells

Calcium dependent

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18
Q

Location of iNOS

A

Found in macrophages (also most nucleated cells)

Induced - not calcium dependent

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19
Q

Location of eNOS

A

Vascular endothelial cells

Calcium dependent

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20
Q

What can induce production of iNOS?

A

Inducible in the presence of inflammatory cytokines

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21
Q

How is NO synthesis regulated in the vascular endothelium?

A

Main regulation is via movement of blood past the endothelial wall - sheer stress opens calcium channels - calcium enters the endothelial cells - production of eNOS

Also via binding of ACh to the ACh recepors on the endothelium allows the entry of calcium

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22
Q

Pathway of eNOS activation in the vascular endothelium

A

Calcium - activates calmodulin

Calmodulin activates eNOS

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23
Q

Three cofactors required for synthesis of eNOS

A

Biopterin H4
FMN
FAD

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24
Q

Composition responsible for the production of activated eNOS from inactivated eNOS

A

Ca2+ + calmodulin

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25
What does NO activate in smooth muscle cells?
Guanylate cyclase
26
What is the mechanism of action of guanylate cyclase?
Conversion of guanosine triphosphate in the smooth muscle to cyclic guanosine monophosphate (cGMP)
27
Effect of cGMP on the vascular smooth muscle?
cGMP - relaxation of vascular smooth muscle - vasodilation
28
Mechanism of action of NO causing smooth muscle relaxation
NO diffuses from endothelium to smooth muscle cells NO activates guanylate cyclase Guanylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate (cGMP) cGMP causes smooth muscle relaxation
29
Effect of vasodilation?
Vasodilation increases local blood flow | This maintains low peripheral vascular resistance and a normal blood pressure
30
Effect of whole body inhibition of eNOS by drug?
This causes increased blood pressure esp. pulmonary arterial pressure
31
Two antagonisers of NO i.e. vasoconstrictors of the blood vessels?
Noradrenaline | Angiotensin
32
Damage to the NO system results in what complication?
Hypertension
33
Effect on blood flow to exercising muscles?
Blood flow increases over ten fold
34
Effect on blood flow to heart during exercise
Blood flow increases up to three fold
35
Effect on blood flow to kidney during exercise
Blood flow decreases by nearly half
36
Effect on blood flow to skin during exercise
Blood flow increases nearly four fold
37
Effect on blood flow to brain during exercise
Blood flow to the brain does not change
38
Receptors causing vasoconstriction of arterioles
Alpha-1 receptors
39
What causes the vasodilation to exercising muscles?
Chemical factors - NO and adenosine
40
Effect of sympathetic nervous system on arterioles
Vasoconstriction - NO and adenosine overcome this
41
How is NO production increased during exercise?
Increased local blood flow - increased sheering forces and opening of calcium channels - increased activation of eNOS - increased production of NO
42
How is NO produced in anaerobic metabolism?
Depletion of ATP produces lactate which lowers pH | Lowered pH produces nitrous acid HNO2 - can form NO
43
Two effects of exercise on the coronary arterioles and cause
Diameter of the coronary arterioles increases Number of open arterioles (collaterals) increases Caused by NO
44
Cause of angina during exercise
If atheromatous plaque is present - vessel cannot dilate - ischaemia and angina
45
Usage of NO for treatment of angina is given in the form of?
GTN - glycerin trinitrate
46
Two areas where NO has an effect?
``` Smooth muscle (around blood vessels) In the blood ```
47
Effect of NO in RBCs
NO reacts with oxyhaemoglobin to produce nitrosohaemoglobin
48
Effect of nitrosohaemoglobin
This displaces oxygen - increases delivery of oxygen to hypoxic tissue
49
Why does local hypoxia occur during exercise?
Occurs in muscles at the start of exercise | More ATP used than produced
50
Define persistent pulmonary hypertension of the newborn (PPHN)
Reduced pulmonary arterial resistance with the first breath does not occur - lungs are not properly perfused Addition of NO to the inspired gas
51
Effect of low ventilation on NO levels and why?
Low ventilation causes low NO production because O2 is required for the production SO low ventilation equates to low perfusion
52
Effect of exercise on the pulmonary circulation
Exercise causes increased CO - causes increased blood flow - the pulmonary arterial resistance decreases to maintain the BP
53
Receptors causing relaxation of bronchial smooth muscle
Beta 2 receptors
54
Effect of reduced NO in the brain
Reduced NO - reduces the cerebral blood flow
55
Resting blood flow through the brain
50ml/min/100gm
56
Blood loss causing reversible brain damage
Blood flow falls to half of normal - around 25
57
Blood loss causing irreversible brain damage
Blood flow falls to one quarter of normal - around 10-15
58
Function of basal release of NO
Prevention of leucocytes (anti-inflammatory) and platelets (anti-thrombotic) from adhering to the surface of the endothelium
59
Four functions of NO
Direct vasodilation Anti-thrombotic effect Anti-inflammatory effect Anti-proliferative effect
60
How can iNOS lead to shock?
Overproduction of NO from macrophages can result in septic shock - uncontrollable vasodilation
61
Equation for blood pressure
BP = CO x SVR
62
Define cardiac output
Blood flow produced by the heart per minute
63
Define systolic BP
Maximum BP during ventricular contraction
64
Define diastolic BP
Minimum level of BP measured between the contractions of the heart
65
Eight components that can effect BP
``` Activity Temperature Diet Emotional state Posture Physical state Medication usage Ethnic background ```
66
Normal BP
120/80
67
Hypotension level
<90/60
68
Define postural hypotension
When the systolic decreases by 20 or the diastolic decreases by 10 when standing
69
Three causes of postural hypertension
Old age Diabetes Drugs
70
CNS effects of hypotension x4
Dizziness Impaired cognition Lethargy and fatigue Visual disturbances (hypoperfusion of brain)
71
Muscle effects of hypotension x2
``` Paracervical backache (upper back) General fatigue ```
72
Boundary for hypertension
140/90 persistently
73
Range of prehypertensio
130-139/85-89
74
Range of prehypertensio
130-139/85-89
75
Are prehypertensives candidates for drug therapy?
No - lifestyle modification
76
Isolated systolic hypertension
Systolic: >140 Diastolic: <90
77
Three lifestyle modifications to reduced BP
Weight loss Increased physical activity Limited alcohol consumption
78
What should be avoided prior to blood pressure measurements (x3) and for how long?
Caffeine Exercise Smoking At least 30 minutes
79
Which BP increases with age?
Systolic
80
Four adverse effects of hypertension
Stroke Coronary heart disease Renal impairment Peripheral vascular disease
81
Each 20/10mmHg increase in BP increases the risk of mortality by what rate? What age group is this prevalent in?
Doubles the risk 40-69 years
82
What is HOTT?
Hypertension Optimal Treatment Trial
83
What is HOTT?
Hypertension Optimal Treatment Trial
84
Results of HOTT - what did it tell us?
Lowest incidence of CV events when DBP maintained at 83 and maintained at <80 in diabetics SO especially important to control hypertension in diabetics
85
Concentric hypertrophy
Thickened wall of the left ventricle Decreased lumen diameter Must increase the HR to maintain CO
86
Eccentric hypertrophy
Whole ventricle enlarges - enlarged heart is weaker
87
Effect of chronic hypertension on the heart
Results in concentric hypertrophy SO then the HR increases
88
Effect of chronic hypertension on the eyes x3
Chronic hypertension damages the retina Cotton wool spots Silver wiring Severe cases: swelling of the optic disc i.e. papilledema
89
Define pailledema
This is swelling of the optic disc of the eye
90
Primary hypertension cause
Idiopathic - genetic 90-95% of cases
91
Secondary hypertension cause x5
5% of cases ``` Renal disease Endocrine disease Coarctation of the aorta Iagtrogenic i.e. hormonal/oral contraception, NSAIDs Thyroid - hyper or hypo ```
92
Two systems to control BP
Neuronal - baroreceptors | Hormonal - RAAS
93
Location of baroreceptros
Carotid artery - carotid sinus Aortic arch These are mechanoreceptors
94
Timescale of the RAAS system to maintain BP
Maintenance of steady, long term pressure
95
Timescale of the RAAS system to maintain BP
Maintenance of steady, long term pressure
96
RAAS pathway
Angiotensinogen to angiotensin I via renin | Angiotensin I to angiotensin II via ACE
97
Effects of angiotensin II x3
Increased sympathetic action Release of aldosterone Increased secretion of ADH
98
Increased levels of what may be present in patients with hypertension? x2
Increased renin | Increased angiotensin II
99
Effect of hypertension on salt and water and why?
Excess salt retention - raised water levels causes change in osmotic pressure Retention of water - raised ADH
100
Two key treatments in hypertension (non-pharmacological)
Dietary salt restriction | Diuretics
101
Normal sodium levels
Between 135 and 145mmol/L
102
Hyponatremia
Sodium levels <135mmol/L
103
Three symptoms of mild hyponatraemia
Loss of energy and fatigue Confusion Muscle weakness
104
Six symptoms of severe hyponatraemia
``` Nausea and vomiting Headache Spasms Restlessness and irritability Seizures Coma ```
105
Prevalence of hypertension in type II diabetics at age 45
40%
106
Prevalence fo hypertension in type II diabetics age 75
60%
107
BMI for obesity
>30
108
Five factors that are raised in obese patients that can result in the onset of hypertension
Increased renal renin release Increased angiotensin formation Increased sodium retention High levels of leptin - increased sympathetic vasoconstriction Hyperinsulaemia - insulin induced hyperkalaemia
109
First line treatment for hypertension
Lifestyle changes - exercise, increased fruit and veg and decreased salt, reduced weight if obese
110
First line pharmacological treatment for hypertension
Thiazide diuretic
111
Name of thiazide diuretic used in the treatment of hypertension
Bendroflumethazide
112
Second and third line treatment of hypertension
Thiazide + beta blocker or ACE inhibitor Angiotensin receptor blocker
113
Fourth line treatment of hypertension
Calcium channel blocker
114
Final line treatment of hypertension
Alpha blocker
115
First line pharmacological treatment for hypertensive diabetics
ACE inhibitors or angiotensin receptor blockers
116
Most important first line treatment for obese hypertensives
Exercise and try to lose weight
117
Therapeutic target for hypertensives
<140/85 in clinic | <130/80 at home
118
Therapeutic target for diabetic hypertensives
<140/80 in clinic | <130/75 at home
119
Define erythropoesis
Production of red blood cells
120
Sites of erythropoesis prior to brith
1-3 week - yolk sac and mesothelial layers of the placenta 6 week - liver and spleen 3 month - bone marrow as the bones form
121
0-5 years - site of erythropoiesis
Bone marrow of all bones
122
5-20/25 years site of erythropoiesis
Bone marrow of the long bones
123
25 years + site of erythropoesis
Bone marrow of membranous bones - vertebrae, sternum, ribs, cranial bones, ileum
124
Name the 5 membranous bones
``` Verterbae Sternum Cranium Ribs Ileum ```
125
Define myeloid tissue
Bone marrow
126
Red bone marrow function
Site of erythropoiesis
127
Yellow bone marrow function
Contains large amounts of fat droplets and cells
128
Stages of production of an erythrocyte
``` Haematopoetic stem cell Common myeloid progenitor cell (committed at this stage) Proerythroblast Early erythroblast Late erythroblast Erythroblast Normoblast Reticulocyte Erythrocyte ```
129
Cytoplasm of what cell stains blue?
Proerythroblast
130
How to recognise proerythroblast?
Bright blue rim of cytoplasm around blue nucleus
131
How to recognise early erythroblast?
Polychromatic i.e. many coloured nucleus
132
Cells that contain ribosomal RNA in them are?
Reticulocytes
133
Define diapedesis
Passing of the erythrocytes through pores in the capillary membranes from the bone marrow into the blood
134
Diameter of erythrocytes
7.8um
135
Volume of erythrocyte
90cu mm
136
Volume of RBC in microcytic anaemia
<79/80fl
137
Volume of RBC in macrocytic anaemia
>100fl
138
Normal RBC count - general
Around 5 million per microlitre
139
Normal lifespan of RBC
120 days (+/- 30 days)
140
RBC count in men
5.2 x0.3x10^6
141
RBC count in women
4.7 x0.3x10^6
142
Component that controls erythropoiesis is?
EPO - erythropoietin
143
Production site of EPO
Fibroblasts in the kidney - at the proximal convoluted tubule Glomus cells of the carotid body
144
Why is EPO only produced in these specific locations?
Oxygen levels here are not affected by exercises or BP changes - steady usage of oxygen
145
What are EPO secreting cells sensitive to?
Hypoxia Hypoxia stimulates increased EPO release
146
Anaemia caused by kidney damage and why?
Kidney damage - reduced EPO production | This can cause microcytic anaemia
147
Charge on erythrocytes
Outside negative surface charge due to presence of glycoproteins - causes them to repel and not stick to each other
148
Define rouleaux
Clumping of erythrocytes caused by reduced charge on their surface
149
Cause of rouleaux x2
Inflammatory reactions Bacteria in the blood
150
Define ESR
Erythrocyte sedimentary rate
151
Significance of raised ERS
Non-specific marker for infection in the blood (due to formation of rouleaux)
152
Two reasons RBCs need ATP
Sodium pumps in the membrane | GLUT1 transporters to consume glucose
153
Metabolism of RBCs
Anaerobic glycolysis (and pentose phosphate pathway)
154
Name the four myeloid cells
``` M M Me Megacaryocyte Mast Cell Myeoblast Erythrocyte ```
155
Cells and site of removal of RBCs from the body
Removed via macrophages when passing through the spleen
156
Three signals indicating need for removal of RBCs
Cell surface antigens of old cells differ to that of young cells Increased levels of methaemoglobin RBCs become more rigid and trapped in splenic capillaries
157
Breakdown of haem via what enzymes
Haem to biliverdin via haemoxygenase | Biliverdin to bilirubin via biliverdin reductase
158
Colour of biliverdin
Green
159
Globin proteins are broken down into what?
Amino acids
160
Unconjugated bilirubin
When bilirubin is bound to albumin in the splenic macrophages and released into the blood
161
Conjugated bilirubin
Occurs in the liver | Bilirubin attaches to glucoronic acid via hepatocytes and is now more soluble
162
How is conjugated bilirubin excreted?
Converted to urobilnogen in the small intestine - passes out in faeces (10% in urine)
163
Site of haemoglobin to biliverdin
Spleen
164
Site of biliverdin to bilirubin
Liver
165
Site of bilirubin to urobilnogen
Small intestine
166
Acid that binds to bilirubin to form conjugated bilirubin
Glucoronic acid
167
Stercobilin
10% of urobilnogen converted to this - excreted in the urine
168
Define arteriosclerosis
Thickening of an arterial wall which then loses elasticity | Sclerosis - hardening
169
Most common form of ateriosclerosis
Athersclerosis
170
Three stages of atherosclerosis
Endothelial damage (and activation) Uptake of modified LDLs, adhesion and infiltration of macrophages Smooth muscle proliferation and formation of fibrous cap
171
Four functions of the endothelium
Vasomotor tone Thrombosis - antithrombotic properties Production of inflammatory factors Production of cellular adhesion molecules (CAMs) - receptors for monocytes
172
Four causes of endothelial damage
Shear stress e.g. turbulent blood flow Toxic damage e.g. free radicals High levels of lipids Viral or bacterial infection
173
Function of lipoproteins
Transportation of fat in the blood
174
Five types of lipoproteins
``` Chylomicrons VLDL LDL IDL HDL ```
175
LDL vs. HDL
LDL - bad - composed of mainly cholesterol | HDL - good - composed of mainly protein
176
Two ways in which LDLs can become modified
Oxidation | Glycation
177
Glycation of LDLs is prevalent in?
Diabetes mellitus - high glucose levels
178
Effect of oxidised LDL?
This can act to cause endothelial damage itself
179
Infiltration of macrophages occurs as?
Increased monocytes bind to CAM - crosses endothelium and transformed into macrophages
180
Define foam cells
Lipid laden macrophages
181
How are foam cells formed?
Macrophages pick up excess levels of modified LDL via scavenger receptor and grow larger and larger LDL apolipoprotein B100
182
Apoliprotein B100 present on?
VLDL IDL LDL
183
Apoliprotein present on chylomicrons?
B48
184
Fatty streak of atheroma occurs in which layer of the artery?
Occurs in the tunica intima
185
Component causing smooth muscle proliferation in arteriosclerosis?
Platelet derived growth factor (PDGF)
186
Two cell types that release PDGF?
Endothelial cells | Macrophages
187
What are the two types of smooth muscle?
Resting - contractile | Proliferating - secretion of extracellular materials
188
What is broken down by the proliferating smooth muscles?
Internal elastic lamina
189
How is a thrombus formed by the smooth muscle cells?
Proliferating smooth muscle cells Secretion of extracellular materials e.g. collagen Collagen - platelets will stick to this and form a thrombus
190
Four common sites of atheroma formation
Carotid bifurcation Aortic bifurcation Lateral walls of the common iliac arteries Coronary arteries
191
Unmodifiable risk factors for atheroma formation x3
Age Sex Family history
192
Modifiable risk factors for atheroma formation x5
``` Dyslipidaemia Smoking Hypertension DM Physical activity ```
193
Define dyslipidaemia
Elevated LDL/cholesterol levels
194
Desirable total cholesterol levels in adults
<200mg/dl
195
Desirable LDL and HDL levels in adults
LDL - <130 | HDL - <40
196
Three emerging risk factors for the onset of atherosclerosis
Homocysteinaemia Lipoprotein a Infection
197
Three treatment options for atheroma formation
Modifiable risk factors Plasma lipid reduction - statins Polypill usage
198
What is contained in the polypill? x5
Statin Three BP lowering drugs - thiazide, beta blocker, ACE inhibitor Folic acid Aspirin
199
Complications from atheroma formation x5
``` Coronary artery disease - MI/angina Peripheral vascular disease Stroke Aneurysm Renal artery stenosis ```
200
Surgical interventions for atherosclerosis x3
CABG PCI Stent
201
Arterial stent generally done in which artery?
Generally done via radial artery rather than the femoral artery
202
Two types of angina and causes
Stable - coronary artery disease | Unstable - acute myocardial infarction
203
Typical history of stable angina (from the patient)
Central chest pain comes on following exertion | Stops when exertion is ceased
204
Two main causes of angina
Decreased myocardial oxygen supply | Increased myocardial oxygen demand
205
Two causes of reduced myocardial oxygen supply
Coronary heart disease | Severe anaemia
206
Three causes of increased myocardial oxygen demand
Left ventricular hypertrophy Right ventricular hypertrophy Rapid tachyarrythrmias
207
Five indications for cardiac referral of a patient
New onset angina Exclusion of angina in high risk individuals with atypical symptoms Worsening angina in patient with previously stable symptoms New or recurrent angina in patient with history of e.g. MI Assessment of occupational fitness eg. airline pilots
208
Four methods for diagnosis of angina
Clinical assesment Electropcardiography LV wall motion analysis Perfusion imaging
209
Diagnostic features for assessment of angina x6
``` HISTORY Character - tight Location - chest central Radiation - arms, throat, jaw Duration - 5-10 minutes at the most Provocation - exertion ```
210
ECG results of patient stable angina - resting vs. exercise ECG
Resting ECG - can be normal | Exercise ECG - abnormal
211
Exercise ECG - stable angina appearance
Planar or down-sloping ST depression
212
ST depression is indicative of what?
ST depression - indicates ischaemia
213
Main non-invasive investigation for angina
Exercise ECG
214
Functional imaging investigations for angina x3
Isotope perfusion imaging MR perfusion imaging Dobutamine stress echo
215
Drugs to increase O2 delivery for angina x4
Nitrates Calcium channel blockers Nicorandil Revasc
216
Drugs to reduced oxygen demand in angina
``` Beta blockers Nitrates Nicorandil Calcium channel blockers Trimetazidine Ivabridine ```
217
Secondary prevention of angina
Aspirin and statins primarily | Also ACE inhibitors
218
Surgical interventions for the management of angina
CABG | PCI
219
Diagnostic criteria for MI
Change in the troponin levels (increase) PLUS at least one of: Symptoms of ischaemia New ST segment/T wave changes Pathological Q waves Imaging evidence of lack of wall motility Presence of thrombus on angiograph
220
Increased troponin levels indicate?
MI - cardiac muscle damage
221
Where is troponin found?
Found only in cardiac myocytes
222
Change on ECG required for MI?
Not for NSTEMI | YES for STEMI - ECG is diagnostic for STEMI
223
Two types of MI
NSTEMI - non-ST elevation myocardial infarction | STEMI - ST elevation myocardial infarction
224
STEMI vs. NSTEMI
STEMI - ruptured coronary plaque and occlusive thrombus NSTEMI - ruptured coronary plaque and subocclusive thrombus
225
Type 1 AMI and cause
Spontaneous AMI | Plaque rupturing
226
Five cardiac signs of AMI
``` Chest pain 4th heart sound Low grade fever Leucocytosis and raised inflammatory markers Troponin leak (increased levels) ```
227
Three autonomic symptoms of AMI
Tachycardia Sweating Vomiting
228
Five traits that may result in a delay for calling for help when experiencing an AMI
``` Older people Women Nocturnal or weekend pain No previous AMI People with diabetes ```
229
What percentage of people who die from an AMI do so before reaching the hospital?
33%
230
What is the mortality rate after one year of an AMI?
40%
231
Major cause of morbidity in AMI patients?
Cardiogenic shock - left ventricular failure
232
Treatment for STEMI
Reduction of the size of the infarct via thrombolytic drugs and reperfusion therapy
233
Two main types of thrombolytic drugs
Streptokinase | Tissue plasminogen activator (tPA)
234
What are thrombolytic drugs?
These work to dissolve the blood clots
235
Action of streptokinase
Lysis of fibrin in the thrombus
236
Action of tPA
Converts plasminogen to plasmin --> this lysis the fibrin in the thrombus
237
Main method for reperfusion therapy?
Primary PCI
238
What should be provided prior to primary PCI?
Anti-platelet drugs i.e. aspirin/heparin
239
Prevention treatment for AMI following discharge?
Lifestyle - smoking, diet, exercise Prevention durgs - aspirin, statin, beta blocker, ACE-inhibitor , tricagrelor Prevention devices e.g. ICD
240
Should tricagrelor be given for life treatment?
No
241
How many patients with AMI are smokers?
20%
242
How many patients with AMI under 60 years are smokers?
50%
243
What percentage of AMI sufferers quit smoking?
33%
244
Volume of RBCs in the body
24x10^12
245
RBC lifespan
120 days - about 4 months
246
RBCs make up what proportion of all body cells?
1/3
247
RBC approximate death rate
2x10^11
248
Average diet contains how much iron per day?
15mg
249
What is the total quantity of body iron?
3-5mg
250
Most iron in the body is in what form?
Circulating haemoglobin - 2mg
251
Where is the majority of iron absorbed in the body?
Duodenum
252
Cells that absorb iron are? Location?
Enterocytes in the duodenal lining
253
Two forms in which iron can be absorbed
Free iron in the ferrous form Fe2+ | Protein e.g. haem
254
Ferrous iron formula
Fe2+
255
Ferric iron formula
Fe3+
256
Function of ferric reductase on iron
Ferric reductase reduces Fe3+ to Fe2+ (for absorption)
257
What component regulates the level of free iron in the plasma?
Transferrins
258
What component transports iron from the bone marrow into the blood?
Transferrins
259
How many iron atoms can transferrins hold and in what form?
Can hold two iron atoms in the ferric (Fe3+) form
260
Location of transferring receptor
Erythroblast
261
Release of iron from transferring occurs where?
Within the cell i.e. erythroblast via endocytosis
262
Free iron in the erythroblast is taken up by?
Ferritin
263
How is iron stored in cells?
Bound to ferritin
264
How is iron released from ferritin?
Controlled fashion - when needed
265
Common diagnostic test for iron deficiency anaemia
Serum ferritin levels - indirect marker of stored iron
266
Define anaemia
Low hb. level <13.5g/dl male and <11.5g/dl female
267
Most common blood disorder of patients
Anaemia
268
Anaemia hb. level in child 6 months to 6 years
<11g/dl
269
Anaemia hb. level in child 6 years to 14 years
<12 g/dl
270
Three variables that alter normal hb. level
Age (decreases with age) Sex Racial background
271
Five further tests if hb. is low
``` History and examination Full blood count and blood film Serum 12, folate, ferritin Renal and liver function tests ESR ```
272
Symptoms of anaemia x5
``` Tiredness Fainting Shortness of breath Worsening angina/claudication Palpitations ```
273
Signs of anaemia x6
``` Pallor Rapid heart rate Bounding pulse Systolic flow murmur Cardiac failure Retinal haemorrhages ```
274
Causes of reduced production of RBCs leading to anaemia x6
``` Iron deficiency B12/folate deficiency Marrow infiltration e.g. cancer Chronic disease Infections e.g. HIV/parvovirus ```
275
Causes of increased destruction of RBCs leading to anaemia x1
Haemolytic anaemia
276
Causes of increased loss of RBCs leading to anaemia x1
Bleeding
277
Two most common causes of anaemia
Iron deficiency and B12/folate deficiency
278
MCV of microcytic anaemia
<76fl
279
MCV of macrocytic anaemia
>96fl
280
Volume of normocytic anaemia
76-96fl
281
Two main microcytic anaemias
Iron deficiency anaemia | Thalassaemia
282
1ml of blood contains how many mg of iron?
0.5mg
283
Major source of haem iron is?
Food of animal origin
284
Factors that can enhance iron absorption x6
``` Haem iron - meat Ferrous salts - Fe2+ Acidic pH Iron deficiency Pregnancy Hypoxia ```
285
Factors that can impair iron absorption x5
``` Non-haem iron i.e. veg Ferric salts - Fe3+ Alkaline pH Iron overload Inflammatory disorders ```
286
Common drug that can decrease iron absorption
Protein pump inhibitors for acid reflux/indigestion
287
Causes of iron deficiency anaemia x10
``` Menorrhagia Varices Ulcer Inflammatory bowel cancer Coeliac Atrophic gastritis Growth spurts Pregnancy Elderly Vegans Hookworm ```
288
Histological cell which signifies iron deficiency anaemia is?
Pencil cell
289
Tablets given to treat iron deficiency anaemia?
Ferrous sulphate
290
Four causes of normocytic anaemia
Acute blood loss Chronic disease Cancer Haemolysis
291
Three causes of macrocytic anaemia
B12/folate deficiency Alochol/liver disease Myelodysplasia
292
Specific function of B12/folate
Conversion of homocysteine to methionine (DNA synthesis)
293
B12 and folate deficiency result in what type of anaemia?
Macrocytic - cells fail to divide
294
B12/folate - which is destroyed by cooking?
Folate
295
How long is B12 stored for in the body?
Three years
296
How long is Folate stored for in the body?
Four months
297
Where is B12 absorbed?
Ileum - bound to IF
298
Where is folate absorbed?
Duodenum and jejunum
299
What is B12 bound to in the body?
Intrinsic factor
300
Cells that produce IF are?
Parietal cells of gastric mucosa
301
Lack of IF results in?
Pernicious anaemia
302
Histological appearance of B12/folate deficiency?
Hypersegmented neutrophils
303
Two main causes of B12 deficiency
Nutritional - lack in diet | Malabsorption - gastric i.e. IF or intestinal e.g. chron's disease
304
Pernicious anaemia?
Lack of IF | Autoimmune disorder - action of autoantibody
305
Autoantibody in pernicious anaemia attacks what? x2
Gastric mucosa | IF
306
Five signs of pernicious anaemia
``` Insidious - gradual onset Anaemia Glossitis Mild jaundice Neurological symptoms ```
307
Treatment for pernicious anaemia
Intramuscular B12 once every three months for life
308
Four signs of folate deficiency
Insidious Anaemia Glossitis Mild jaundice NO neurological signs!
309
Treatment for folate deficiency
Oral folic acid
310
Define haemolytic anaemia
Lifespan of RBC <120 days
311
Three signs of haemolytic anaemia
Jaundice Increased LDH levels Spherocytosis
312
Three signs of haemolytic anaemia - explain
Jaundice - increased release of bilirubin (can lead to gallstones) Increased levels of LDH - released from the cells Spherocyte formation
313
Four haemolytic anaemias
Hereditary spherocytosis Sickle cell disease Thalassaemia Glucose-6-phosphate dehydrogenase deficiency
314
Signs of haemolytic anaemia x4
Pallor and anaemia Jaundice Gallstones Splenomegaly
315
Inheritance pattern of hereditary spherocytosis
Autosomal dominant
316
G6PD function
Prevents/reverses the oxidation of Hb. membrane SO prolongs the lifespan of RBC
317
Inheritance of G6PD deficiency
X-linked
318
Immunoglobulin involved in autoimmune haemolytic anaemia
IgG
319
Investigation for autoimmune haemolytic anaemia
Direct Coombs test/Direct antiglobulin test
320
Define stroke
Interruption of cerebral blood flow causing ischaemia and hypoxia
321
Two causes of stroke
Infarction - blockage of artery | Haemorrhage - rupture of aneurysm
322
Two divisions of haemorrhagic stroke
Parenchymal - into the brain tissue | Subarachnoid - into the subarachnoid space
323
Stroke is the ____ most common cause of death in the UK? After what?
Third most common Heart disease Cancer
324
Direct Coombs test/direct antiglobulin test is used for?
Investigation of autoimmune haemolytic anaemia
325
Stroke symptoms are quick or gradual?
QUICK
326
Symptoms of stroke
Sudden numbness/weakness of face/limbs Sudden confusion Sudden trouble with vision Sudden severe headache
327
FAST pneumonic for symptoms
Face Arms Speech Time
328
Stroke golden hour
Interventions in the first hour following stroke make significant difference to outcome
329
Four types of stroke
TIA Thrombotic - ischaemic Embolic - ischaemic Haemorragic
330
Maximum length of a TIA
24 hours - clinically this is only for 85% of patients
331
Typical length of a TIA
<1 hour
332
Cause of TIA
Release of small emboli from a thrombus | Temporary downstream blockage of vessel
333
What is thrombotic stroke?
Development of atheroma in a cerebral vessel - ruptures and forms local clot
334
What is embolic stroke?
Embolism occurs from an original thrombus | Original thrombus in this case is not in cerebral arteries
335
Main feature of embolic stroke?
Rapid development of neurological signs
336
Thrombotic and embolic strokes make up what percentage of all strokes?
85%
337
Source of embolism in embolic stroke is usually where?
Left side of heart
338
Key feature of haemorrhagic stroke is? x2
Severe headache Stupor/coma that may progress with time
339
Cause of haemorrhagic stroke
Rupture of blood vessel
340
Define lacunar stroke
Occlusion of artery supplying deep structures rather than cortex Basal ganglia, thalamus, pons, cerebellum
341
Presence of cortical infarct signs in lacunar stroke?
Absent
342
Three forms of lacunar stroke?
Motor hemiparesis with dysarthria Ataxia and hemiparesis Dysarthria and clumsy hand
343
Define dysarthria
Difficult or unclear articulation of speech due to poor articulation of the muscles of speech
344
Define ataxia
Loss of full control of bodily movements
345
Main feature of embolic stroke?
Rapid development of neurological signs
346
Thrombotic and embolic strokes make up what percentage of all strokes?
85%
347
Source of embolism in embolic stroke is usually where?
Left side of heart
348
Key feature of haemorrhagic stroke is? x2
Severe headache Stupor/coma that may progress with time
349
Cause of haemorrhagic stroke
Rupture of blood vessel
350
Define lacunar stroke
Occlusion of artery supplying deep structures rather than cortex Basal ganglia, thalamus, pons, cerebellum
351
Presence of cortical infarct signs in lacunar stroke?
Absent
352
Three forms of lacunar stroke?
Motor hemiparesis with dysarthria Ataxia and hemiparesis Dysarthria and clumsy hand
353
Define dysarthria
Difficult or unclear articulation of speech
354
Define ataxia
Loss of full control of bodily movments
355
Motor hemiparesis with dysarthria where is the lesion?
Infarct in the posterior limb of the internal capsule
356
Ataxia and hemiparesis where is the lesion?
Infarct in the posterior limb of the internal capsule
357
Dysarthria and clumsy hand where is the lesion?
Infarct in the anterior limb of the internal capsule
358
Impaired function of cerebral sodium pump results in? x2
Swelling of the brain nerve cells (increased leakage of Na+ and hence water into the cell) This swelling results in increased ICP
359
Why do cerebral nerve cells require a very high level of sodium pumps?
Have a very large surfaced-area to volume ration - increased sodium leakage
360
Hypertension accounts for what percentage of stroke risk?
35-50%
361
Those with AF have what percentage risk of stroke per year?
5%
362
Name five lesser risk factors for stroke
``` Hypercholestrolaemia Migraine Obstructive sleep apnoea Diet low in potassium Thiazide and loop diuretics ```
363
Most common artery for stroke
Middle cerebral artery
364
Why is MCA prone to aneurysms and stroke?
Highly tortuous artery
365
Lenticulostriate arteries - supply and origin
Arteries to the basal ganglia and the internal capsule Leave MCA at 90 degree angle
366
Function of internal capsule
Motor commands from motor cortex to brainstem and sinal cord
367
Function of cerebral sodium pump x2
Maintains the membrane potential | Maintains the nerve cell size and shape
368
Impaired function of cerebral sodium pump results in? x2
Swelling of the brain nerve cells (lack of movement of Na+ and water out of the cell) This swelling results in increased ICP
369
Why do brain cells have the highest consumption of ATP?
Most of the ATP is required to fuel the sodium pump
370
Three main treatment strategies for stroke
Restore blood flow Combat excitotoxicity Combat free radical damage
371
How can blood flow be restored following stroke?
Introduce tissue plasminogen activators - to burst the clots
372
Which cells remove potassium from the extracellular space of the brain?
Glial cells - take up the potassium
373
Hypoxic brain - effect on potassium levels?
In a hypoxic brain, the glial cells do not take up the potassium - increased extracellular potassium levels
374
Superoxide dismutase
Free radical scavenging enzymes against ROS
375
Cause of exocitotoxicity in hypoxic brain
Excess release of nuerotransmitters
376
Two main glutamate receptors
AMPA | NDMA
377
Consequence of excitotoxicity in the brain
Increased influx of calcium in the cell - this increases the metabolic demand - formation of free radicals
378
Define penumbra
Middle region around a stroke focus - the neurones are damaged by they can survive if intervention occurs
379
Three main treatment strategies for stroke
Restore blood flow Combat excitotoxicity Combat free radical damage
380
Three drugs to combat the excitotoxicity
NMDA antagonists AMP antagonist e.g. NBQX Lithium
381
Three methods to reduce free radial damage of the brain
Antioxidants e.g. vitamin C and E Enzymes - superoxide dismutase Cool down the brain
382
Superoxide dismutase
Free radical scavenging enzymes against ROS
383
Define clinical shock
Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in cellular hypoxia
384
Two components of shock syndrome
Hypotension | End organ injury
385
Normal CO
5l/min
386
Normal MAP
100mmHg
387
MAP of shock
MAP <60mmHg
388
Equation for BP
COxSVR
389
Equation for CO
CO = HR x SV
390
Two hormones that act to maintain SVR and their receptors
Noradrenaline - alpha-1 receptors Angiotensin 2 - angiotensin AT1 receptor These are vasoconstrictors
391
What is the most common cause of low CO
Generally due to low SV | HR tends to be compensation
392
Starling's law of the heart
The force of contraction increases as the end diastolic volume increases SO the greater the preload, the greater the force of contraction so the greater the stroke volume
393
Location of alpha-1 receptors and angiotensin receptors
Alpha adrenoreceptor - on the outside | Angiotensin receptor - lumen
394
Three factors that can increase myocardial contractility
Sympathetic NS Catecholamines i.e. adrenaline/noradrenaline Ionotrope drugs
395
Receptor for ionotropoic drugs
Beta-1 receptor
396
Four factors leading to reduced myocardial contractility
Cardiac disease Hypoxia/hypercapnia pH/electrolyte disturbance Drugs e.g. BBs or CCBs
397
How is SVR maintained?
Constriction of arterioles in end organs
398
Two hormones that act to maintain SVR and their receptors
Noradrenaline - alpha-1 receptors Angiotensin 2 - angiotensin receptor These are vasoconstrictors
399
Two local vasodilators
No | Prostacyclin
400
Local vasoconstrictor
Endothelin
401
Cells that produce prostacyclin
Endothelial cells
402
Prostacyclin is produced from what?
Arachidonic acid
403
Two functions of prostacyclin
Inhibits platelet activation | Local vasodilator - reduces calcium entry into smooth muscle
404
Hormone that antagonises the effects of prostacyclin is?
Thromboxane
405
Compensated shock
Initial stage of shock
406
Decompensated shock
Later stage of shock - organs cannot be perfused and start to fail
407
Four main classes of shock
Obstructive shock Distributive shock Hypovolaemic shock Cardiogenic shock
408
Obstructive shock and example
Physical obstruction causing failure of cardiac output e.g. pulmonary embolism
409
Main sign of septic shock
Fever
410
Hypovolaemic shock and eg
where you have bled and lost too much blood so there is not enough circulating blood so that even if you were to increase the heart rate, preload cannot increase e.g. haemorrhage
411
Cardiogenic shock and eg
Failure of the heart to pump efficiently and supply blood to the body e.g. myocardial infarction/heart failure
412
Classic presentation of hypovolaemic shock
``` Low BP High HR Confusion Anxiety Greyish pallor Oligouria ```
413
Effect of breath sounds on obstructive shock
Breath sounds are absent on the affected hemiothorax
414
Volume of blood loss that is life threatening
>40% - >2litres
415
At whcih stage of hypovolaemic shock will treatment be required
Stage 3 - prior to this can be compensated for
416
Immediate compensation to shock
Increased sympathetic - HR and contractility via baroreceptors Release of ADH vasopressin
417
Longterm compensation to shock
Renin, aldosterone release, increased thirst sensation, increased EPO production
418
Name of cells that produce EPO
Peritubular fibroblasts
419
Four stages of hypovolaemic shock
1 - <15% loss of blood 2 - <30% loss of blood 3 - >30% loss of blood 4 - >40% loss of blood
420
Septic shock is a form of which type of shock?
Distributive
421
Composition of feotal hb
Two alpha | Two gamma
422
Composition of adult Hb. (HbA)
Two alpha and two beta
423
Genes for alpha subunit - chromosome?
Alpha subunit - 2 genes on chromosome 16
424
Genes for beta subunit - chromosome?
Beta subunit - 5 genes on chromosome 11
425
Five genes for beta subunit
``` Gamma A Gamma G Epsilon Delta Beta ```
426
HbF compared to HbA
HbF can bind O2 more efficiently than HbA
427
Hb. Gower-1 and composition
Very first form of Hb - first six weeks Two zeta Two epsilon
428
Composition of HbA2
Two alpha | Two delta
429
Beta thalassaemia cause
Mutation on chromosome 11
430
Alpha thalassaemia
Deleted/faulty genes on chromosome 16
431
Beta thalassaemia
Deleted/faulty genes on chromosome 11
432
Four forms of alpha thalassaemia and cause
Minima - one gene defective - silent carrier Minor - two genes defective Hb H disease - three genes defective Hydrops fetalis - four genes defective - incompatible with life
433
Hydrops fetalis stillborn infant cause
Four defective genes on chromoome 16
434
Beta thalassaemia cause
Point mutation on chromosome 11
435
MCV of haemolyic anaemia
6-8g/dL
436
Two forms of beta thalassaemia
Heterozygous - minor | Homozygous - major
437
Consequence of beta thalassaemia major
Cannot produce sufficient levels of HbA either
438
HbE
Hb with single point mutation in Beta chain
439
Mitral valve prolapse
>2mm systolic prolapse of one or both valve leaflets into the LA
440
Cause of SCA
Mutant form of beta subunit | Mutation of glutamic acid to valine (GAG to GTG) at codon 6 of chromosome 11
441
HbC
Hb with abnormal beta subynit
442
HbE
Hb with single point mutation in Beta chain
443
Most common valve lesion
Mitral valve prolapse
444
Symptoms of mitral valve prolapse
Asymptomatic
445
Signs of mitral valve prolapse
Ejection click and late systolic murmur
446
Treatment of mitral valve prolapse
Usually none necessary
447
Symptoms of aortic stenosis x5
``` Dyspnoea Angina Syncope LVF Sudden death ```
448
Three causes of aortic stenosis
Calcific disease Congenital bicuspid valve Rheumatic disease
449
Cause of rheumatic disease
Group A haemolytic strep infection
450
Aortic stenosis indications for surgery
Any symptoms of AS Echocardiographic evidence of worsening LV dilatation Peak systolic pressure gradient >50mmHg
451
Causes of aortic regurgitation
``` Calcification Congenital bicuspid valve Rheumatic disease Infective endocarditis Ankolysing spondylitis Marfan syndrome Aortic dissection ``` SAME AS AORTIC STENOSIS + INFECTIVE ENDOCARDITIS
452
Symptoms of aortic regurgitation x2
NB. Often none Dyspnoea - contractile failure Angina - increased O2 demand of LV
453
Causes of aortic regugitation
``` Calcification Congenital bicuspid valve Rheumatic disease Infective endocarditis Ankolysing spondylitis Marfan syndrome Aortic dissection ```
454
Symptoms of aortic regurgitation
a
455
Signs of aortic regurgitation
Rapidly rising carotid pulse (increased preload) Early diastolic murmur Ejection murmur
456
Rising carotid pulse aortic stenosis vs. aortic regurgitation
Aortic stenosis - slow rising | Aortic regurgitation - rapid rising
457
Effect of aortic regurgitation on the LV
Dilatation due to increased volume/volume overload
458
Investigation for aortic regurgitation
Echo-doppler
459
Aortic regurgitation - indications for surgery
Any symptoms of AR | Echocardiographic evidence of worsening LV dilatation
460
Cause of mitral stenosis
Rheumatic fever
461
Signs of mitral stenosis x3
Fast pulse Mid-diastolic rumble Increased JVP, Basal crepitations, Ankle oedema - due to volume overload
462
Define orthopnoea
Shortness of breath i.e. dyspnoea when lying flat
463
Signs of mitral stenosis x3
Fast pulse Mid-diastolic rumble Increased JVP, Basal crepitations, Ankle oedmea - due to volume overload
464
Investigation for mitral stensos
Echocardiogram + doppler
465
Treatment for mitral stenosis x2
Valvuplasty - replacement of valve | Angioplasty - dilate the valve
466
Mitral valve disease - indications for surgery
Symptoms that fail to respond to medical treatment | Worsening cardiovascular complications
467
Symptoms and signs of mitral regurgitation
Same as mitral stenosis
468
Mitral valve disease - indications for surgery
Symptoms that fail to respond to medical treatment | Worsening cardiovascular complications
469
Location of cardiac plexus
Anterior to the carina - bifurcation of trachea at L4/L5 and posterior to arch of aorta
470
Cardioinhibitory centre
Parasympathetic to the heart - reduces the heart rate Synapse with the vagus To the SAN and the AVN
471
Sympathetic innervation to the heart from?
Sympathetic trunk | Visceral general afferents
472
Cardioinhibitory centre
Parasympethetic to the heart | Synapse with teh vagus
473
Cardioinhibitory centre location
The medulla
474
Three nuclei of the vagus nerve
Dorsal motor nucleus Nucleus ambiguus Solitary nucleus
475
Cardioacceleratory centre function x2
Sympathetic innervation: Increase HR Increase force of contraction
476
Location of cardioacceleratory centre
Medullar - reticular formation
477
Autonomic region of grey matter in the spinal cord?
T1-T4 | Lateral horn
478
Anterior chamber of the heart is?
Right ventricle
479
Surfaces of the heart
``` Anterior Base Right pulmonary Left pulmonary Diaphragmatic ```
480
Anterior chamber of the heart is?
Right ventricle
481
Blood supply to the AVN and the SAN?
Right coronary artery
482
Left dominant heart is what?
If the posterior descending artery comes from the left coronary artery rather than the right coronary artery - 15% of people
483
Blood supply to the AVN and the SAN?
Right coronary artery
484
Three bundle branches of the LAD
Posterior/septal branch fo the left bundle Right bundle Left bundle
485
Bundle of His divides into what?
Right bundle | Left bundle
486
Bachman''s bundle?
This is a bundle coming straight from the SAN
487
ECG presentation of AF?
Absent P waves
488
Causes of concentric hypertrophy x2
Aortic stenosis | Chronic hypertension
489
Why can concentric hypertrophy lead to eccentric hypertrophy?
Reduced compliance results in volume overload
490
Causes of ventricular hypertrophy x2
Aortic stenosis | Chronic hypertension
491
Cause of eccentric hypertropohy
Volume overload/preload
492
Valves open during systole
Aortic and pulmonary
493
Valves open during diastole
Mitral and tricuspid
494
S1-S2 systole or diastole?
Systole
495
S2-S1 systole or diastole?
Diastole
496
Two effects of rheumatic disease
Fibrosis of the valve cusps | Softening of the cordae tendinae
497
When is mitral regurgitation heart?
Systolic murmur
498
When is aortic stenosis heart?
Systolic murmur (mid-systolic)
499
Effect of mitral valve stenosis on left atrium?
Causes left atrial enlargement
500
When is mitral stenosis heard?
Diastolic murmur
501
Oedema in left sided heart failure?
Pulmonary oedema - respiratory crackles
502
Cause of eccentric hypertropohy
Volume overload/preload
503
Valves open during systole
Aortic and pulmonary
504
Valves open during diastole
Mitral and tricuspid
505
Parasympathetic outflow to the heart comes from which vagus nerve nuclei?
Mainly nucleus ambiguus - also some from from dorsal motor nucleus
506
S2-S1 systole or diastole?
Diastole
507
Two effects of rheumatic disease
Fibrosis of the valve cusps | Softening of the cordae tendinae
508
When is mitral regurgitation heart?
Systolic murmur
509
When is aortic stenosis heart?
Systolic murmur (mid-systolic)
510
Effect of mitral valve stenosis on left atrium?
Causes left atrial enlargement
511
When is mitral stenosis heard?
Diastolic murmur
512
Pathological/Inferior Q waves show?
Shows that the patient has had a previous AMI - very likely to suffer from heart failure
513
Oedema in right sided heart failure?
Systemic oedema - swollen ankles
514
Oedema in congestive heart failure?
Symptoms of both
515
CXR signs of pulmonary oedema?
Batwing sign | Kerley B lines
516
Define pulmonary oedema
Excess fluid in the lungs - at the base of the lungs
517
Is heart failure more common amongst men or women?
Men
518
Four causes of heart failure?
Coronary artery disease Hypertension Cardiomyopathy Valvular heart disease Anything that causes something to be wrong with the heart
519
Give four aggravating factors for heart failure
Cardiac arrhythmia e.g. AF Hypertension Anaemia Infections
520
Symptoms of heart failure x3
Fatigue Dyspnoea Oedema
521
Signs of heart failure x8
``` Cool skin Peripheral cyanosis Basal crackles Increased JVP Ankle swelling Ascites Tachycardia Sweating ```
522
Give six potential complications of heart failure
``` Inttravascular thrombosis Infection Functional valvular dysfunction Multi-organ failure Cardiac arrythmias Sudden death ```
523
Three common ECG findings in heart failure
Inferior Q waves Anterior T waves Left bundle branch block
524
What should be present on an ECG for a patient to benefit from cardiac resynchronisation therapy (pacemaker)?
Prolonged QRS interval - >150ms (OR >120ms plus echo signs)
525
Effect of heart failure on the lungs
Patient has wet lungs - pulmonary oedema
526
Define pulmonary oedema
Excess fluid in the lungs
527
Gold standard investigation for heart failure is?
Echocardiogram
528
What is brain natriuretic peptide BNP?
Secreted by myocardial cells in response to raised left atrial pressure Also secreted when ventricles are stretched
529
Functions of BNP x4
Promotes natriuresis and vasodilation | Inhibitors ADH and aldosterone release
530
Effect of pharmacological treatmetn on diastolic failure?
No proven value
531
Define pulmonary effusion
Collection of excess fludi in the pleural cavity - potential space becomes a real space
532
Main treatment groups for heart failure x2
Beta blockers - for sympatho-adrenal activation | ACE inhibitors, ARB, sprionolactone - for RAAS activation
533
Why are diuretics commonly given for heart failure?
For treatment of fluid retention
534
Indications for a heart transplant x4
``` Heart failure without the following: Major organ failure Major co-morbidity Psychological disability Severe pulmonary hypertension ```
535
Prognosis from heart transplant
80% one year survival (bad)
536
Diastolic vs systolic heart failure
Systolic - heart cannot contract effectively | Diastolic - heart cannot relax sufficiently to fill completely
537
Who is diastolic failure more common in? x2
Women | Older patients
538
Treatment of diastolic heart failure x3
Treat the underlying cause - especially hypertension Treat the systolic component if mixed Treat fluid retention
539
Effect of pharmacological treatmetn on diastolic failure?
No proven value
540
Define pulmonary effusion
Collection of excess fludi in the pleural cavity - potential space becomes a real space
541
Define cardiac myopathy
A disease of the heart muscle
542
Cardiac myopathy usually caused by what type of mutations?
Missense mutations
543
Four types of cardiomyopathy are?
Restrictive Hypertrophic Dilated
544
What is restrictive cardiomyopathy?
Lack of stretch/dilatation of the ventricles during diastole due to increased stiffness of the wall Reduced compliance
545
Appearance of the heart in restrictive cardiomyopathy?
Heart appears normal visibly but does not stretch when required
546
What is pericarditis?
Inflammation of the pericardium | Hardening and lack of movement of fluid - restrictive disorder
547
Heart sounds present in restrictive cardiomyopathy?
Third heart sound and fourth heart sound
548
Hypertrophied cardiomyopathy is?
Hypertrophy of the myocytes - increase in size of the cardiac muscle of the ventricular wall
549
Mutations of hypertrophied cardiomyopathy?
Missense mutations
550
Main antihypertensive for under 55 year old
Ace inhibitor or ARB
551
First heart sound caused by?
Closing of the mitral and tricuspid valves
552
Second heart sound caused by?
Closing of the aortic and pulmonary valves
553
Cause of third heart sound?
Ventricular gallop
554
Cause of fourth heart sounds?
Atrial gallop
555
What is pericarditis?
Inflammation of the pericardium | Hardening and lack of movement of fluid - restrictive disorder
556
Main risk factor for CHD?
Atherosclerosis
557
Four main risk factors for CHD?
Hypertension High cholesterol - atherosclerosis Obesity Diabetes
558
Lifestyle interventions to reduced CHD in hypertensives? x7
``` Smoking cessation Diet - reduce body weight Reduce salt intake <100 Reduced alcohol consumption Regular aerobic exercise Fruit and veg Reduce sugar intake ```
559
Target BP for hypertensives
<140/80
560
Second line antihypertensive?
Thiazide-like diuretic
561
Mortality rate for CHD?
50% of cardiovascular disease deaths
562
Calcium antagonist action and s/e
Vasodilation | Flushing and oedema
563
ACE inhibitor action and s/e
Inhibit RAAS and vasodilate | Cough and low BP
564
ARB action and s/e
Block action of angiotensin - vasodilate | Low BP
565
Function of folic acid in polypill
Reduce homocysteine
566
Quantity of aspirin in polypill?
75mg
567
Target BP for hypertensives with diabetes
<130/80
568
Two antihypertensives unsuitable for diabetics + why?
Thiazide diuretics Beta blockers Worsen glucose control
569
Treatment of MI x4
Humidified oxygen Opiates Aspirin Thrombolysis/primary angioplasty
570
Secondary prevention for MI
Beta blockers ACE inhibitors Statins
571
Four components of polypill
Statin Antihypertensives Antplatelet aspirin Folic acid
572
Function of folic acid in polypill
Reduce homocysteine
573
Quantity of aspirin in polypill?
75mg
574
Define autoantibodies
Antibodies that react to self antigens
575
Alloantibodies?
Antibodies that react to foreign antigens
576
Antigens on surface of RBC are?
Sugar - ABO blood type | Protein - Rhesus blood type
577
Protein/sugar antigen on RBC determined by?
Genes
578
Alloantibodies are dangerous when?
Exposed to another blood type e.g. pregnancy or transfusion
579
Sugar antigens present on RBCs?
A or B
580
A antigen on RBC - what antibody do you have?
Have anti-B antibody
581
What type of Ig are RBC antigens?
IgM or IgG
582
Agglutinate means?
Attach to the antigen to prevent it from binding to anything
583
Universal blood type donor?
Blood type O - not agglutinated by any antibody
584
Universal blood type acceptor?
AB blood type - have no antibodies in the plasma
585
Different rhesus blood types?
C or c D or no D (no D is written as d) E or e
586
Are antibodies produced against the rhesus blood types?
Not naturally produced - will be produced by immune system upon exposure
587
Temperature spike during transfusion indicates what?
Transfusion reaction - intravascular haemolysis STOP transfusion immediately!!
588
cdE will be agglutinated by which antibodies?
Anti-c | Anti-E
589
Which rhesus antigen is the most clinically important and why?
D antigen 80% without D antigen will develop anti-D if exposed CcDEe - rhesus D positive Cde - rhesus D negative
590
Haemolytic disease of the newborn (HDN) is what?
Rhesus negative mother develops anti-D antibodies upon exposure Rhesus positive second baby - stillbirth or severe brain damage
591
How is HDN prevented?
Rhesus negative mothers carrying rhesus positive babies are given prophylactic anti-D antibodies
592
Five risks of blood transfusion
``` Transmit infection Alloimmunisation - antibody can compromise future transfusion Incompatible transfusion Iron overload from multiple transfusions Circulatory overload ```
593
Purpose of indirect antiglobulin test?
Screen for atypical antibodies in the patient's plasma
594
Temperature spike during transfusion indicates what?
Transfusion reaction - intravascular haemolysis STOP transfusion immediately!!
595
Thrombosis vs. embolism
Thrombus - pathological clot formation | Embolism - part of clot breaks off and becomes obstructed in smaller vessels
596
Composition of venous vs. arterial thrombi
Venous thrombi - RBCs | Arterial thrombi - platelets
597
Two main types of venous thromboembolism (VTE)?
DVT | PE
598
Location of distal DVT?
Calf veins only
599
Location of proximal DVT?
Popliteal veins or above
600
Three main causes of VTE and what is this known as?
Virchow's triad: Reduced blood flow - stasis Vessel wall disorder Hypercoagulability
601
Four genetic risk factors for VTE
Antithrombin deficiency Protein C deficiency Protein S deficiency Factor V Leiden
602
Six major risk factors for VTE
``` Fracture of the hip/pelvis Hip/knee replacement surgery Major general surgery major trauma Spinal cord injury Hospitalisation with acute medical illness ```
603
Four complications of DVT
PE Extension of clot Recurrent VTE Post-thrombotic syndrome
604
Five weak risk factors for VTE
``` Bed rest>3 days Travel-related Obesity Day-case surgery Varicose veins ```
605
DVT presentation? x8
``` Pain Erythema Tenderness Swelling Palpable cord Warmth Ipsilateral oedema Superficial venous dilation ```
606
WHY IS IT SO IMPORTANT TO HAVE CORRECT DIAGNOSIS OF VTE?
90% of presenting patients do not have VTE and drugs can be fatal
607
What is D-dimer?
Fibrin degradation marker Non-specific for clot formation
608
Investigations for DVT
D-dimer | Radiology e.g. ultrasound, CT
609
Scoring system used for DVT?
Wells score: >2 DVT likely and <1 unlikely
610
What is post-thrombotic syndrome?
Recurrent pain and swelling in the leg - venous hypertension
611
Three signs of PE
Tachypnoea Tachycardia Crepitations and pleural rub
612
Three main investigations for PE
ECG CXR Arterial blood gasses
613
Wells score for likely PE?
>4
614
Other conditions that D-dimer may be raised in are? x4
Infection Cancer Inflammation Pregnancy
615
Define thrombocytopenia?
Deficiency of platelets
616
Half life of LMWH?
4 hours
617
What is fondaparinux?
Anticoagulant
618
Half life of fondaparinux?
18 hours
619
When is fondaparinux unsuitable?
Patients with renal impairment
620
Three side effects of heparin?
Major bleeding - 1-5% of patients Heparin induced thrombocytopenia Osteoporosis - exposure over several weeks
621
Lifestyle treatment for VTE?
Graduated knee stockings
622
What is warfarin?
Vitamin K antagonist
623
Half life of warfarin
36 hours
624
Function of warfarin
Affects INR - reduces risk of recurrence by 90%
625
Who should warfarin not be used in?
Pregnancy - teratogenic
626
Two surgical interventions for VTE?
Thrombolysis | Inferior vena cava filter
627
Lifestyle treatment for VTE?
Graduated knee stockings
628
Define haemostasis
Stopping of blood flow
629
Vessel damage causes which two reactions?
Platelet release reaction | Coagulation cascade
630
Vasomotor change during vessel injury is what and why?
Vasoconstriction occurs - to reduced blood flow
631
What causes the vasoconstriction during vessel injury?
Serotonin
632
Function of vWF?
Adherence of platelets to one another and to teh sites of vascular damage
633
Factor that activates the coagulation cascade is?
Platelet phospholipid
634
Primary haemostasis is?
Formation of primary platelet plug via platelet aggregation and reduced blood flow
635
Secondary haemostasis is?
Coagulation cascade - stabilisation of primary platelet plug
636
What is Von Willebrand factor? vWF?
Glycoprotein in the plasma
637
Site of vWF synthesis?
Bone marrow and endothelial cells
638
Receptors for vWF on platelets?
Primary - GpIb | Secondary - GpIX, GpV
639
what is Von Willebrand disease?
Deficiency in/defective vWF - lack of ability to clot
640
Inheritance of Von Willebran disease?
Autosomal
641
Bernard Soulier syndrome is what?
Lack of GpIb
642
Glanzmann's syndrome is what?
Lack of GpIIb
643
Platelet lifespan
8-14 days
644
Roles of glycoproteins
Receptors for adhesive proteins, coagulation factors and proteins
645
Three most abundant glycoprotein molecules
GpIIIa GpIb GpIIb
646
Treatment for VWD?
Desmopressin
647
DRAW OUT PATHWAY FROM ARUN
DRAW OUT PATHWAY FROM ARUN
648
Function of thrombin
Fibrinogen to fibrin
649
what is the activated partial thromboplastin time (APTT)?
Time taken for the intrinsic pathway of the coagulation cascade
650
Four components responsible for the regulation of coagulation
Antithrombin Protein C Protein S Fibrinolytic clot
651
What is the thrombin time?
Time taken for the final common pathway of the coagulation cascade
652
Haemophilia A affects which factor?
VIII
653
Haemophilia B affects which factor?
IX
654
Five symptoms of haemophilia
``` Soft tissue bleeds Bleeding into joint cavities Psoas bleeding Intracranial bleeds Bleeding at operative sites ```
655
Function of protein C
Inactivates Va and VIIIa
656
What activates protein C?
Thrombin
657
Risk factors for DIC x6
``` Infection Malignancy Shock Liver disease Transmplantation Snake bite Intravascular haemolysis ```
658
Where is vitamin K produced?
Liver
659
What are the vitamin K dependent factors?
II, VII, IX, X
660
Disseminated intravascular coagulation (DIC) is what?
Underlying condition activates coagulation cascade - pathological blood clots
661
Risk factors for DIC x6
``` Infection Malignancy Shock Liver disease Transmplantation Snake bite Intravascular haemolysis ```
662
ECG - what shows HR?
RR intervals
663
PR interval shows?
Action potential from the atria to the Bundle of His
664
P wave shows?
Atrial depolarisation
665
HR normal range?
RR interval | 60-100 bpm
666
P wave normal wave
80ms - 2 squares
667
RR interval shows?
HR
668
PR interval normal length?
120-200ms
669
QRS interval normal length?
<120ms
670
PR interval >200ms indicates?
Heart block
671
QRS complex shows?
Ventricular contraction
672
Normal HR?
60-100bpm
673
Normal P wave length?
<80ms
674
Sinus tachycardia is?
HR > 100bpm
675
Normal QRS duration?
<120ms
676
Sinus bradycardia is?
HR < 60bpm
677
Sinus bradycardia normally seen when?
In patients on beta blockers
678
Tachycardia is?
HR > 100bpm
679
Ventricular tachycardia is?
Very very high rate - 180-190bpm
680
Ventricular tachycardia on ECG?
No P wave
681
Ventricular tachycardia vs ventricular fibrillation?
Tachycardia - regular | Fibrillation - irregular
682
Ventricular fibrillation on ECG?
HIGH RATE - 300+!!! Absent P wave No QRS seen
683
First degree heart block?
PR interval - fixed constant duration >200ms
684
Second degree heart block type 1?
AKa. Wenkenbach PR interval progressively longer - finally absent QRS Regularly irregular
685
Second degree heart block type 2?
Irregularly regular rate- random absence of QRS
686
Third degree heart block on ECG?
Bradycardia Ventricle contracts independently of atria Inverted QRS
687
When is heart block present?
If the PR interval is >200ms
688
ECG of AF?
Cannot see P wave or PR interval
689
Cause of AF?
Many separate sites of the atria are generating electrical impulses
690
P wave inverted in which lead in junctional rhythm?
Inverted in lead II
691
ECG of Atrial flutter?
P wave replaced with multiple F waves | 300bpm
692
What is junctional rhythm?
AVN takes over as the normal pacemaker
693
ECG appearance of junctional rhythm
Bradycardia Normal QRS Absent P wave (or inverted)
694
P wave inverted in which lead in junctional rhythm?
Inverted in lead II
695
Ventricular tachycardia is?
Very very high rate - 180-190bpm
696
Ventricular tachycardia on ECG?
No P wave
697
Ventricular tachycardia vs ventricular fibrillation?
Tachycardia - regular | Fibrillation - irregular
698
Ventricular fibrillation on ECG?
HIGH RATE - 300+!!! Absent P wave No QRS seen
699
First degree heart block?
PR interval - fixed constant duration >200ms
700
Second degree heart block type 1?
AKa. Wenkenbach PR interval progressively longer - finally absent QRS Regularly irregular
701
ELECTRICAL AXIS OF THE HEART LOOK AT
ELECTRICAL AXIS OF THE HEART LOOK AT
702
Third degree heart block on ECG?
Bradycardia Ventricle contracts independently of atria Inverted QRS
703
When is heart block present?
If the PR interval is >200ms
704
ECG of AF?
Cannot see P wave or PR interval
705
Cause of AF?
Many separate sites of the atria are generating electrical impulses
706
Cause of Atrial flutter?
SAN firing too fast - prior to completion of ventricular contraction
707
ECG of Atrial flutter?
P wave replaced with multiple F waves | 300bpm
708
What is dextrocardia?
Where the primiive heart folds to the left instead of right - the heart (apex) is on the right side of the body rather than the left Aorta loops towards the right
709
ECG appearance of junctional rhythm
Bradycardia Normal QRS Absent P wave (or inverted)
710
P wave inverted in which lead in junctional rhythm?
Inverted in lead II
711
What is supraventricular tachycardia?
Tachycardia generated in the atria
712
What are endocardial cushions and what do these become?
Four areas of growth in the heart | Become the mitral and tricuspid valve - two each
713
Most common supraventricular tachycardia is?
AVNRT
714
AVNRT more common in men or women?
Women
715
ECG appearance of a bundle branch block? x2
Prolongation/widening of the QRS complex | Notch on the R wave or double R wave
716
What is represented by the ST segment?
The time during which both ventricles are fully depolarised
717
Charge of the ST segment is?
Isoelectric
718
Downsloping/depressed ST segments indicative of what? x2
Coronary ischaemia OR Hypokalaemia
719
Diagnosis of STEMI requires what from an ECG trace?
New ST elevation in two or more adjacent ECG leads
720
NSTEMI indicates what?
Cardiac ischaemia
721
ELECTRICAL AXIS OF THE HEART LOOK AT
ELECTRICAL AXIS OF THE HEART LOOK AT
722
Primitive heart tube forms/completes on what day of development?
21
723
Heart starts to beat on what day?
22
724
What is an atrial septal defect likely to be caused by?
Lack of development of the septum primum or the septum secondum
725
Bulbus cordis becomes what?
Right ventricle
726
Heart tube doubles in length at which day of development?
Day 22 to day 24
727
Why does the heart loop when lengthening?
Contained within pericardial sac
728
What is dextrocardia?
Where the primiive heart folds to the left instead of right - the heart (apex) is on the right side of the body rather than the left
729
What situs inversus?
Organs are all in the reversed region
730
Prevalence of situs inversus?
1:7000
731
What is the AV canal during development adn what does this become?
Communication between atria and ventricles - becomes the mitral and tricuspid valves
732
What is a cyanotic heart lesion?
Lesion with a shunt going from right to left - deoxygenated shunted to the left adn merges with oxygenated blood Teratalogy of fallt Transposition Truncus arteriosus
733
What is an acyanotic heart lesion?
Lesion where oxygenated blood joints deoxygenated blood ASD VSD PDA Coarctation
734
What are the four characteristics of the teratalogy of fallot?
Overriding aorta Right ventricular hypertrophy Ventricular septal defect Narrow RV outflow
735
What is the significance of the endocardial cushions in embryology?
Abnormalities can often occur here - cardiac malformations form
736
What day does atrial partitioning occur and how?
Day 28 | Septum primum
737
What is at the free edge of the septum primum?
Ostium primum
738
Where is the foramen ovale in teh developing heart?
Septum secondum
739
What is the function of the foramen ovale?
Shunting of blood from th right atria to the left atria
740
Why do you require the foramen ovale in teh developing heart?
The foetus does not use it's lungs
741
What is the septum primum and it's function?
Acts as a flap/valve over the foramen ovale
742
How does the foramen ovale close following birth?
Increaed pressure in the left atrium - septum primum pushes up against septum secondum adn they seal
743
What is the remnant of the foramen ovale known as in adults?
Fossa ovale
744
What is an atrial septal defect likely to be caused by?
Lack of development of the septum primum or the septum secondum
745
When do the ventricles start to form in the developing heart?
End of the 4th week
746
Umbilical arteries - how many and what do these carry?
There are two of these from foetus to placenta | Carry deoxygenated blood
747
Umbilical veins - how many and what do these carry?
One of these Placenta to baby Oxygenated blood
748
What does the umbilical vein become at birth?
Ligamentum teres of the liver
749
Umbilical arteries and veins are under high or low pressure?
High
750
What is the ductus arteriosus?
Connects the pulmonary artery to the descending aorta
751
What causes the ductus arteriosus to close?
Increased paO2
752
What is a cyanotic heart lesion?
Lesion with a shunt going from right to left - deoxygenated shunted to the left adn merges with oxygenated blood
753
What is an acyanotic heart lesion?
Lesion where oxygenated blood joints deoxygenated blood
754
What are the four characteristics of the teratalogy of fallot?
Overriding aorta | Rijt ventricular hypertrophy
755
What is a persistent truncus arteriosus?
Single artery arises from the heart - supplies both aorta and the pulmonary artery
756
How does persistent truncus arteriosus present?
Progressive heart failure
757
What is meant by transposition of the great vessels?
Right ventricle pumps into the aorta and the left ventricle pumps into the pulmonary artery
758
What is teh presentation of the transposition of great vessles and what should be done?
BLUE BABY | Immediate surgical intervention
759
Three symptoms of atrial septal defects
Exercise intolerance Dyspnoea on extertion Fatigue
760
What is the most common cardiac defect?
Ventricle septal defect - 25%
761
What are atrial and ventricular septal defects?
Opening between teh two atria/the two ventricles
762
What is a patent ductus arteriosus?
Connection between descending aorta and the pulmonary trunk
763
Treatment of patent ductus arteriosus?
Prostaglandin inhibitor e.g. ibuprofen Then surgery
764
Treatment for coarctation of the aorta
Balloon angioplasty
765
Medical term for breathlessness is?
Dyspnoea
766
Define breathlessness
Undure awareness of breathing or awareness of difficulty breathing
767
Two respiratory centres adn where are these located?
Pneumotaxic centre Apneustic centre In the pons
768
Nerve groups involved with breathing and what do these innervate? x2
Phrenic nerve - diaphragm | Intercostal nerves - intercostals
769
Ten causes of breathlessness
``` Hypoxia Metabolic acidosis Hypotension/reduced CO Pulmonary oedema Obstruction of the pulmonary artery Anaemia Exercise Pregnancy Anxiety, pain Breathing CO2 ```
770
Hormone involved in pregnancy causing breathlessness
Progesterone
771
Receptors involved in metabolic acidosis causing breathlessness
Peripheral chemoreceptors
772
Receptors involved in the lungs causing breathlessness during pulmonary oedema are?
J receptors
773
Six associated factors for breathlessness
``` Smoking Hypertension DM Hyperlipidaemia Obesity Family history ```
774
What is meant by 'shunting'?
An area of the lung that is perfused but is not ventilated
775
Most important sign of respiratory failure and why?
Tachypnoea - >25 adn definately >30 This is the first sign to appear - all the others appear late
776
Define tachypnoea
Abnormally rapid breathing
777
Ten signs of respiratory failure
``` Tachypnoea Use of accessory msuscles Nasal flaring Intercostal or suprasternal recession Tachycardia Hypertension Sweating Cyanosis Flapping tremor Boundign pulse ```
778
Type 1 respiratory failure is?
``` Hypoxaemia only (and hypocapnia) PaO2 < 8kpa ```
779
Type II respiratory failure is?
Hypoxiaemia and hypercapnia PaO2 < 8kPa PaCo2 >6.5kPa
780
Cause of type I respiratory failure is?
Due to damage to the lung tissue - prevents adequate perfusion of the tissue but can still excrete Co2
781
Cause of type II respiratory failure is?
Ventilatory failure - alveolar ventilation is insufficient to excrete the Co2 being produced
782
Four examples of type I respiratory failure
``` Pneumonia Pulmonary oedema Asthma/COPD PE Pneumothorax ```
783
Main of type II respiratory failure
Hypoventilation e.g. airway obstruction, nerve trauma
784
First line treatment for respiratory failure?
Provide O2
785
Second line treatment of respiratory failure? x2
Control secretions | Treat lung infection - antibiotics
786
Final line of treatment for respiratory failure?
Respiratory support - invasive OR non-invasive
787
Three types of oxygen delivery masks?
Oxygen masks - nasal cannulae Face mask with resevoir bag Venturi mask
788
Indication for use of oxygen mask with nasal cannulae?
Patient with normal vital signs e.g. post-op
789
Indication for use of face mask with reservoir bag?
High O2 concednration needed by patient | E.g. asthma attach, pneumonia, sepsis
790
Indication for use of venturi mask?
Controlled treatment required in long term respiratory failure e.g. COPD
791
Oxygen saturation level required in human?
SpO294%
792
What does pulse oxometre tell you?
Oxygenation of patient - not ventilation
793
Five sources of error with pulse oximetry?
``` Poor peripheral perfusion Dark skin - over reads False nails/nail varnish Bright ambient light Lipidaemia ```
794
Desired partial pressure of O2?
PaO2 > 10kPa
795
If unsure of the cause of respiratory failure in the patient, what treatment should you administer whilst coming to a diagnosis?
High flow oxygen
796
What is the volume for the tidal volume?
Half a litre
797
Three factors that affect vital capacity
Age Height Sex
798
Best method to analyse obstructive diseases?
Peak flow
799
When should peak flow be measured?
Once in morning, once in evening
800
Indication of asthma severity via peak flow?
The greater the peak flow difference between morning and evening, the more severe the asthma
801
Define vital capacity
Volume from maximum expiration to maximum inspiration
802
How to measure forced expiratory volume?
Vitalograph
803
What is a vitalograph?
An electric peak flow metre
804
Obstructive vs restrictive lung disease on a vitalograph?
Obstructive - FEV1 is reduced due tot eh narrow airways but the FVC will be the same Restrictive - FEV1 AND FVC are reduced
805
FEV1/FVC ration in obstructive and restrictive disease?
Obstructive - ratio is reduced | Restrictive - ratio is teh same (both reduce)
806
When plotting from vitalograph, what is on each axis?
Y axis - volume, l | X axis - time, s
807
FEV1/FVC ratio showing no obstruction?
>70%
808
FEV1/FVC ratio showing mild obstruction?
61-69%
809
FEV1/FVC ratio showing moderate obstruction?
45-60%
810
FEV1/FVC ratio showing severe obstruction?
<45%
811
Smoking causes what type of lung disease?
Obstructive
812
Key test result for obstructive disorders is?
Reduced peak flow rate
813
Key test result for restrictive disorders is?
Reduced vital capacity
814
Two main obstructive disorders are?
Asthma | COPD
815
Three characteristics of asthma?
Reversible airway obstructive Hyper-responsiveness of airways Atopoic
816
Three key features of the pathophysiology of asthma?
Bronchoconstriction Secretion of mucous Airway inflammation
817
What is the cause of asthma?
Oversupplied IgE receptors
818
Immediate response of asthma pathophysiology?
Inhaled allergens bind to Ige on mast cells and release inflammatory mediators - histamine
819
Effect of inflammatory mediators/histamine released in asthma?
Increased mucous secretion Bronchonconstrction Oedema
820
Asthma delayed response is?
Mast cells activate eosinophils and release proteisn to damage epithlial cells
821
Common protein released by eosinophils in asthma is?
Eosinophil peroxidase
822
Function of proteins released by eosinophils in asthma?
Damage to epithelium - stimulate afferent nerves | Activation of parasympathetic nerves - muucous secretion and airway constriction
823
What autonomic control is involved in asthma?
Parasympathetic
824
Why is there a build up of mucous in an asthmatic?
Increased mucous secretion BUT damaged epithelium SO cannot clear the mucous
825
Four substances that can trigger asthma
Dusts Polles Medications Food
826
Five symptoms asthma
``` Troublesome cough - at night/after exercise Wheezing Chest tightness after exposure Colds last more than ten days Relief upon medication usage ```
827
Two key tests to diagnose asthma?
Peak flow | FEV1/FVC measuremetn
828
Three long term medications to treat asthma
Inhaled corticosteroids LABA - long acting beta-2 agonists Leukotriene modifiers
829
Function of long term medications x3
Reduce inflammation Relax airway muscles Improve lung function
830
Quick relief asthma medication and function
Short acting beta-2 agonists | used in acute episodes
831
Advantage of spacers?
Improve penetration of the drug into the lung | Reduce potential adverese effects from occurring
832
Indications for use of nebulisers for asthma treatment?
Small children | Severe asthma episodes
833
COPD is a combination of?
Chronic bronchitis | Emphysema
834
Time period for bronchitis to become diagnosed?
Chronic productive cough for more than half the time over two years
835
Main cause of emphysema?
Smoking
836
Main structure present in emphysema?
Bullae
837
Pathophysiology of bronchitis?
Proliferation of squamous cells | Massive mucous gland enlargment
838
Enzyme involved in emphysema?
Serine elastase
839
What is inactivated in emphysema?
Elastase inhibitor alpha-antitrypsin
840
Steroids are useful in the treatment of which obstructive lung disease?
Asthma
841
Four restrictive disorders of the lung?
``` Pneumonia Pneumothorax Pulmonary fibrosis Pleura thickening Ankolysing spondylitis ```
842
Normal PaO2
95
843
Normal PaCo2
40
844
Normal PaHCO3-
24
845
PvO2 (venous blood gas)
30-40
846
PvCO2?
50
847
What is respiratory acidosis?
Build up of CO2 in the blood - reduces pH
848
Five main causes of respiratory acidosis
``` Hypoventilation - drugs Diseases of the airways - asthma Diseases of the chest - scoliosis Disease affecting nerves/muscles Severe obesity - restricted expansion of the lungs ```
849
pH is controlled by the ratio of what?
HCO3-/CO2
850
Respiratory acidosis effect on pCO2 and HCO3-?
CO2 increases a lot | HCO3- increases slightly
851
Eight symptoms of respiratory acidosis?
``` Headache Drowsiness Lethargy Anxiety Sleepiness Fatigue Memory loss Restlessness Muscle weakness ```
852
Five signs of respiratory acidosis?
``` Slowed breathing Gait disturbance Tachycardia Tremor Reduced BP Papilledema ```
853
What is the main cause of the signs and symptoms from respiratory acidosis?
Due to a low CNS pH - causes reduced cerebral blood flow
854
What is the cerebral blood flow dependent on?
Dependent on plasma pH i..e CO2
855
pH and pCO2 in respiratory acidosis?
pH <7.35 | pCO2 >45mmHg
856
Treatment for respiratory acidosis
Oxygen Bronchodilators Stop smoking Treat underlyign lung condition
857
Effect of respiratory acidosis on the kidneys and consequence of this?
Retention of K+ by the kidneys - hyperkalaemia
858
Effect of respiratory acidisos on the heart and why?
Respiratory acidosis causes hyperkalaemia | This causes heart arrythmias - disrupts resting potential
859
Acute respiratory acidosis test results?
PaCO2 > 6.3kPa/47mmHg and pH <7.35
860
Chronic respiratory acidosis test results?
PaCo2>6.3kPa/47mmHg BUT pH is normal/near normal High HCO3-
861
Acute vs. chronic respiratory acidosis?
Acute - reducded pH | Chronic - nromal pH due to renal compensation
862
Cause of respiratory alkalosis?
Hyperventilation
863
Four symptoms of acute respiratory alkalosis?
``` Hyperventilation Dizziness Light headedness Confusion Cramps ```
864
Five other acuses of respiratory alkalosis?
``` Meningitis Stroke Anxiety Cirrhosis Sepsis Hypoxia ```
865
Symptoms of chronic respiratory alkalosis?
Generally symptomless
866
Three matbolic changs in respiratory alkalosis?
Constriction of cerebral blood vessels Increased neuromuscular activity Hypoklaemia
867
Blood test results for respiratory alkalosis
pH > 7.44 | PaCo2 < 35mmHg
868
Type I respiratory failure is?
Hypoxia with normal or low PCO2
869
Type II respiratory failure is?
Hypercapnia with or without hypoxia
870
What is the more common type of respiratory failure?
Type I
871
Ventilation/perfusion mismatch occurs in whcih type of respiratory failure?
Type I
872
Anion gap in rspiratory acidosis?
High
873
CO2/HCO3 ratio in respiratory acidosis?
High
874
CO2/HCO3 ratio in respiratory alkalosis?
Low
875
What is dependent on the CO2/HCO3 ratio?
pH
876
What is meant by 'shock'?
Inadequate maintainance of CO
877
Cells involved in innate immunity are? x4
Neutrophils Monocytes Eosinophils Mast cells
878
Cells involved in adaptive immunity are? x2
B adn T lymphocytes
879
What are the two main features of the adaptive immune system?
Self-tolerace | Memory
880
Clonal deletion is?
Deletion of B or T lymphocytes expresseing receptors for self antigens
881
Clonal expansion is?
Proliferation of B or T lymphocyte once it binds to foreign antigen
882
Which lymphocytes mature in the thymus?
T-lymphocytes
883
Function of IgG?
Block pathogen binding Activate complement Opsonise antigen for phagocytes
884
Role of IgG in pregnancy?
Specially transported across the placenta
885
Function of IgM?
Block pathogen binding, activate complement
886
Function of IgA?
Block pathogen binding | NB. no activation of complement
887
Where is IgA found?
Tears | Digestive juices
888
Function of IgE?
Activation of MAST cells
889
Function and secretion of IgD?
Both of these are unknown?
890
Proteins generated via complenet? x2
C3a | C5a
891
Role of histamine in type 1 hypersensitivity?
Increased permeability of venules Vasodilation of arterioles Itch Contraction of smooth muscle - bronchial tree
892
Role of leukotrienes in type 1 hypersensitivity?
Increased permeability of venules | Chemotaxis
893
Role of prostaglandins in type 1 hypersensitivity?
Arteriolar dilatation Pain Fever
894
Cells activated in type I hypersensitivity?
MAST cells
895
Five clinical manifestations of anaphylactic shock
``` Drop in blood pressure Warm peripheries Urticaria - hives Erythema Sore red itchy eyes Swelling of face, lips, hands, feet Bronchoconstriction Nuasea and vomiting Headache Cardaic arrest Death ```
896
Four antigens that can trigger anaphylaxis
``` Drugs - penicillin, beta-lactams, NSAIDS, aspirin Latex Foods - peanuts, fish Arthropon venoms Exercise can predipose ```
897
Acute treatment of anaphylaxis x5
``` Intramuscular adrenaline - 500mg Oxygen high flow Fluids iv Antihistamines Glucocorticoids ```
898
What is omalizumab and why is this not used?
Monoclonal antibody against IgE Very very expensive and impractical - intravenous injections lifelong
899
Interleukin involved primarily in allergens and shock?
IL4
900
Main significance of lower respiratory tract infections?
One of three most important infective causes of death in children under the age of 5
901
Five bacteria causing respiratory tract infections
``` Streptococcus pneumonia Haemophilius nfluenza Staphylococcus aureus Streptoccus pyogenes Mycoplasma pneumonia ```
902
Two viruses causing respiratory tract infections
Influenza | Respiratory syncytial virus (RSV)
903
Protozoa causing respiratory tract infections and in who?
Toxoplasma gondiii | In the immunocompromised
904
Community acquired pneumonia occurs in who typically?
Very young and very old Also those with co-morbidities
905
Pathogens taht can cause community acquired pneumonia are grouped into which two groups?
Typical OR atypical pathogens
906
What can community acquired pneumonia be secondary to?
Viral respiratory tract infection
907
How frequently can the cause of community acquired pneumonia not be identified?
40-60% - even after extensive testing for known respiratory pathogens
908
How common is hospital acquired pneumonia in the world?
Third commonest nosocomial infection
909
What is the mortality rate of hospital acquired pneumonia?
Nosocomial infection with the highest mortality rate
910
Five risk factors for hospital acquired pneumonia
``` Abnormal conscious state Intubation Ventilation Surgery Immunosuppression ```
911
cteria type typically causing hospital acquired pneumonia is?
Gram negative
912
Most common cause of typical lobar pneumonia - community acquired?
Streptococcus pneumoniae
913
Typical presentation of community acquired pneumonia? x4
Sudden onset of chills Fever Pleuritic chest pain Productive cough
914
Investigation to identify S. pneumoniae?
Gram stain of sputum
915
Presentation of atypical pneumonia?
Non-productive cough Fever Headache Chest x-ray is more normal than typical pneumonia
916
Top five organisms causing atypical penumonia
``` Mycoplasma pnumonia - most common Chlamydia pneumoniaae C.pittaci Legionella pneumophilia Coxiella burnetti ```
917
Mycoplasma pneumonia - how is this transmitted?
Droplet infection
918
Mycoplasma pneumonia who does this typically occur in?
School age children and young adults
919
Symptoms of M.pneumoniae?
``` Fever Headache Myalgia Earache Dry cough ```
920
Oragnism causing Q fever
Coxiella Burnetti
921
Three typical complications associated with pneumonia are?
Pleural effusion Empysema thoracis Lung abscess
922
Hospital acquired pneuminia occurs in whom?
Immuno-compromised patients
923
What is the mortality rate of hospital acquired pneumonia?
20-50%
924
What is the CURB65 score used for?
TO determine who requires treatment for pneumonia
925
What does CURB65 stand for?
``` C - confusion U - urea >7mmol R - respiratory rate >30 B - blood pressure <90mmHg 65 - age >65 ``` Increased risk of death as the score increases - score 0-5
926
CURB-65 score of 0 equates to?
Low risk of death - do not require hospitalisation
927
CURB-65 score of 1/2 indicates?
Increased risk of death - consider hospitalisation
928
CURB-65 score of 3+ indicates?
High risk of death - requires urgent hospital admission
929
Treatment for community acquired pneumonia?
Beta lactams
930
Risk of death with CURB-65 score of 0?
0.7%
931
Risk of death with a CURB-65 score of 5?
57%
932
Which community acquired pneumonia pathogen should not be treated with beta lactams?
M. pneumoniae
933
Pathogen that causes TB is?
Mycobacterium turburculosis
934
Five symptoms of TB?
``` Dry cough Poor appetite Weight loss Weakness Fever ```
935
M. turburculosis gram negative or positive?
Negative
936
What is the Mantoux test?
To identify TB immunology
937
Vaccine protecting against TB?
BCG
938
Efficacy of BCG vaccine against TB?
60-80% <16y/o
939
What is the upper respiratory tract?
Nose, paranasal sinuses, middle ear, nasopharynx, oropharynx, laryngopharynx, tonsils, adenoids
940
Four most common infections of the upper respiratory tract are?
Colds Pharyngitis - sore throat Tonsilitis SInusitis (adults)and otitis media (children)
941
Most common pathogen group responsible for upper respiratory tract?
Viruses
942
Four most common virsuses causing upper respiratory tract infections?
Adenovirus Parainfluenza virus Respiratory syncytial virus Rhinovirus
943
Virus most responsible for colds?
Strains of rhinovirus - 50%
944
Bacteria most responsible for URTIs?
Group A strep - pharyngitis
945
Significance of epiglottitis?
This is a medical emergency
946
Three symptoms of epiglottitis
Fever Sore throat Dysphagia Rapid onset of these
947
ORganism group mostly responsibel for epiglotttitis
bacteria
948
Organism responsible for Whooping cough?
Bordetella Pertussis
949
Treatment for whooping cough?
Erythromycin
950
Bordetella Pertussis positive or negative gram staining?
Negative
951
Pathogen causing glandular fever?
Epstein Barr virus
952
Which organs enlarge in EBV?
Hepatosplenomegaly
953
Intercostal muscles are innervated by which nerves?
Anterior rami of thoracic spinal nerves
954
Where is the intercostal VAN found in the anterior thoracic wall?
Between the intercostal and the innermost intercostal muscles
955
Define thoracocentesis?
To sample the pleural fluid
956
Where is the needle inserted in the thoracentesis and why?
Superior to the rib to avoid damage to teh nerves (intercostal)
957
What level is thoracocentesis carried out
9th mid-axillary line
958
Where is a chest drain inserted?
5th intercostal space - mid-axillary line
959
Innervation of diaphragm is?
Phrenic nerve C3, 4, 5
960
Three muscles of inspiration
External intercostal Diaphragm (Also internal intercostal but only to a small degree)
961
Two accessory muscles of inspiration are?
Sternoceidomastoid | Scalene muscles
962
Muscle/mechanism of expiration is?
Elastic recoil
963
Muscles that carry out forced expiration? x2
Internal intercostal | Abdominal muscles
964
Nerve root of phrenic nerve
C3, 4, 5
965
Nerve roots of intercostal nerves
T2 - T12
966
Nervous innervation to the parietal pleura?
Intercostal nerves
967
Nervous innervation to the visceral pleura?
Sympathetic trunk and parasympathetic vagus
968
Nervous innervation to the diaphragmatic pleura?
Phrenic nerves
969
Bronchial tree is included in which pleural type?
Visceral pleura
970
Normal CXR - is the pleura of the lungs visible?
No
971
Lung apex is at what level?
2cm above the clavicle
972
Cardiac notch is at what level?
4th rib
973
Where does the vena cava leave the diaphragm?
T8
974
Where does he oesophagus leave the diaphragm?
T10
975
Where does the aorta leave the diaphragm?
T12
976
What are the pleural boundaries?
T8, T10, T12
977
Divisions of the bronchial tree are? x7
Trachea - main bronchi - lobar bronchi - segmental bronchi - terminal bronchioles - conducting bronchioles - respiratory bronchioles
978
Emphysema is ?
Ddestruction fo the avleolar walls - permenant enlargement of air spaces
979
Cartilage shape in teh trachea?
C shaped rings
980
Cartilage shape in teh bronchi?
Plates - all the way around
981
Cartilage shape in the bronchioles?
No cartilage in the bronchioles
982
Superior mediastinum is found above which landmark?
Angle of Louis
983
Function of recurrent laryngeal nerve?
Vocal cord innervation
984
Hoarsness of voice - damage to which nerve?
Recurrent laryngeal nerve
985
Recurrent laryngeal nerve loops around which structure? - left and right
Arch of the aorta - left | Subclavian artery - right
986
Long thoracic nerve supplies what?
Serratous anterior muscle
987
When are lung tumours felt and why?
Once they reach teh parietal pleura | The visceral pleura has no sensory innervation
988
Blood supply and drainage of lungs?
Bronchial arteries and bronchial veins
989
Origin of bronchial arteries?
Descending aorta
990
Bronchial veins drain to?
Azygous and hemi-azygous veins
991
The pulmonary trunk is?
Blood vessel from the right ventricle - bifurcates into the left and right pulmonary arteries
992
Trachea is where is relation to teh oesophagus?
Trachea is anterior to the oesophagus
993
Level of the dome of the left diaphragm is?
Lower boarder of the 5th rib
994
At what level does the vagus nerve perforate the diaphragm?
With the oesophagus - T8 Through the oesophageal hiatus
995
Anterior intercostal arteries originate from where?
The internal thoracic artery
996
Two terminal branches of the internal thoracic artery?
Superior epigastric artery | Musculophrenic artery
997
Superior epigastric artery originates from where?
Internal thoracic artery
998
Three effects of the sympathetic innervation to the bronchi, bronchioles and pulmonary vessles?
Bronchodilation Vasoconstriction Inhibition of glandular secretion
999
Three effects of parasympathetic innervation to teh bronchi, bronchioles and pulmonary vessles?
Bronchoconstriction Vasodilation Stimulation of glancular secretion
1000
Three functions fo the diaphragm
Separate abdominal and thoracic cavities Inspiration Expiration
1001
Muscle type of the diaphragm?
Skeletal
1002
Nerve type of teh phrenic nerve?
Mixed - somatic and autonomic
1003
Origin of intercostal arteries?
Internal thoracic artery
1004
Intercostal veins drain to where?
Anterior - intenral thoracic vein | Posterior - azygous adn hemiazygous
1005
Pleural reflection is?
Extent of the lung pleura whcih the lung does not extend to
1006
Position of trachea in tension pneumothorax?
AWAY from the affected side
1007
What si teh most preferred orientation of a CXR?
PA - posteriro to anterior
1008
Why is PA CXR preferred?
Can accurately comment on size of the heart
1009
When might you use an AP CXR?
Bed bound patietn
1010
What is teh problem with an AP CXR? x3
Heart appears larger Scapula is over the lung field Clavicles are horizontal
1011
Trachea will be deviated away from? x2
Mass | Tension pneumothorax
1012
Trachea will be pulled towards? x4
Collapsed lung Loss of lung volume Consolidation Fibrosis
1013
Consolidation of the lung appears as?
Dense (white) material
1014
Four causes of consolidation are?
Pneumonia Haemorrage Fluid - pulmonary oedema Cells - cancer Anything increasing teh density
1015
Characteristic features of pneumothorax on CXR? x2
Asymmetrical | Lack of lung marking to the edge of the lung field
1016
Pleural effusion is?
Collection of fluid in the pleural space - lowest part
1017
Recognise pleural effusion from CXR?
White | Meniscus
1018
Abnormal cardiothoracic ratio is?
>50%
1019
What is below right dome of diaphragm?
Liver
1020
What is below left dome of diaphragm?
Bowel
1021
Emphysema on CXR visible when?
More than 6 anterior ribs/more than 8 posterior ribs Flattening of hemidiaphragm
1022
Five signs of congestive cardiac failure?
``` Alveolar oedema Kerly B lines Cardiomegaly - boot shaped Upper lobe divisions Bilateral effusions ```
1023
Anterior vs. posterior ribs CXR
Posterior - attached to the sternum | Move forwards and become teh anterior ribs
1024
Diapghram at the level of which rib?
7
1025
Two causes of emphysema
Smoking | Air pollution
1026
Three risk factors of TB?
HIV Diabetes Smoking
1027
Four symptoms of pneumonia?
Cough Fever Dyspnoea Chest pain
1028
Horner's syndrome is what?
Daamge to sympathetic nerves
1029
Horner's syndrome caused by tumour at whch part of the lung?
Apex
1030
Signs of Horner's syndrome
Constricted pupil (meiosis) Drooping upper eyelid (ptosis) Local inability to swear on ne side of teh face
1031
Three features of asthm
Hypertrophy fo airway wall muscle - decreased lumen Increased mucous production Inflammatory cell infiltration
1032
Two main symtptoms of asthma
Producing a wheeze cough | Breathlessnes
1033
DDx for wheeze?
Infection
1034
Asthma - allergens activate what cells?
Th2 cells
1035
Th 2 cells asthma - these release what?
IL4
1036
IL4 of asthma activates what?
B cells and MAST cells
1037
Interleukins that activate B cells in asthma are? x2
IL4 | IL13
1038
Interleukins that activate Mast cells in asthma are?
IL4 IL6 IL9
1039
Immunoglobulin in asthma activates what?
IgE activates Mast cells
1040
Action of B cells in asthma?
Production of IgE - activates Mast cells
1041
Four inflammatory components released by mast cells?
Histamine PGD3 LTC4 Kinins
1042
Summarise pathogenesis of asthma
``` ALlergens activate Th2 Th2 activates B cells and MAST cells B cells produced IgE IgE activates Mast cells, along with Il4 Mast cells release inflammatory mediators ```
1043
Function of inflammatory mediators in asthma? x4
Activate nerve endings Make mucous Produce airway oedema Bronchoconstriction
1044
Four triggers for asthma
Allergens Irritants Infection Exercise
1045
Two DDx for wheeze when not asthma
Brnchiolitis - children | COPD
1046
Bronchodilator treatment for asthma causes FEV1 to increased by how much?
15% / 200ml
1047
Asthma attack - vital capacity increases or decreases?
Decreases
1048
ASthma - airway resistance is greatest where?
In the larger airways
1049
Asthma - compliance increases or decreases and why?
Increases - reduced alveolar elastic recoil
1050
What is peak flow?
Person's maximum speed of expiration
1051
Peak flow morning vs/ evening
Wrose in teh morning adn better in teh eveing
1052
Significance of peak flow in asthmatic?
Difference between morning and evening is greater in asthmatic
1053
Airflow through a tube is dependent on which four variables?
Radius of the tube Viscosoty fo the gas Pressure difference across teh tube Length fo teh tube
1054
Four stimulus challenges to monitor asthma?
Histamine challenge Metacholine challenge Allergen challenge - risky Cold air
1055
What is the reason for challenge testing in asthmatic?
To see which stimuli the asthmatic responds to
1056
What is reactive airways dysfunction syndrome RADS?
Bronchial hyperreactivity following infection - set off by irritants
1057
Does RADS involve reacting to an allergen?
No
1058
Untreated asthma over time has what effect on teh bronchi?
Chronic narrowing of the bronchi
1059
Five common allergens for asthma?
``` Dust Grass Tree pollen Pet fur Urine ```
1060
Three common irritants for asthma?
Sulphur dioxide Nitrogen dioxide Ozone
1061
Whic infection isthhas the worst effect on asthma?
Viral infection
1062
Why can exercise cause asthma?
Exercise - increased ventilation - cooling - cooling causes spasm
1063
Significance fo asthma at night?
Asthma gets worse at night
1064
Two main reasons asthma is worse at night?
Allergens in teh bed? | Did teh patient take their inhaler at night?
1065
Menstrual asthma affects what percentage of women?
30%
1066
Poor control of asthma can result in what?
COPD
1067
First line treatmetn for asthma
Salbutamol as required
1068
Second line treatment for asthma
Regular inhaled steroids
1069
Fourth line treatment for asthma?
theophyllines | Leukotrient antagonists
1070
Last line treatment of asthma
Oral steroids Anti-IgE therapy Steroid sparing agents
1071
Treatment for acute severe asthma?
Immediate treatment with inhaled high dose bronchodilators, oxygen adn steroids
1072
Acute severe asthma causes how many deaths per year?
1200
1073
Two ways smoking leads to asthma
Increases NFkB | Blocks steroid response HDAC2
1074
Prevalence of asthma in children
20%
1075
Prevalence of asthma in adults
15%
1076
Normal respiratory rate is?
<25 per minute (6-28)
1077
Main facotor that can cause a change in respiratory rate?
Equipment usage e.g. mouthpieces
1078
Most common test for measurement of lung function?
Spirometry
1079
Normal FEV1/VC result?
75% FEV1/VC ratio
1080
FEV1/VC ratio for obstructive lung disease?
<75%
1081
FEV1/VC ratio for restrictive lung disease?
75% (reduced FVC) | SO >75% ratio
1082
What is the Fick principle?
Volume of gas per unit time which diffuses across a tissue sheet is prportional to teh area of teh sheet Inversely proportional to the thickness
1083
Fick principle is dependent on?
Permeability coefficient for the gas that is diffusing
1084
Graham's law is?
The rae of diffusion of a gas is inversely proportional to the square root of it's molecular weight (big things diffuse slower)
1085
Four components that reduces gas transfer?
Reduced surface area Increased thickness fo teh memrbrane Reduced oxygen concentration Inadequate time for gas transfer to occur
1086
Pathogen responsible for majority of TB cases?
Mycobacteria tuberculosis
1087
Five bacteria that cause TB
M. tuberculosis M. bovis M. microti M. canetti
1088
Mycobacteria that does not cause TB?
M/.avium complex
1089
Four factors affecting likelihood of TB inheritance
Infectiousness of the person with TB environment in which exposure occurs Length of teh exposure Virulence (strength) of teh tubercle bacilli
1090
Pharmacological treatmetn for TB x4
Isoniazid Rifampicin Pyrazinamide Ethambutol
1091
How long should Ethambutol be provided for the treatmetn of TB?
2 months
1092
How long should Rifampicin adn Isoniazid be provide for the treatmetn of TB?
4 months
1093
What is DOTS in TB therapy?
OTS - directly observed therapy | This is used if you think that the patient is not likely to follow the therapy as they should
1094
Why does hypoxia occur at high altitude?
PaO2 is reduced at high altitude so lungs are less saturated with oxygen The drive to increase ventilation is suppressed by chemoreceptors to prevent teh excess loss of Co2
1095
Hypoxic drive controlled by which site?
Carotid bodies
1096
Hypoxic drive kicks in at what concentration of O2?
PO2 <60mmHg
1097
what happens if there is a rapid ascent to high altitude?
Pulmonary circulation reacts to hypoxia with vasoconstriction - worsens the case of hypoxia SO pulmonary arterial hypertension
1098
At what altitude will affects of hypoxia start to occur?
200m
1099
People without respiratory disease can eventually acclimatise to what altitude?
2000-6000m
1100
what altitude is regarded as the death zone?
7500m
1101
Majority of time that can be spent in teh death zone is?
2-3 days
1102
Significant hypoxia occurs at which altitude, even in the most experienced climbers?
7000m
1103
What are the three components that occur during acclimatisation?
Metabolic acidosis Increased erythrocyte number - increased haematocrit Reduced pulmonary vascular resistance
1104
Why does metabolic acidosis occur at high altitude?
To compensate for the respiratory alkalosis - reduced renal excretion of acid
1105
How is haematocrit increased at high altitude?
Increased production of EPO
1106
How can increased haematocrit prove to be fatal?
Increased haematocrit can increase teh viscosity of the blood which can lead to increased pulmonary vascular resistance adn lead to pulmonary arterial hypertension Rigth heart failure
1107
Effect of high altitude on pulmonayry vascular resistance?
Increaes
1108
What happens to the pulmonary vascular resistance upon acclimatisation?
The pulmonary vascular resistance will fall | increased NO production
1109
What is acute mountain sickness? AMS
Ascent to hgih altitude is too rapid - first sign taht something is wrong
1110
HACE vs HAPE
HACE - high altitude cerebral edema - neurological condition | HAPE - hgih altitude pulmonary edema - pulmonar condition
1111
SYmtoms of AMS x5
``` Headache - essential for diagnosis Poor sleep Tiredness Loss of appetite, nausea, vomiting Dizziness ``` Think alcohol hangover
1112
How are the symptoms of AMS scored?
Each symptoms is scored 0-3 for severity and >3 is diagnosis fo AMS
1113
At what height will everyone suffer from AMS?
5000m
1114
What si teh treatmetn for mild AMS?
rest and no further ascent
1115
hat is the treatmetn for severe AMS? x4
Descent Oxygen Acetaxolamide Dexamethasone
1116
What is acetaxolamide?
Carbonic anhydrase inhibitor
1117
Function of carbonic anhydrase?
Renal reabsorption of bicarbonate
1118
Location of carbonic anhydrase?
Proximal convoluted tubule
1119
Normally - how much bicarbonate is reabsorbed?
All of it

Year 2 CR (37 decks)

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