CR physiology Flashcards
Types of antibodies against ABO antigens
IgM
What is mixed in forward blood grouping?
Patients blood with known antibodies
What is mixed in reverse blood grouping?
Patients blood with known blood cells
Types of antibodies against Rhesus antigens
IgG
Most clinically important Rhesus antigen?
D
When does HDN occur?
Rh- negative most carrying second Rh+ child
What type of alleles are A and B?
Codominant
Which are the most common blood groups seen in Caucasians?
A and O
What is the most common blood groups seen in Asians?
B
Rhesus - innate or immune antibodies?
Immune
When can Rh sensitisation occur?
Transfusion
Pregnancy
Transplant
Which is more common - Rh+ or Rh-?
Rh+
How is HDN prevented?
Anti-D injection to all Rh- mothers
Treatment of acute transfusion reaction?
Stop transfusion
Saline for hypotension
Frusemide to maintain renal perfusion
DIC treatment
What does a direct Coombes test test for?
Autoimmune antibodies to own RBCs
What does an indirect Coombes test test for?
Detects unbound antibodies present in patients plasma
Used to look for rare antibodies
Used in cross matching
Step 1 antihypertensive treatment
<55 = ACEI
>55 or black = CCB
Step 2 antihypertensive treatment
ACEI + CCB
Step 3 antihypertensive treatment
ACEI + CCB + thiazide
Step 4 antihypertensive treatment
Above + further diuretics or alpha/beta blocker
Side effects of CCBs
Flushing, oedema
Side effects of ACEIs
Cough, hypotension
Side effects of ARBs
Hypotension
Side effects of Thiazides
Low K+, impotence
Side effects of beta blockers
Bronchospasm, lethargy
MI immediate treatment
Oxygen
Aspirin
Opiates
Thrombolysis/PCI
Secondary MI prevention
Beta blockers
ACEIs
Statins
Lifestyle
Polypil contents
Aspirin (75mg)
Statin
3 BP lowering drugs
Folate
1 small square on ECG
= 0.04s
1 big square on ECG
= 0.2s
P wave duration
<0.08
<2 small squares
PR interval duration
<0.2s
<5 small squares
QRS complex interval
<0.12s
<3 small squares
First degree heart block
Regular
PR intervals >0.2s
Second degree heart block type 1
Each successive PR interval gets longer until a QRS complex is dropped
Second degree heart block type 2
QRS complexes randomly dropped
Third degree heart block
No synchrony between atrial and ventricular rhythms
Often bradycardic
AF
Irregular rhythm
Rate = 100-160
Atrial flutter
Regular rhythm
F waves instead of P waves
Rate = 110
F wave rate = 300
Junctional rhythm
AVN takes over as pacemaker
Rate = 40-60
P wave may be seen and may be inverted
SVT
Rate = 140-200
Regular rhythm
Due to AF, AF or Wollf-Parksinson-White syndrome
P waves often absent
AV nodal re-entrant tachycardia
Regular
P waves often seen after QRS complex
Reentry circuit within to just next to the AVN
Pathology of WPW syndrome
Extra electrical pathway connecting atria and ventricles
Shortened PR interval
Delta wave
Bundle branch block
Prolonged QRS
Notched R waves in V1 in RBBB
Notched R waves in V6 in LBBB
Causes of LAD
LVH
Inferior MI
Causes of RAD
RVH LV atrophy Lateral MI COPD, tall, thin Dextrocardia
Sites of RBC production in foetus
3-6 weeks = yolk sac
6 weeks - 3 months = liver and spleen
3 months onwards = bone marrow
Which bones become the final haematopoietic bones?
Vertebrae, sternum, ribs, cranial bones, ilium
Appearance of proerthyroblast
Large cell with large nucleus
Basophilic cytoplasm
Perinuclear halo
Nucleoli
Appearance of early erythroblast
= basophilic normoblast
Still dark blue cytoplasm
Less cytoplasm
Loss of perinuclear halo
Appearance of intermediate erythroblast
= polychromatophillic normoblast
Nucleus getting smaller
Reduced blue staining of cytoplasm
Appearance of late erythroblast
= orthochromic normoblast
Cytoplasm almost completely pink
Nucleus even smaller
Appearance of a reticulocyte
Expulsion of nucleus
Slightly bigger than mature RBC
Blue hue remains to cytoplasm
When does a reticulocyte become an erythrocyte?
After 1 day in circulation
Erythrocyte diameter
7.8um
Normal erythrocyte levels
= 5.2x10 6 /uL in males
= 4.7x10 6 /uL in females
Where is EPO produced?
Kidney fibroblasts
Type I glomus cells of carotid body
What does increased ESR show?
Infection of the blood
What structures are formed when ESR is high?
Rouleaux
GLUT transporters in RBCs
GLUT1
What enzyme breaks open haemoglobin?
Haemoxygenase
What is biliverdin?
Openen pophyrin ring without iron
What converts biliverdin –> bilirubin?
Biliverdin reductase
Where does biliverdin –> bilirubin take place?
Within macrophages
What conjugated bilirubin?
Glucoronic acid
What does bacteria convert bilirubin to?
Urobilinogen
What is urobiliogen further oxidised to?
Stercobilin
Average VO2 max
250ml/min
Local dilatory factors released by muscle
NO, adenosine, phosphates, carbon dioxide, H+, K+
Pulmonary ventilation at rest
8L/min
Pulmonary ventilation in peak levels of exercise
100L/min
Which way does oxygen dissociation curve shift in exercise?
To the right
Improves oxygen delivery to tissues
What causes this Bohr shift?
Increased CO2 and H+
Increased local temperature
Platelet diameter
1-4um
Normal platelet range in blood
140-400x10 9 /L
Lifespan of platelets
8-14 days
How are platelets removed?
By the reticuloendothelial system
What does GpIb bind to?
vWF
What does GpIIB/IIIA bind to?
vWF and fibrinogen
What do alpha granules release?
Proteins –> vWF, fibrinogen, TPAI-1
What do delta granules release?
ADP
What disorder = lack of GpIb?
Bernard Soulier syndrome
What disorder = lack of GpIIb/IIIa?
Glanzmann’s syndrome
What factors do platelets release that cause attractions and aggregation?
Serotonin, ADP, TXA2
Treatment of mild VWF disease?
DDAVP
Extrinsic pro-tenase complex
TF + VIIa
Intrinsic pro-tenase complex
VIIIa + IXa
Which enzymes does thrombin enhance the activity of?
5,8,9,11,13
Haemophilia A
Factor 8 deficient
Haemophilia B
Factor 9 deficient
Haemophilia A treatment
DDAVP, factor VIII
Haemophilia B treatment
factor IX
Where are common bleeding sites?
Soft tissue
Joints
Operative sites
Cranium
What does antithrombin inhibit?
2, 7, 9, 10, 11, 12
What does protein C inhibit?
5 and 8
What are vitamin K dependant?
2, 7, 9, 10, protein C, protein S
What does tPA activate
Plasminogen –> plasmin
Fibrin –> fibrinogen
What does fibrin breakdown produce?
D-dimer
What is the reaction that produces NO?
L-arginine + oxygen
–> NO + citrulline
Where is NOS I found?
In the brain
Calcium dependant
Where is NOS II found?
Most nucleated cells
Particularly in macrophages
What activates NOS II?
Inflammatory cytokines
Calcium independant
Where is NOS III found?
Vascular endothelial cells
How is NOS III activated?
Sheer stress from blood friction opens calcium channels
Calcium activated calmodulin
Calmodulin activates eNOS
With cofactors –> biopterin H4, FMN, FAD
Can also be stimulated by ACh –> calcium entry
Nitric oxide action
Diffuses from endothelium –> smooth muscle cells
Activates guanylate cyclase
Converts GTP –> cGMP
Causes vascular smooth muscle relaxation
How is NO produced in exercise when there is a lack of oxygen?
Exercise converts nitrate to nitrous acid
Reduced –> NO
What happens to eNOS in atherosclerosis
Endothelium damaged so cannot produce NO by eNOS
Coronary vessels cannot dilate in exercise
–> angina and acidosis
How does NO improve oxygen delivery?
NO enters blood
Binds to haemoglobin to displace oxygen
Forms nitrosohaemoglobin
How does acid base balance alter blood brain flow?
Increased in acidosis
Decreased in alkalosis
Where can clots commonly form?
Auricles of the atria
Deep veins of the calf
When does hypoxic ventilation drive begin?
PO2 <60mmHg
When do we initially suffer the effects of altitude?
Over 2000m
Where is the death zone?
7500m and above
How is a metabolic acidosis generated by the kidney?
Decreased H+ ATPase activity in DCT
Increased bicarbonate excretion
How is an increased erythrocyte number generated?
Increased EPO secretion
How is pulmonary vascular resistance decreased?
Collateral circulations
Increased NO synthesis
What is the action of Diamox
= acetazolamide
Carbon anhydrase inhibitor
Prevents bicarbonate reabsorption in the PCT
Speeds up acclimatisation
High doses can also block carbon dioxide transport by Hb to decrease respiratory loss
Treatment of high altitude cerebral oedema
Oxygen Descent Diamox Dexamethasone Hyperbaric chamber
Treatment of high altitude pulmonary oedema
Oxygen Sit upright Descent Hyperbaric chamber Nifedipine (CCB) --> reduces PAH Viagra (sildenafil) --> slows down cGMP breakdown
Causes of respiratory acidosis
Hypoventilation Narcotics + alcohol COPD, asthma Scoliosis Severe obesity Neuromuscular damage
Treatment of respiratory acidosis
Underlying cause
Bronchodilators
CPAP/BiPAP
Oxygen
Signs and symptoms of respiratory acidosis
Those of low CNS pH
Headache, drowsiness, anxiety, fatigue, memory loss, muscle weakness
Slowed breathing, gait disturbance, blunted tendon reflexes, tremor, papilloedema, tachycardia, hypotension
Maximum bicarbonate levels that can be reached
45mmol/L
Minimum bicarbonate levels that can be reached
12mmol/L
Respiratory alkalosis causes
Hyperventilation Anxiety, pain Pregnancy Sepsis and fever Altitude Salicyclates and progesterone CVA
Symptoms of respiratory alkalosis
Dizziness, confusion, cramps and tingling in hands and mouth, blurred vision, spasms, seizures, irregular HR, tetany
Diagnostic FEV1/FVC ratios
<75% = obstructive >75% = restrictive
Peak flow in asthma
Diurnal variation
Reversibility testing
400mg salbutamol by inhaler
2.5mg salbutamol by nebuliser
30mg/day steroids for 2 weeks
Peak flow must improve by >15% and >200ml
When is total lung carbon monoxide increased?
Increased cardiac output, polycythaemia, alveolar haemorrhage
When is total lung carbon monoxide decreased?
Decreased perfusion, decreased ventilation, V/Q mismatch, anaemia
Causes of reduced lung surface area
Lobectomy, pneumonectomy, airway obstruction, increased dead space, emphysema
Causes of hypovolaemic shock
Haemorrhage
Cholera
Causes of cardiogenic shock
MI, valve disease, myocarditis, heart failure
Causes of obstructive shock
PE
Cardiac tamponade
Causes of distributive shock
Sepsis
Anaphylaxis
How are mast cells activated
Cross linking with IgE
Via complement C3a and C5a
Via nerves –> substance P
Via direct contact with pathogen
What do mast cells release?
Histamine
Leukotrienes
Prostaglandins
What does histamine do?
Increases capillary permeability
Vasodilation
Itching
What do leukotrienes do?
Increase capillary permeability
Cause chemotaxis
What do prostaglandins do?
Arteriolar dilation
Pain
Fever
What is angioedema
Swelling of subcutaneous tissues Face Lips Hands and feet Pharynx Larynx
What drugs commonly trigger anaphylaxis?
Beta lactase Aspirin NSAIDs Insulins Anaesthetics
Anaphylaxis treatment
500mg adrenaline in 0.5ml Epipen = 300mg adrenaline in 0.3ml High flow oxygen Saline Antihistamines (chlorpheniramine) Corticosteroids (hydrocortisone)
Total body iron
3-5g
Where is iron absorbed?
Duodenum
How is iron absorbed?
As Fe2+
Ferric reductase can reduce Fe3+ to 2+
Transferrin
Iron binding plasma protein
Carries two Fe3+ ions
Binds to transferring receptor and is endocytose
Releases iron
Ferritin
Intracellular iron store
Buffer
Cytoplasmic
Diagnostic for iron deficiency
Anaemia Hb levels
Adult male <13.5g/dl
Adult female <11.5g/dl
6-14 <12g/dl
6m-6yrs <11g/dl
Anaemia cell sizes
<76fl = microcytic 76-96fl = normocytic >96fl = macrocytic
Causes of microcytic anaemia
Iron deficiency
Thalamssaemia
Causes of normocytic anaemia
Chronic disease
Acute blood loss
Cancer
Haemolysis –> sickle cell
Causes of macrocytic anaemia
B12/folate deficiency
Alcoholic liver disease
Factors enhancing iron absorption
Iron in meat Fe2+ iron Pregnancy Acid pH Hypoxia Iron deficiency
Factors reducing iron absorption
Iron in vegetables Fe3+ iron Alkaline pH Iron overload Inflammatory disorders
Vitamin B12
Water soluble Found in meat, eggs, animal protein Not destroyed by cooking Can be stored Absorbed in ileum bound to IF
Signs of pernicious anaemia
Insidious onset
Glossitis
Mild jaundice
Neurological symptoms
Treatment of pernicious anaemia
IM B12 every 3 months
Folate
Water soluble vitamin Found in liver, greens, yeast Destroyed by cooking Very little can be stored Absorbed in the duodenum and jejunum
Features of haemolytic anaemia
Jaundice
Raised LDH
Extravascular haemolysis
Sickle cell disease Thalassaemia Antibody induced Rhesus mismatched transfusion Hereditary spherocytosis
Intravascular haemolysis
ABO mismatched transfusion
Mechanical trauma
Snake bites
Infection
Extra vs intravascular haemolysis
Extra = spherocytes present Intra = haemoglobin in blood, very high LDH, haemoglobinuria
Triggers to G6PD deficiency
Fava beans
Infection
Drugs
Autoimmune haemolytic anaemia
IgG antibodies against membrane components
Extravascular haemolysis
Diagnosing angina
HISTORY
Exercise ECG
Functional imaging
Common sites of atheromas
Arterial branch points -Carotid -Aortic -Iliac Renal arteries Coronary arteries
Endothelial factors
Vasodilators --> NO, prostacyclin Vasoconstrictors --> AgII, endothelin Pro-fibrinolysis --> tPA Anti-fibrinolysis --> TPAI-1 Anti-inflammatory --> NO Pro-inflammatory --> E-selectin Cell adhesion --> VCAM, ICAM, IL-8
LDL modification
Oxidation by ROS
Glycation by DM
Actions of oxidised LDL
Inflammatory mediator production
Cell adhesion molecule production
How does modified LDL lead to lipid accumulation?
Does not bind to normal LDL receptor Binds to scavenger receptor This has no negative feedback --> massive lipid accumulation --> foam cell
What causes smooth muscle proliferation and migration?
Growth factors from endothelial cells and macrophages
E.g. PDGR
Which cells form foam cells?
Macrophages
Smooth muscle cells
What does a stable plaque cause?
Stable angina pectoris
What does an unstable plaque cause?
Thrombus formation
MI
What does the LDL receptor recognise
Lipoprotein B100
What happens when a plaque ruptures
Haemorrhage
Release of tissue factor
Collegen exposure
Lipid blood levels
TC <200mg/dl
LDL <130mg/dl
HDL >40mg/dl
Where are alpha genes found?
Chromosome 16
Where are beta genes found?
Chromosome 11
Forms of alpha gene
2 alpha genes
1 zeta gene
Forms of beta gene
Epsilon Gamma G Gamma A Delta Beta
What is Hb Gower 1?
Produced in the yolk sac up to 6 weeks
Zeta 2 epsilon 2
What is HbF?
Produced after 6 weeks in utero from the liver and spleen
Alpha 2 gamma 2
What happens when 3 alpha genes are missing?
Haemoglobin H disease
Haemoglobin H (beta 4) and haemoglobin Barts (gamma 4) are formed
These have a higher affinity for oxygen
–> poor tissue perfusion
What happens when 4 alpha genes are missing
All haemoglobin is haemoglobin Barts (gamma 4)
Baby cannot survive
–> hydrops foetalis
Manifestations of beta thalassaemia major
Hypochromic, microcytic anaemia Bone marrow expansion Splenomegaly Extra medullary erythropoietic masses Failure to thrive CCF
What is the problem caused by iron overload?
Fenton reaction
Ferrous irons react with hydrogen peroxide
Forms destructive hydroxyl radical
–> cirrhosis, diabetes, glandular dysfunction
Iron chelating agents
Desferrioxiamine = SQ Deferiprine = oral
Mutation in HbS
Glutamic acid –> valine
Consequences of HbS
Anaemia
More infections
Vaso-occlusive crisis
Chronic tissue damage
ECG in heart failure
Pathological Q waves
LBBB
Anterior T waves
AF and other arrhythmias
BNP
Produced by ventricles in response to excessive myocyte stretching
Promotes naturiesis and vasodilation
Inhibits ADH and aldosterone release
>100pg/ml in heart failure
Cardiac resynchronisation therapy
Must be in sinus rhythm
If QRS prolongation >150ms
If LVEF <35%
If grade III/IV symptoms
Implantable cardiac defibrillator
Used of AMI >4 weeks previously
LVEF <30%
QRS >120ms
Acute heart failure causes
AMI Tachyarrythmias Valve disease --> MS, chordal rupture Infection Failure to take drugs
Immediate AHF treatment
IV diuretic
Oxygen
Ventilation
Hypotension BP
<90/60mmHg
Hypertension damage to the eye
Arteriolar narrowing
Silver or copper wire arterioles in the centre due to reflected light
Causes of secondary hypertension
Renal disease Pheochromocytoma (chromatin cells) Cushing's syndrome Conn's syndrome (hyperaldosteroneism) Acromegaly Hypothyroidism CoA Iatrogenic
MI ECG features
ST elevation
Pathological Q waves
Classification of MI
1 = spontaneous 2 = ischaemic imbalance from spasm, embolism, dissection or hypotension 3 = death from presumed AMI 4a = from PCI 4b = from stent 5 = from CABG
Clinical consequences of MI
Chest pain 4th heart sound Fever Sweating Vomiting Tachycardia
Features of VW disease
Bruising Epistaxis Gingival haemorrhage Post-surgical bleeding Menorrhagia
Clotting times for VW disease
High APTT and bleeding time (low VIII)
Normal PT, TT and platelet count
Haemorrhage disease of the newborn
Prevented by vitamin K at birth
Due to low vitamin K at birth, immature liver and low vitamin K in breast milk
How does liver disease cause bleeding problems?
Failure to produce clotting factors Failure to absorb or use vitamin K Abnormal fibrinogen production Portal hypertension --> splenomegaly --> decreased platelet count --> prolonged PT, APTT, TT --> high fibrooge degradation products --> thrombocyopaenia
How does kidney disease cause bleeding problems?
Leads to uraemia
Impairs platelet function
–> prolonged bleeding time
–> abnormal platelet aggregation studies
Pathology of DIC
Due to excessive activation of the haemostatic system
- -> microvascular thrombus and tissue damage
- -> depletion of platelets and clotting factors can cause bleeding
Causes of DIC
Gram negative sepsis Malignancy Obstetric disorders Shock Liver disease Acute transplant rejection ABO incompatibility Snake bite
When does massive transfusion syndrome occur?
> 5L of blood in 24 hours
50% blood loss in 3 hours
80% of blood replaced
Diagnosis of shock
MAP <60mmHg Clinical signs of hypo perfusion - tachycardia - tachypnoea - confusion - pallor
Where do noradrenaline and angiotensin II act in the vascular wall?
Noradrenaline = release outside the arteriole and acts on alpha receptors in smooth muscle AgII = carried in plasma and acts on endothelium lining and smooth muscle
Action of thromboxanes
Vasoconstriction
Platelet aggregation
Action of prostacyclins
Vasodilation
Inhibit platelet aggregation
Immediate shock compensation
Mediated by baroreceptors Increased SNS outflow ADH release ANP release inhibited --> water retention
Long term shock compensation
Kidney mediated Increased renin secretion Thirst sensation Albumin synthesis EPO release
Hypovolaemic shock classes
1 = <15% = <750ml 2 = 15-30% = 750-1500ml 3 = 30-40% = 1500-2000ml 4 = >40% = >2000ml
Septic diagnosis
Temp >38 and <36
HR >90
RR >20 or paCO2 <32mmHg
WBC >12x10 9/L
Septic shock
= sepsis with hypotension
Pathology of sepsis
Bacterial infection leads to excessive host response
LPS stimulates cytokine release
Vasodilation occurs
Reduced SVR and therefore BP
What causes TIA
Small emboli pinged off from a thrombus
Symptoms duration of TIA
Typically less than an hour
Must be less than 24 hours
Types of ischaemic stroke
Thrombotic
Embolic
Lacunar
What is a lacunar stroke?
Occlusion of arteries supplying deep brain rather than cortex
- -> motor hemiparesis with dysarthria
- -> ataxia and hemiparesis
- -> dysarthria and clumsy hand
Consciousness in stroke
Loss in hemorrhagic
Usually maintained in ischaemic
Lenticulo-striate arteries
Branches from MCA
Supply basal ganglia and internal capsule
Excito-toxicity
K+ not removed Depolarises cells Causes excessive NT release Excess stimulation of NMDA (fast) and AMPA (slow) channels Increases metabolic demand of cells Leads to free radical formation
Stroke treatment
TPAs NMDA antagonists (cerestat) AMPA antagonists (NBQX) Lithium Antioxidants Superoxidase dimutase enzymes
What is found in aortic stenosis?
Ejection systolic murmur Soft S2 Slow rising carotid pulse Narrow pulse pressure S4 and ejection click
What causes aortic stenosis?
Calcific disease
Congenital bicuspid valve
Rheumatic disease
What are the symptoms of aortic stenosis?
Dyspnoea
Angina
Syncope
Sudden death
What is found in mitral regurgitation?
Pan systolic murmur Soft S1 AF S3 RV heave Right heart failure signs
What causes mitral regurgitation
Valve prolapse, rheumatic disease, endocarditis
Chordal rupture, papillary muscle dysfunction
LV dilation
What are the symptoms of mitral regurgitation?
Dyspnoea
Palpitations
Systemic emboli
What is found in mitral stenosis?
Mid-diastolic rumble Sound S1 with opening snap AF RV heave Right heart failure signs
What is seen on mitral stenosis ECG?
Bifid P waves
What causes mitral stenosis?
Rheumatic disease
Whats are the symptoms of mitral stenosis?
Dyspnoea
Palpitations
Systemic emboli
What is found in aortic regurgitation?
Early diastolic murmur with decrescendo Rapidly rising carotid pulse Collapsing pulse Systolic ejection murmur Wide pulse pressure Very displaced apex beat
What causes aortic regurgitation?
Calcific disease, congenital bicuspid valve, rheumatic disease, endocarditis
Marfan syndrome, ankylosing spondylitis, aortic dissection, Ehlers danlos
What are the symptoms of aortic regurgitation?
Often none
Dyspnoea
Angina
Definition of mitral prolapse
> 2mm systolic prolapse of 1 or both valve leaflets
Signs of mitral prolapse
Ejection click and late systolic murmur
Ddx of DVT
Musculo-tendinous trauma Tendinitis Ruptured Baker's cyst Cellulitis Lymphedema Haematoma
Post thrombotic syndrome
Recurrent pain and swelling
Pigmentation and ulceration
More common in proximal DVT
PE classic symptoms
Dyspnoea
Pleuritic chest pain
Haemoptysis
Signs of PE
Tachypnoea
Tachycardia
Crepitations
Pleural rub
ECG signs of PE
Tachycardia
T wave inversions (anterior leads)
S1Q3T3 pattern
CXR signs of PE
Focal oligaemia
Peripheral wedge shape above diaphragm
Small pleural effusion
DDx of PE
Acute coronary syndrome Pneumonia Bronchitis COPD exacerbation Asthma attack
Diagnosis of PE
CTPA V/Q scanning (must have normal CXR) Echo Pulmonary angiogram D-dimer
UFH half life
60-90 mintes
LMWH half life
4 hours
Fondaparinux half life
18 hours
Warfarin half life
36 hours
Causes of thrombophilia
Factor V Leiden Prothrombin gene mutation Protein C deficiency Protein S deficiency Antithrombin deficiency
Pathology of factor V Leiden
Cannot be degraded by protein C
Antiphospholipid syndrome pathology
Autoimmune antiphospholipid antibodies
Increases chance of clot formation
Antibodies seen in antiphospholipid syndrome
Lupus anticoagulant
Anticardiolipin antibodies
Anti-B2-glycoprotein 1 antibodies
Consequences of antiphospholipid syndrome
Stroke, TIA
PE
Pregnancy problems –> pre-eclampsia, miscarriage
DVT
Asthma treatment ladder
Salbutamol \+ inhaled steroid \+ LABA \+ theophylline + leukotriene antagonist + anticholergic \+ oral steroid
Inputs of the respiratory centre
Baroreceptors Central and peripheral chemoreceptors Hypothalamus Progesterone Anaemia Skeletal muscle afferents Occlusion of PA Pulmonary stretch receptors J receptors Cortex
Outputs of the respiratory centre
DRG –> pharyngeal muscles, intercostal muscles, diaphragm
VRG –> expiratory muscles
How does pulmonary oedema cause dyspnoea?
Stimulates pulmonary J receptors
Sitting watching TV
1 MET
1 flight of stairs without stopping
4 METs
Walking 2mph
2 METs
CURB 65
C = confusion U = urea >7mmol R = respiratory rate >30 B = SBP <90mmHg 65 = age >65
CURB 65
C = confusion U = urea >7mmol R = respiratory rate >30 B = SBP <90mmHg 65 = age >65
How does smoking cause emphysema?
Activation of polymorphonuclear leucocytes
Release serine elastase
Smoke also inactivates the inhibitor of elastase, alpha-antitrypsin
Causes if type 2 respiratory failure
Brainstem injury Metabolic encephalopathy Depressant drugs Spinal cord lesion Neuropathy Respiratory muscle damage Airway obstruction Decreased lung/chest wall compliance
Sources of pulse oximetry error
Poor peripheral perfusion Dark skin False nails Bright light Excessive motion Carboxyhaemoglobin
