These include:
Absent Oesophagus
Short Oesophagus
Tracheo-oesophageal fistulae
Oesophageal Atresia
Diverticulae
Congenital Stenosis
Sunday, 4 April 2010
Heart Block - in degrees...
The heart is a pretty sophisticated bit of equipment, which doesn't stop it from fouling up in many various and irritating ways. Here are some of them.
Heart Block
"interference of the conduction process"
First Degree
Prolonged PR Interval
Causes:
Normal variant/acute MI/CAD/acute rheumatic carditis/digoxin toxy/electrolyte distub.
No Tx
Second Degree
Three types
Intermittent failure of conduction
Benign. No Tx.
Tx. Poss heralds 3rd Degree HB.
Tx. Poss heralds 3rd Degree HB.
Causes:
acute MI/IHD
Mobitz I & II = No Tx
2:1 = temp/perm pacing (*slow Vn rate)
Third Degree
Look at every PR interval in ECG (I know).
No conduction at all of atrial contractions.
No relationship between P wave, and ORS complex.
Abnormal QRS complexes. Ventricles depolarising from an ectopic foci in V muscle, via a slow 'escape mechanism'.
Causes:
conducting tissue disease (*fibrosis): transient - acute MI/chronic - fibrosis in Bundle of His/both bundles blocked
Tx = temp/perm pacing
Heart Block
"interference of the conduction process"
First Degree
Prolonged PR Interval
Causes:
Normal variant/acute MI/CAD/acute rheumatic carditis/digoxin toxy/electrolyte distub.
No Tx
Second Degree
Three types
Intermittent failure of conduction
- Mobitz Type 1 - "Wenckebach"
Benign. No Tx.
- Mobitz Type II
Tx. Poss heralds 3rd Degree HB.
- 2:1/3:1
Tx. Poss heralds 3rd Degree HB.
Causes:
acute MI/IHD
Mobitz I & II = No Tx
2:1 = temp/perm pacing (*slow Vn rate)
Third Degree
Look at every PR interval in ECG (I know).
No conduction at all of atrial contractions.
No relationship between P wave, and ORS complex.
Abnormal QRS complexes. Ventricles depolarising from an ectopic foci in V muscle, via a slow 'escape mechanism'.
Causes:
conducting tissue disease (*fibrosis): transient - acute MI/chronic - fibrosis in Bundle of His/both bundles blocked
Tx = temp/perm pacing
The Cardiac Axis
Cardiac Axis
This is the average spread of depolarisation through the ventricles, when seen from the front.
Positive Lead I + Negative Lead II = Left Axis Deviation
Negative Lead I + Positive Lead II = Right Axis Deviation
Left axis deviation can imply
This is the average spread of depolarisation through the ventricles, when seen from the front.
You need only look at leads I and II for this, as the normal cardiac axis is considered to be anywhere between -30 degrees and +90 degrees.
Positive Lead I + Positive Lead II = Normal Cardiac AxisPositive Lead I + Negative Lead II = Left Axis Deviation
Negative Lead I + Positive Lead II = Right Axis Deviation
Left axis deviation can imply
- Left Anterior Hemiblock
- Inferior MI
- Left Ventricular Hypertrophy (though it is not diagnosed this way)
- Normal finding in short fat adults
- artificial cardiac pacing
- emphysema
- hyperkalaemia
- Wolff-Parkinson-White syndrome - right sided accessory pathway
- tricuspid atresia
- ostium primum ASD
- injection of contrast into left coronary artery
- Left Posterior Hemiblock
- Anterolateral MI
- Right Ventricular Hypertrophy
- Normal finding in children and tall thin adults
- chronic lung disease even without pulmonary hypertension
- pulmonary embolus
- Wolff-Parkinson-White syndrome - left sided accessory pathway
- atrial septal defect
- ventricular septal defect
ECGs #2 - Some Basics
Conduction of the heart
SA Node - AV Node - Bundle of His - Right Bundle Branch & Left Bundle Branch (posterior & anterior fascicles) - Purkinje Fibres
Leads - "an electrical picture of the heart"
The ECG views the heart from two planes.
The 'standard' or limb leads view the heart vertically (e,g, from sides and feet), while the chest leads view it horizontally (e.g. straight on and left side).
It's like someone has poked a bunch of holes in the chest, and you only catch glimpses of the heart through each, and you assemble what must be going on in your head. It would be great if you had X-ray vision like Superman and could just *buzz* and see what's happening to a person's chest, but y'know - real life and all that jazz...
The different views of the heart:-
I, II and VL - Left Lateral
II, III and VF - Inferior
VR - Right Atrium
V1 and V2 - Right Ventricle
V3 and V4 - Interventricular Septum/Anterior of Left Ventricle
V5 and V6 - Anterior and Left Lateral of Left Ventricle
or another way to frame it...
I, VL, V5 & V6 = Lateral Leads
II, III and VF = Inferior Leads
V1, V2, V3 & V4 = Anterior Leads
Depolarisation
When the the muscle is depolarising towards a lead, the lead records it as the the stylus going up, and when the electrical wave moves away from a lead, the leads moves down. You might think of it like the doppler effect. As an ambulance drives towards you, its siren goes up in frequency, and as it whizzes past, the sound dies out.
Quickly calculating the rate
R-R Interval (in large squares) divided into 300
P Wave
Atrial Contraction
Usu. 3x3mm
Usu. assess in Lead II
PR Interval
Beginning of P wave to beginning of QRS complex
Conduction through SA Node - Atria - AV Node - Bundles of His - Ventricular Muscle
n. = 120 - 200ms
QRS Complex
Ventricular Conduction
n. = 120ms
Q Wave - first negative deflection after P
- Normal in Lateral Leads and Lead III - 'septal Q waves', as the IV septum depolarises from left to right
R Wave - first positive deflection after P
S Wave - first negative deflection after R
Transition Point
As waveform progress from V1 to V6, the R waves starts small, and then get bigger, while the S wave starts big and eventually disappears. The point where the R wave = the S waves in the QRS complex is know as the 'transition point', where the IV septum should theoretically lie.
n. V3 & V4
Clockwise Rotation
If the TP shifts towards more lateral leads, then the right ventricle is taking up more space in the precordium. When the heart is seen from below this moving of the TP is clockwise, and therefore known is as 'clockwise rotation'.
This occurs in chronic lung disease.
VR tends towards having the inverse picture from lead II. This is normal. Don't panic.
SA Node - AV Node - Bundle of His - Right Bundle Branch & Left Bundle Branch (posterior & anterior fascicles) - Purkinje Fibres
Leads - "an electrical picture of the heart"
The ECG views the heart from two planes.
The 'standard' or limb leads view the heart vertically (e,g, from sides and feet), while the chest leads view it horizontally (e.g. straight on and left side).
It's like someone has poked a bunch of holes in the chest, and you only catch glimpses of the heart through each, and you assemble what must be going on in your head. It would be great if you had X-ray vision like Superman and could just *buzz* and see what's happening to a person's chest, but y'know - real life and all that jazz...
The different views of the heart:-
I, II and VL - Left Lateral
II, III and VF - Inferior
VR - Right Atrium
V1 and V2 - Right Ventricle
V3 and V4 - Interventricular Septum/Anterior of Left Ventricle
V5 and V6 - Anterior and Left Lateral of Left Ventricle
or another way to frame it...
I, VL, V5 & V6 = Lateral Leads
II, III and VF = Inferior Leads
V1, V2, V3 & V4 = Anterior Leads
Depolarisation
When the the muscle is depolarising towards a lead, the lead records it as the the stylus going up, and when the electrical wave moves away from a lead, the leads moves down. You might think of it like the doppler effect. As an ambulance drives towards you, its siren goes up in frequency, and as it whizzes past, the sound dies out.
Quickly calculating the rate
R-R Interval (in large squares) divided into 300
P Wave
Atrial Contraction
Usu. 3x3mm
Usu. assess in Lead II
PR Interval
Beginning of P wave to beginning of QRS complex
Conduction through SA Node - Atria - AV Node - Bundles of His - Ventricular Muscle
n. = 120 - 200ms
QRS Complex
Ventricular Conduction
n. = 120ms
Q Wave - first negative deflection after P
- Normal in Lateral Leads and Lead III - 'septal Q waves', as the IV septum depolarises from left to right
R Wave - first positive deflection after P
S Wave - first negative deflection after R
Transition Point
As waveform progress from V1 to V6, the R waves starts small, and then get bigger, while the S wave starts big and eventually disappears. The point where the R wave = the S waves in the QRS complex is know as the 'transition point', where the IV septum should theoretically lie.
n. V3 & V4
Clockwise Rotation
If the TP shifts towards more lateral leads, then the right ventricle is taking up more space in the precordium. When the heart is seen from below this moving of the TP is clockwise, and therefore known is as 'clockwise rotation'.
This occurs in chronic lung disease.
VR tends towards having the inverse picture from lead II. This is normal. Don't panic.
Saturday, 27 March 2010
Hydration
Assessing hydration in a patient
A popular OSCE question. Which makes it surprising that it's always such a surprise, maybe because - Surprise! - we've never been taught it.
Situations where assessing the fluid status is important eg dehydration:-
-Vomiting
-Sepsis
-Bowel obstruction
-Bleeding
-Recent Surgery
-Diarrhoea
-Fever
Causes of fluid overload:-
-Right heart failure
-Constrictive pericarditis
-Hypoalbuminaemia
Anyhoo - how to assess someone's hydration status, whether dehydrated or fluid overloaded:
General Inspection
I'm looking at the environment to see if there are any important clues into the patient's fluid status. This includes
-fluid restriction,
-drugs
-drips
-lines
-catheter bags,
-or nutritional supplements.
I am then looking at the patient to see if there is any obvious signs of them being
-dehydrated
-or fluid overloaded, e.g. oedema.
Hands
Starting with the hands I am
-feeling them
-and testing the capillary refill to see if there are signs of peripheral shutdown.
Dehydration would be indicated if the cap refill was prolonged.
Normal <2s.
Wrist
I am palpating the
-pulse.
Both dehydration and fluid overload would cause a tachycardic pulse.
Arm
I am testing
-the blood pressure,
-both sitting and standing.
If there was a decrease in the pressures this could indicate dehydration.
Wait 3 minutes between sitting and standing.
Fall in >20mmHg Systolic or >10mmHg Diastolic = Postural Hypotension
Neck
I am looking at the patient's neck to assess
-the JVP, as its height is an indicator of intravascular volume.
Normal = 2cm above sternal angle
If it is diminished, this indicates dehydration.
If it is raised it can indicate fluid overload.
Face
I am looking at
-the eyes, to see if there are sunken orbits. This can indicate moderate to severe dehydration.
I am also looking in
-the mouth to see if there is a lack of moisture, which indicates dehydration.
Chest
Looking at the chest, I am assessing
-the skin turgor by pinching a fold of skin at the sternum (this could also be done on the forearm) for a few moments and then releasing it.
If the skin resumes its place quickly the skin turgor is normal, but if takes a longer amount of time the skin turgor is reduced, and this indicates dehydration.
NB This test, however, is of less use in the elderly when there is loss of skin elasticity.
Oedema
I am checking
-the sacral region
-and legs for signs of oedema, and therefore fluid overload.
Auscultation
I am listening to
-the lungs for the presence of fine inspiratory basal crackles, which could indicate pulmonary oedema
-additional heart sounds to indicate a hyperdynamic state
And to finish off...
I'd like to check the patient's
-temperature
- obs chart (temperature, BP, O2 sats, pulse, RR)
-urine output/catheterise
- fluid balance chart
Inputs (IV fluids, oral intake)
Outputs (urine, stool, drains, stoma bags etc) - vomiting? diarrhoea?
- drug chart – is patient on any diuretics?
- notes - recent surgery?
- further Ix i.e. U&Es, FBC, central line monitoring
A popular OSCE question. Which makes it surprising that it's always such a surprise, maybe because - Surprise! - we've never been taught it.
Situations where assessing the fluid status is important eg dehydration:-
-Vomiting
-Sepsis
-Bowel obstruction
-Bleeding
-Recent Surgery
-Diarrhoea
-Fever
Causes of fluid overload:-
-Right heart failure
-Constrictive pericarditis
-Hypoalbuminaemia
Anyhoo - how to assess someone's hydration status, whether dehydrated or fluid overloaded:
General Inspection
I'm looking at the environment to see if there are any important clues into the patient's fluid status. This includes
-fluid restriction,
-drugs
-drips
-lines
-catheter bags,
-or nutritional supplements.
I am then looking at the patient to see if there is any obvious signs of them being
-dehydrated
-or fluid overloaded, e.g. oedema.
Hands
Starting with the hands I am
-feeling them
-and testing the capillary refill to see if there are signs of peripheral shutdown.
Dehydration would be indicated if the cap refill was prolonged.
Normal <2s.
Wrist
I am palpating the
-pulse.
Both dehydration and fluid overload would cause a tachycardic pulse.
Arm
I am testing
-the blood pressure,
-both sitting and standing.
If there was a decrease in the pressures this could indicate dehydration.
Wait 3 minutes between sitting and standing.
Fall in >20mmHg Systolic or >10mmHg Diastolic = Postural Hypotension
Neck
I am looking at the patient's neck to assess
-the JVP, as its height is an indicator of intravascular volume.
Normal = 2cm above sternal angle
If it is diminished, this indicates dehydration.
If it is raised it can indicate fluid overload.
Face
I am looking at
-the eyes, to see if there are sunken orbits. This can indicate moderate to severe dehydration.
I am also looking in
-the mouth to see if there is a lack of moisture, which indicates dehydration.
Chest
Looking at the chest, I am assessing
-the skin turgor by pinching a fold of skin at the sternum (this could also be done on the forearm) for a few moments and then releasing it.
If the skin resumes its place quickly the skin turgor is normal, but if takes a longer amount of time the skin turgor is reduced, and this indicates dehydration.
NB This test, however, is of less use in the elderly when there is loss of skin elasticity.
Oedema
I am checking
-the sacral region
-and legs for signs of oedema, and therefore fluid overload.
Auscultation
I am listening to
-the lungs for the presence of fine inspiratory basal crackles, which could indicate pulmonary oedema
-additional heart sounds to indicate a hyperdynamic state
And to finish off...
I'd like to check the patient's
-temperature
- obs chart (temperature, BP, O2 sats, pulse, RR)
-urine output/catheterise
- fluid balance chart
Inputs (IV fluids, oral intake)
Outputs (urine, stool, drains, stoma bags etc) - vomiting? diarrhoea?
- drug chart – is patient on any diuretics?
- notes - recent surgery?
- further Ix i.e. U&Es, FBC, central line monitoring
Tuesday, 23 March 2010
Pancreatitis
Pancreatitis
Your friend and mine... actually scratch that, pancreatits is pretty sucky as diseases go, mainly because the pancreas is not encased in a protective lining like other organs are.
Consequently, when it gets damaged and starts releasing its digestive enzymes it has no where to go but on itself - leading to a sort of auto-digestion, and the surrounding organs - ew. This creates all sorts of inflammation. As I said, pretty sucky. Plus, ma-hoo-sive 3rd space losses means gallons of extracellular fluids get trapped in the gut, peritoneum and retroperitoneum (meaning 'behind the peritoneum', from the original Greek - peritoni-, meaning 'lining', and retro- 'meaning from the 70s' - due to the tiny disco ball found lying behind there*). The body decompensates rapidly in this condition, and so the patient, as a result, becomes very unpredictable - able to be chatting one minute, and in severe shock the next.
There are several kinds:
Acute
Chronic
Obstructive
(due to obstruction of the pancreatic duct, but basically shares features with the acute and chronic forms)
Tachycardia
Causes
Using the infamous GET SMASHED
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune (PAN)
Scorpion Sting (Trinidadian)
Hyperlipidaemia/Hypercalcaemia/Hypothermia
ERCP
Drugs
plus Pregnancy and Idiopathic, Infections, Ischaemia
Gallstones & Chronic alcoholism = 70%
Idiopathic = 20%
Poor ol', IDIOtic Amy, she got SMASHED, & woke up PREGNANT. You'd think she's have more sense.
RANSON criteria indicates clinical outcome
Glasgow Criteria for assessing severity of pancreatitis
(NB only validated for gallstones & ethanol as the cause)
PANCREAS
PaO2 <8kPA
3/3+ positives within 48hrs = severe pancreatitis. Transfer to ITU/HDU.
Pathology
Mild
Macro
Tx
*Total BS
Your friend and mine... actually scratch that, pancreatits is pretty sucky as diseases go, mainly because the pancreas is not encased in a protective lining like other organs are.
Consequently, when it gets damaged and starts releasing its digestive enzymes it has no where to go but on itself - leading to a sort of auto-digestion, and the surrounding organs - ew. This creates all sorts of inflammation. As I said, pretty sucky. Plus, ma-hoo-sive 3rd space losses means gallons of extracellular fluids get trapped in the gut, peritoneum and retroperitoneum (meaning 'behind the peritoneum', from the original Greek - peritoni-, meaning 'lining', and retro- 'meaning from the 70s' - due to the tiny disco ball found lying behind there*). The body decompensates rapidly in this condition, and so the patient, as a result, becomes very unpredictable - able to be chatting one minute, and in severe shock the next.
There are several kinds:
Acute
Chronic
Obstructive
(due to obstruction of the pancreatic duct, but basically shares features with the acute and chronic forms)
Acute Pancreatitis
10-20/100 000 West society
*mild/self-limiting
1/5 - severe = shock/organ failure/death
Symptoms
Central/epigastric pain radiating to the back. +/- nausea, vomiting. Possibly relieved on sitting forwards.Symptoms
Tachycardia
Causes
Using the infamous GET SMASHED
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune (PAN)
Scorpion Sting (Trinidadian)
Hyperlipidaemia/Hypercalcaemia/Hypothermia
ERCP
Drugs
plus Pregnancy and Idiopathic, Infections, Ischaemia
Gallstones & Chronic alcoholism = 70%
Idiopathic = 20%
Poor ol', IDIOtic Amy, she got SMASHED, & woke up PREGNANT. You'd think she's have more sense.
Pathogenesis
Enzymatic auto-digestion of pancreas
Acinar cell damage = release of pro-enzymes into interstitium, where activated
Mechanisms
- Direct - Trauma/infection/alcohol
- Oxidative stress
- Acinar cell ischaemia (retained pancreatic secretion, inflammation, oedema, vascular constriction)
leading to...
Acute inflammation
Microvascular leakage
Oedema
Fat necrosis
Proteolysis
Vascular destruction
Haemorrhage
Ix
Increased WCC
Increased plasma pancreatic enzyme levels x3 (within 24 hours)Ix
Increased WCC
RANSON criteria indicates clinical outcome
Glasgow Criteria for assessing severity of pancreatitis
(NB only validated for gallstones & ethanol as the cause)
PANCREAS
PaO2 <8kPA
Age >55yrs
Neutrophils WBC >15x10
Calcium <2mmol/L
Renal function Urea >16mmol/L
Enzymes LDH >600iu/L & AST>200iu/L
Albumin >32g/L
Sugar BM>10mmol/L
3/3+ positives within 48hrs = severe pancreatitis. Transfer to ITU/HDU.
Pathology
Mild
Interstitial oedema
Focal fat necrosis
Pancreas swollen
Superficial white plaques of fat necrosis (fatty acids + Ca)
Severe
Necrotizing
Affects acini, ducts, islets
Affects acini, ducts, islets
= w/spread necrosis and Hg
Macro
Yellow/white chalky fat necrosis, with areas of black haemorrhage
Peritoneum = brown, serous fluid - fat globules & chalky deposits
Micro
Micro
Interstitial oedema
Peri-pancreatic fat necrosis
Peri-pancreatic fat necrosis
Severe
Extending necrosis
Extending necrosis
Acini and blood vessels destruction
With septal acute inflammation cell reaction and haemorrhage
With septal acute inflammation cell reaction and haemorrhage
Tx
Mild episode & majority of cases
Resolve with supportive treatment
Min organ dysfunction
Resolve with supportive treatment
Min organ dysfunction
Course and Cx
Severe episode
Pancreatic necrosis (Dx at CT)
Local damage
Pancreatic abscesses
Pancreatic pseudocysts
Duodenal obstruction
Path = complete resolution/focal fibrosis
Multi-organ failure
DIC
ARDS
Death - 30% in severe acute pancreatitis
Early deaths = organ failure
Death - 30% in severe acute pancreatitis
Early deaths = organ failure
Late deaths = infection
5% mortality = shock w/i 1 week of perforation
*Total BS
Causes of Haemolytic Anaemia
SHEEP TIT
ew, but there you go
Sickle cell disease
Hereditary spherocytosis
Enzyme deficiencies (G6PD, pyruvate kinase)
Erythroblastosis fetalis
Paroxysmal nocturnal haemoglobinuria
Trauma to RBCs (mechanical heart valves, DIC, cardiac haemolysis)
Immunohaemolytics (warm Ab, cold Ag, drug induced, transfusion reaction)
Thalassaemias
or TASTE the PuB DISH
Thalassaemia
Autoimmune (warm Ab, cold Ag, drug induced, transfusion reaction, haemolytic disease of the newborn)
Sickling disorders
Trauma to RBCs (mechanical heart valve, cardiac haemolysis, MAHA)
Enzyme deficiencies (G6PD, pyruvate kinase)
the
Paroxysmal nocturnal haemoglobinuria
u
Burns
DIC
Infection (malaria, septicaemia)
Spherocytosis
Hypersplenism
with help from:
http://www.scribd.com/MemorableMedicine
... I really hope that this is relevant...
Otherwise I'd feel like a bit of a tit, making all this effort.
Or a sheep tit, if you will.
ew, but there you go
Sickle cell disease
Hereditary spherocytosis
Enzyme deficiencies (G6PD, pyruvate kinase)
Erythroblastosis fetalis
Paroxysmal nocturnal haemoglobinuria
Trauma to RBCs (mechanical heart valves, DIC, cardiac haemolysis)
Immunohaemolytics (warm Ab, cold Ag, drug induced, transfusion reaction)
Thalassaemias
or TASTE the PuB DISH
Thalassaemia
Autoimmune (warm Ab, cold Ag, drug induced, transfusion reaction, haemolytic disease of the newborn)
Sickling disorders
Trauma to RBCs (mechanical heart valve, cardiac haemolysis, MAHA)
Enzyme deficiencies (G6PD, pyruvate kinase)
the
Paroxysmal nocturnal haemoglobinuria
u
Burns
DIC
Infection (malaria, septicaemia)
Spherocytosis
Hypersplenism
with help from:
http://www.scribd.com/MemorableMedicine
... I really hope that this is relevant...
Otherwise I'd feel like a bit of a tit, making all this effort.
Or a sheep tit, if you will.
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