Gastro-Oesophageal Reflux Disease, Ulcerations & Strictures, oh my!

GORD!!! Can you believe it?! GORD!!!
Enough of that.

Gastro-duodenal contents can enter the lower oesophagus, just for the hell of it, and a small amount of reflux, as it is known, can be perfectly normal. When abnormal reflux causes oesophagitis, however, this is known as Gastro-Oesophageal Reflux Disease.
Only a % of these actually have symptoms, though.

Symptoms:
Dysphagia

Regurgitation

Nocturnal asthma

Aetiology
Increased abdominal pressure

(pregnancy/obesity/trauma/vomiting)
Lower oesophageal sphincter incompetence
(smoking/alcohol/hiatus hernia/systemic sclerosis)
Decreased muscosal protection
(NSAIDs)

Ix
Endoscopy
 - normal/erythema
Biopsy +/- Barium Swallow

Histology
NB there is a poor correlation between symptom severity and the actual histological findings.
There are 3 diagnostic histological features in biopsies:

1. Epithelial Hyperplasia
2. Congestion of the lamina propria
3. Chronic inflammatory cells within muscosa

Neutrophils are suggestive of ulceration

Complications

• Mucosal erosions
• Ulceration
• Lower oesophageal stricture
• Bleeding
• Barrett's Oesophagus

Erosive & Ulcerative Oesophagitis
Well visualised at endoscopy.
Similar to those found in PUD.


Benign Strictures
Occur when recurrent/persistent ulceration leads to oesophageal fibrosis
These can be focal/circumferential = stenosis & dysphagia

Tx
Underlying causes/Sx

Oesophagitis

Oesophageal inflammation.
Affects 5% of the adult Western population.

Symptoms:
Retro-sternal burning (heartburn)
 - worse with leaning forward, or drinking hot liquids
Severe Presentation:
Dysphagia/Bleeding/Haematemesis/Melaena

Pathology:
Occurs due to damage to the oesophageal mucosa

Aetiology:
Risk factors include -
*GORD
Infection (candida/herpes/CMV/bacteria)
Chemicals (NSAIDS/toxins)
Radiotherapy
Crohn's

Acute Oesophagitis
http://library.med.utah.edu/WebPath/GIHTML/GI002.html
Neutrophils infiltrate the submucosa and squamous mucosa

Normal Oesophagus
http://library.med.utah.edu/WebPath/GIHTML/GI209.html

Hiatus Hernia

Definition:
"partial or total herniation of the stomach/gastro-oesophageal junction (GOJ) through the diaphragmatic hiatus, into the thoracic cavity"

Presentation:
Common, mostly > 50yrs
Can be asymptomatic/symptoms of reflux oesophagitis

Aetiology
Increased abdo pressure
Low residue diet
Laxity of diaphragmatic hiatus or peri-oesophageal attachments

Classification:
There are two main types of hiatus hernia:

• Sliding (most common)

In this, the GOJ is pulled up through the diaphragmatic hiatus (DH) +/- the stomach

• Para-oesophageal (5%)

In this, a part of stomach (*greater curve), slides up through the hiatus, between the oesophagus & the diaphragm. The GOJ remains secure.
It is x 4 more common in females.
Extreme cases - "upside down stomach" when the entire stomach herniates into the thoracic cavity.

Complications
Similar to reflux oesophagitis:

• mucosal erosions
• ulceration
• lower oesophageal stricture
• bleeding
• Barrett's Oesophagus

Congenital Abnormalities of the Oesophagus

These include:

Absent Oesophagus
Short Oesophagus
Tracheo-oesophageal fistulae
Oesophageal Atresia
Diverticulae
Congenital Stenosis

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

• Mobitz Type 1 - "Wenckebach"

Progressive prolonging of PR, then complete failure of conduction, then conducted beat with shorter PR interval. Cycle which repeats. Imagine a wonky cycle that gets harder and harder to pedal, until you fall off, and then you hurriedly get back on and start all over again.
Benign. No Tx.

• Mobitz Type II

Occasional failure to conduct atrial contraction. Imagine an old Casion keyboad on Mobitz setting that randomly doesn't keep the beat.
Tx. Poss heralds 3rd Degree HB.

• 2:1/3:1

x2/3 the no. of P Waves to QRS complexes. Note when the P wave may be hidden in the T wave - it can be identified as a regular distortion.
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.

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 Axis
Positive Lead I + Negative Lead II = Left Axis Deviation
Negative Lead I + Positive Lead II = Right Axis Deviation

Left axis deviation can imply

1. Left Anterior Hemiblock
2. Inferior MI
3. Left Ventricular Hypertrophy (though it is not diagnosed this way)
4. Normal finding in short fat adults

and less common -

• 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

Right axis deviation can imply

1. Left Posterior Hemiblock
2. Anterolateral MI
3. Right Ventricular Hypertrophy
4. Normal finding in children and tall thin adults 

 and anything causing a right-sided strain eg pulmonary disorders -

• 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.