Massive haematemesis: H2 receptor antagon – no use in UGI bleed. PPI IV i.e. IV OMEPRAZOLE PPI. Endoscopy. || Angio + tagged red cell scan. Octreotide.
Massive haemoptysis = 100ml to 600m lover 24 horus. 6 units = GI Bleed.
Tx: Lung resection. Ligation.
Haemoptysis: Usually acute bronchitis when <100ml.
Tx: Semi-recumbent, affected side down to prevent aspiration into good lung. Abx. Narcotics for cough suppression.
Left ventricular failure
Recurrent pulmonary thrombo-emboli
Pulmonary vasculitis —
Goodpasture’s syndrome (anti-glomerular basement antibody disease)
Haematemesis + maleana = Peptic ulcer i.e. gastric + duodenal (esp. prox duodenum) ulceration (H PYLORI). Oesophageal varices. Gastritis or duodenitis.
USUALLY oesophageal varices 2o to portal HTN. Or GORD. Or duodenal ulcer.
Dyspepsia = duodenal ulcer, gastric ulcer, non-ulcer dyspepsia, reflux oesphagitis, gastric ca, gallstone.
In extremis: O neg.
Band varices. Inject EtOh/Epi. GI bleed –> 6 units!
PUD: H pylori.
Diagnose H pylori: Urea breath test or urease test or antral biopsy.
PPI = Omeprazole. Can cause false negatives hence, stop PPI’s 2 weeks before breath-testing.
Duoedenal (posteriors bleeders – gastroduodenal artery) >>> gastric ulcers.
Pain (dull or burning), several hours after meal, wakes at night. Relieved by food and antacids. Ulcer = very specific location of pain.
Gastric ulcers invaded by splenic artery = torrential bleed.
NSAID’s ===> bleed from gastric ulcer. Esp w nsaids c aspirin.
Antacids (Mg –> diarroea; Al –> constip). Relieve pain. H2 antag: Cimeditine/Ranitidine. RANITIDINE is a H2 antagonist. Omeprazole is a PPI – better than ranitidine. Great if NSAID’s are used. Sucralfate covers the ulcer.
Eradicate H pylori: Special abx + PPI.
DU ulcer > Gastric ulcer (oldies).
DC Barium (gas + barium in stomach).
PEPTIC (DU + GA) ULCERS –> Antacid/H2 blocker (ranitidine)/Omeprazole (PPI). Oi, and eradication too.
If NSAIDs + gastric ulcers –> PPI given together.
UPPER GI BLEED = coffee-ground + malaena. Hcl on blood = coffee ground vom. Tarry black poo = maleana.
Dull donut. Then lean towards you and percuss the dull donut which is now resonant.
[Other signs of ascites may be present due to its underlying etiology. For instance, in portal hypertension (perhaps due to cirrhosis or fibrosis of the liver) patients may also complain of leg swelling, bruising, gynecomastia, hematemesis, or mental changes due to encephalopathy. Those with ascites due to cancer (peritoneal carcinomatosis) may complain of chronic fatigue or weight loss. Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and exercise intolerance.]
Failures = transudate because they are trans i.e. everywhere. (Transudate via portal vein due to increased portal venous pa. Low protein, low LDH, alkaline, normal glucose.
Salt restrict (lets you diurese) + SPIRO to counter aldosterone. Shunt TIPS.
(Exudates – cancer actively secreting it. Lots of protein, LDH, low pH, low glucose.)
Exudate = cancer. DRAIN OFF.
Ascites cause fluid retention. Can cause SBP.
HF = rise in hydrostatic pressure. Nephrotic/liver failure = Fall in oncotic pressure.
LVF – pulm oedema + pleural effusions.
OEDEMA = Big hydrostatic (e.g. water/Na retention) or low oncotic pressure or increased permeability or reduced lymphatic clearance.
LVH – It’s so big, the L goes onto the right hand side.
Bright red poo = haematochezia = lower GI bleed.
Aspirin is for ARTERIAL stuff. Dalteparin is for VENOUS stuff.
Stop aspirin 7 days pre-op.
LMWH: DVT. Anti-XA. Beware with aspirin – bleeders! Protamine antidote. Check no HIT. Heparin APTT.
Warfarin – Give Vit K to reverse warfarin. Can reverse with PCC or short-lived FFP.
Low insulin: DKA Type I. HONK Type II.
Hyperglycaemia – Dietary indiscretion/DKA/HHS/New onset diabetes. Ppt: MI/Infection/Cocaine/Surgery/Trauma.
DKA – Hyperpneic respirations (fast and deep Kaussmaul respirations). Neurologic symptoms (seizures, focal weakness, lethargy, coma, death) – more prevalent in HHS.
” The Ligament of Treitz which extends from the small intestine at the duodenojeunal junction serves as the anatomic landmark.
Type I = insulin dependent. Beta cells destroyed.
Type II = non-insulin dependent. Insulin resistance.
Gastric and duodenal ulcer
Gastritis and esophagitis
Esophageal and gastric varices
Colitis (infectious, ischemic, inflamma
The presence of clubbing is associated with non-small-cell bronchogenic carcinoma, bronchiectasis, and chronic lung abscess.
The presence of diastolic rumble, with opening snap, loud S1, and loud P2 in the precordial examination, suggest the presence of mitral stenosis.
symptoms + 11.1 random
2 hours post 7g OGTT: 11.1
Else impaired fasting/impaired glucose tolerance
Diabetes – Type II:
1. Metformin (reduces gluconeogenesis). Metformin can cause lactic acidosis. Doesn’t cause hypo’s.
2. Glicazide sulphonylurea – hypo’s and weight gain with glicazide but not metformin.
3. Pioglitazone aka thiazolidindediones. Not in HF.
If that doesn’t work —> then insulin. If you have ketosis –> insulin asap!
Glargine/determir = basal long-acting.
ACEi (ramipril)/thiazides/CBB for BP. Statins.
Type I – Insulin! Glargine lantus + levemir determir = Long-acting for basal’s.