ASSCC 6 Flashcards
Define rhabdomyolysis:
Breakdown of muscle tissue, releasing potentially toxic muscle cell components into systemic circulation
6 Causes of Rhabdomyolysis:
1) Crush injury / blunt trauma
2) Extreme exercise
3) Prolonged immobilisation on hard surface
4) Hypothermia
5) Malignant hyperthermia
6) Acute ischaemic + reperfusion injury
7) Drugs: statins, vibrates, alcohol
Mx of rhabdomyolysis:
1) Fluid resuscitation
2) Diuretics
3) Alkalinisation of urine with sodium bicarbonate
4) Correct electrolyte abnormalities
What is the MoA of ADH?
- Increased plasma osmolarity causes increase ADH release from posterior pituitary
- ADH causes insertion of aquaporins into the DCT and CD
- Promotes reabsorption of water, preventing diuresis
5 actions of RAAS:
1) Increased sympathetic activity
2) Increased Aldosterone secretion
3) Tubular Na+, Cl-, H20 reabsorption
4) Tubular K+ excretion
5) Arteriolar vasoconstriction = ^BP
6) Increased ADH secretion
5 risk factors for gastric ulcer:
1) NSAIDs
2) H pylori
3) Steroids
4) Previous peptic ulcers
5) Malignancy
How do NSAIDs cause peptic ulceration?
- Topical irritant on gastric epithelium
- Suppression of gastric PG synthesis
- Reduction of gastric mucosal blood flow
- Impaired barrier properties of mucosa
- Impaired repair of injury to mucosa
Management of perforated gastric ulcer:
1) Omental patch repair
2) Peritoneal wash out
3) Intra-abdominal drain
4) Biopsy to rule out malignancy
5) Long term PPI
MoA of PPI:
Proton pump inhibitor
Binds irreversibly to H+/K+ ATPase on gastric parietal cells
Prevents H+ ions pumped into stomach
Reduces acidity of stomach acid
4 Actions of HCL in stomach:
1) Antibacterial
2) Activates pepsinogen to pepsin
3) Stimulates duodenum to release CCK and secretin
4) Promotes absorption of Ca2+ and iron in small intestine
3 phases to regulate gastric secretions:
1) Cephalic phase: stimulates HCL secretion
2) Gastric phase: stimulates HCL + gastrin
3) Intestinal phase: stimulates HCL initially, then secretin + CCK
4 Differentials of sudden onset haematemesis:
1) Bleeding oesophageal varices
2) Bleeding peptic ulcer
3) Borhaave syndrome
4) Mallory-Weiss tear
How does alcohol cause cirrhosis?
- Changes in lipid metabolism
- Decreased export of lipoproteins
- Cell injury caused by reactive oxygen species and cytokines
- Scarring and nodular regeneration
Pathogenesis of portal HTN in liver cirrhosis:
- Cirrhosis is characterised by fibrosis, scarring and nodular regeneration
- Fibrosis obstructs portal venous return = portal hypertension
- Arteriovenous shunts within the liver contribute to portal hypertension
3 contributing factors to ascites:
1) Hypoalbuminaemia
2) Increased formation of hepatic and splanchnic lymph
3) Retention of salt and water due to increased aldosterone and ADH levels
Cause of confusion in liver disease:
Hepatic encephalopathy
Type of anaemia in chronic alcoholism:
Macrocytic anaemia
Factors:
- Toxic effect on bone marrow
- Malnutrition (vit B12/folate def)
What is the main cause of hypersplenism in chronic alcoholics?
Portal hypertension
4 causes splenomegaly:
1) Infective: TB, Malaria
2) Blood diseases: SCA, hereditary spherocytosis, ITP
3) Neoplastic: Lymphoma
4) Vascular: Portal HTN, infarction
How does vitamin B12 deficiency cause macrocytic anaemia?
- Vit B12 necessary in DNA synthesis
- Cell cycle unable to progress from G2 to M stage
- Cell unable to divide
= Macrocytosis
Sites of portosystemic anastomosis:
1) Lower oesophagus
2) Upper anal canal
3) Umbilical
4) Bare area of liver
5) Retroperitoneal
Portosystemic veins causing lower oesophageal anastomosis:
- Oesophageal branches of left gastric
- Azygous vein
Portosystemic veins causing upper anal canal anastomosis:
- Superior rectal veins
- Middle/inferior rectal veins
Portosystemic veins causing umbilical anastomosis:
- Veins of ligamentum teres
- Superior/inferior epigastric veins
Surgical treatment options for cirrhosis + portal hypertension :
1) TIPSS
2) Stapled oesophageal transection
3) Orthoptic liver transplant
Why are uraemia pts anaemic?
1) Deficiency of erythropoietin
2) Circulating bone marrow toxins
3) Bone marrow fibrosis during osteitis fibrosa cystica
4) Red cell fragility due to uraemic toxins
