ASSCC 6 Flashcards
(26 cards)
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
