- PATHOPHYSIOLOGIES -

Question 1

Outline the pathophysiology of HELLP sydrome

Answer 1

• Generalized endothelial and microvascular injury from activation of the complement and coagulation cascades
• increased vascular tone
• platelet aggregation
• This results in areas of hemorrhage and necrosis within the liver and may evolve to large hematomas, capsular tears, and intraperitoneal bleeding

Question 2

Outline the pathophysiology of Pre-eclampsia

Answer 2

• decreased placental perfusion due to defective spiral artery remodeling
• placental production of a toxic substance endothelin’
• endothelial cell damage
• intravascular congestion
• vasospasms
• increased thromboxane
• fluid shift intravascular to intracellular

Question 3

Outline the pathophysiology of Ectopic pregnancy

Answer 3

• fertilised ovum implants outside the uterine cavity
• most commonly in the fallopian tube
• causing tubule rupture
• erodes submucosal blood vessels
• severe bleeding into tubal lumen

Question 4

Outline the pathophysiology of Post-partum haemorrhage

Answer 4

• 88% of major PPH occur in first 4 hours
• Some loss expected for up to 6 weeks
• Rubra to Serosa to Alba
Secondary PPH (24h‐12 weeks after birth)
• Infection
• Retained products of conception
• Delayed involution
• Return to bright red loss , clots
• Can be sudden and catastrophic

Question 5

Outline the pathophysiology of Bowel obstruction

Answer 5

. - obstruction occurs

• lack of rapid movement of HCI and chyme
• bacteria flourish as a result
• fluiid, gas and intestinal products accumulate proximal to the obstruction
• distal bowel collapses
• distention reduces absorption
• increased pressure leads to increassed capillary permeability and leak of fluid into the peritoneal cavity
• this results in hypotesion and hypovolaemic shock

Question 6

Outline the pathophysiology of cholecystitis

Answer 6

• Inflammation of the gallbladder due to obstruction of the CBD by gallstones
• Causes distension of the gallbladder
• pressure decreases blood flow
• bacterial invasion / infection : (E.coli, streptococcus or salmonella)

Question 7

Outline the pathophysiology of liver failure

Answer 7

• injury to liver (hepatitis, ETOH, drugs, poisoning, obesity, DM, metabolic and genetic disorders)
• inflammation
• immune system stimulation
• increase in oxygen free radicals
• decrease in hepatic perfusion
• hepatic atrophy
• hepatic fibrosis (cirrhosis)
• portal hypertension
• fuild shift
• ascites, peripheral oedema, oesophageal varices
• hepatic decompensation
• renal failure

Question 8

Outline the pathophysiology of GI bleed

Answer 8

Patho:

• injury to the epithelial layer of the GI tract
• GIB
• hypovolaemia
• compensate with peripheral vasoconstriction and increased CO
• Renal Na and water retention
• blood flows to vital organs
• further bleeding or inadequate compensation
• hypovolaemic shock
• insufficient blood to organs
• MODS
• death

Question 9

Outline the pathophysiology of liver cirrhosis

Answer 9

• Damage to hepatocytes
• Kupffer cells activated
• release inflammatory mediators
• reactive oxygen species
• growth factors
• activation of fibrogenic fibroblasts
• fibrosis alters or obstructs blood flow
• altered and reduced blood flow
• leads to ischemia, necrosis and atrophy

Question 10

Outline the pathophysiology of acute pancreatitis

Answer 10

Pancreas:

• inflammation of the pacreas
• back up of pancreatic secretions
• activation and release of enzymes (trypsin, chymeotrypsin, lipase, elastase)
• autodigestion
• Vascular damage, coagulative necrosis, fat necrosis and formation pseudocysts
• oedema
• ischaemia and necrosis

Systemically:

• Pro-inflammatory cytokines & vasoactive peptides released
• Activation leucocytes
• Injury to vessel walls
• Coagulation abnormalities
• third spacing of fluid in the peritoneum
• Vasodilation
• Hypotension
• Shock
• Multisystem failure
• SIRS

Question 11

Outline the pathophysiology of seizures

Answer 11

• TONIC PHASE
• firing of abnormal group of neurons due to irritation
• increase in intensity and excitability
• threshold reached for discharge and can spread through the cortex, thalamus and brain stem
• causes muscle contraction
• CLONIC PHASE
• inhibitory neurons in the cortex, thalamus and basal ganglia interrupt the cortical stimulation
• causing alternation contraction and relaxation of muscles

Question 12

Outline the pathophysiology of a thrombolytic stroke

Answer 12

• Thrombus or embolis
• causes a blockage in the blood vessels
• reduced/nil blood supply
• lack of O2 and glucose to the cell
• cell death and oedema
• affected area becomes soft and discoloured
• necrosis and swelling
• loss of brain tissue, function of neurons and myelin sheath altered
• cell membranes depolarise, altered uptake of neurotransmitters
• calcium accumulates in the cell
• degrading enzymes activated
• lactic acid accumulates
• acidosis impedes cerebral vasomotor functions

Question 13

Outline the pathophysiology of a haemorrhagic stroke

Answer 13

• hypertension or trauma
• ruptured blood vessels
• mass blood forms
• increased ICP
• reduced/nil blood supply
• lack of O2 and glucose to the cell
• cell death and oedema
• further increasing ICP

Question 14

Outline the pathophysiology of meningitis

Answer 14

• inflammation of the leptomeninges
• triggered by autoimmune disease (e.g. lupus)
• or an adverse reaction to medication (intrathecal)
• or infection (most common) caused by bacteria, virus or fungus
• pathogen enters CSF through direct or haematological spreads
• endotoxins from bacteria
• inflammatory mediators are released
• endothelial layer becomes leaky
• protein and fluid leak out of the capillaries
• hypovolaemia
• cerebral oedema
• inflammation increases production of CSF
• raised ICP
• this causes headaches, fever, nuchal rigidity and photophobia

Question 15

Outline the pathophysiology of gastroentiritis

Answer 15

• Gastroenteritis is the inflammation and infection of the stomach, small and
large intestine.
• Caused by either a virus or bacteria and less commonly by parasites

Question 16

Outline the pathophysiology of Appendicitis

Answer 16

• inflammation of the vermiform appendix that spreads to its other parts
• due to infection from obstruction of the appendiceal lumen
• accumulation of WBC and pus
• increase inintraluminal pressure
• causes ischaemia, epithelial rigidity and bacterial invasion

Question 17

Outline the pathophysiology of Intussusception

Answer 17

• Folding (telescoping) of one segment of intestine into another
• Results in bowel obstruction
• Compresses vessels leading to swelling and obstruction
• Necrosis and/or perforation

Question 18

Outline the pathophysiology of Hypertrophic pyloric stenosis

Answer 18

• IHPS occurs secondary to hypertrophy and hyperplasia of the muscular layers of the pylorus
• causing a functional gastric outlet obstruction

Question 19

Outline the pathophysiology of Nephrotic syndrome

Answer 19

Nephrotic syndrome is a clinical disorder characterised by heavy proteinuria, hypoalbuminaemia and oedema
The key acute complications of nephrotic syndrome are hypovolemia, infection and thrombosis

Question 20

Outline the pathophysiology of sepsis in the neonate

Answer 20

• Specific microbial factors (infection obtained from mother e.g. group B strep), intrauritine, meningitis, pneumonia
• Host factors predisposing newborn (poor cellular and humeral immunity and barries broken down easily

Question 21

Outline the pathophysiology of guillain-barre syndrome

Answer 21

• Neuro-immunological response involving the body’s immune system attack of the peripheral nervous system
• immune attack is initiated to fight an infection and that some chemicals on infecting bacteria and viruses resemble those on nerve cells, which, in turn, also become targets of attack.
• Antibodies or white cells attack the myelin sheath of nerves.
• This causes the nerves to inflame, slowing communication to and from the brain.
• Eventually, the brain will not be able to effectively communicate with the peripheral nerves, causing a state of paralysis