- PATHOPHYSIOLOGIES - Flashcards
1
Q
Outline the pathophysiology of HELLP sydrome
A
- 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
2
Q
Outline the pathophysiology of Pre-eclampsia
A
- 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
3
Q
Outline the pathophysiology of Ectopic pregnancy
A
- 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
4
Q
Outline the pathophysiology of Post-partum haemorrhage
A
• 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
5
Q
Outline the pathophysiology of Bowel obstruction
A
. - 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
6
Q
Outline the pathophysiology of cholecystitis
A
- 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)
7
Q
Outline the pathophysiology of liver failure
A
- 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
8
Q
Outline the pathophysiology of GI bleed
A
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
9
Q
Outline the pathophysiology of liver cirrhosis
A
- 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
10
Q
Outline the pathophysiology of acute pancreatitis
A
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
11
Q
Outline the pathophysiology of seizures
A
- 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
12
Q
Outline the pathophysiology of a thrombolytic stroke
A
- 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
13
Q
Outline the pathophysiology of a haemorrhagic stroke
A
- 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
14
Q
Outline the pathophysiology of meningitis
A
- 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
15
Q
Outline the pathophysiology of gastroentiritis
A
• 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
