Flashcards in Review posters 20/05/2016 Deck (69):
Exocrine pancreatic cancer
Endocrine pancreatic cancer
Insulinoma, gastrinoma, glucagonoma
Produces insulin- causing the body to store sugar rather than burn it
Produces gastrin causing increase stomach acid
Produces glucagon- increaseing blood sugar levels
Symptoms of pancreatic cancer
Jaundice, back pain, weight loss (anorexia, nausea and vomiting)
Risk factors for pancreatic cancer
Obesity and physical inactivity
Investigations into pancreatic cancer
CT scan- first
Staging of pancreatic cancer
T- goes from Tis (carcinoma in situ) up to T4 (bad)
N- N0 or N1- N1 means it has invaded lymph nodes
M- M0 or M1- M1 means it has metastasised
Treatment of pancreatic cancer
Whipples resection- attach the bile duct straight to the duodenum
Total pancreatomy- remove whole pancreas
If not resectable-
Where do T cells stem from?
Haematopoeitic stem cells
What occurs in the thymus?
Immature T cells undergo selection (only 10% survive)
Failure to make neutrophils, macrophages, lymphocytes, platelets
Severe combined immunodeficiency
Failure to produce lymphocytes.
Clinical findings of severe combined immunodeficiency
Unwell by 3 months
Failure to thrive
Infections of all types- SPUR
Unusual skin disease- graft versus host disease- colonisation of infants empty bone marrow by maternal lymphocytes
Family history of early infant death
What immunoglobulin is transported to the child across the placenta?
What immunoglobulin is in breast milk?
Causes of severe combined immunodeficiency
Deficiency of cytokine receptors
Deficiency of signalling molecules
Treatment of SCID
Aggressive treatment of existing infections
Antibody replacement (IV immunoglobulin)
Stem cell transplantation
Commonest form of SCID
Mutation of interleukin 2 receptors - results in inability to respond to cytokines
Failure of T cell and NK development
Normal or increased B cells
Poorly developed lymphoid tissue and thymus
Funny looking child, low down folded ears. Small mouth, high forehead, cleft palate.
Oesophageal atresia (top of the oesophagus doesn't connect to the bottom)
Complex congenital heart disease
T cell lymphopenia- low T cell count
Genetics of DiGeorge syndrome
Caused by chromosomal deletion- 22q11- cumulative effect of deletion of several genes.
Results in T cell immunodeficiency
Infections and DiGeorge syndrome
Recurrent viral infections- CD8 T cells normally deal with virus'
Recurrent bacterial infections- Can't signal to B cells to kill these
Frequent fungal infections- T cells are needed for fungal defence
Lab investigations into DiGeorge syndrome
Absent/decreased T cells
Increased/normal B cells- however poor antibody response.
Normal NK cells
Management of DiGeorge syndrome
Correct cardiac abnormalities
Early and aggressive treatment of infection
T cell function improves with age.
Disorders of T cell effector function
IL 12 receptor of gamma interferon production
T- B cell communication
Clinical features of T cell deficiencies
Recurrent infections-viral, bacterial, fungal, intracellular pathogens, opportunistic infections
Investigation into T cell deficiencies
First line- Total WCC
Quantitation of lymphocyte subpopulations
Functional tests of T cell
Activation and proliferation
B cell deficiencies
Upper and lower resp tract and GI infections. Often by common organisms
Viral infections less common but could occur
Clinical features of B cell deficiencies
Antibody mediated autoimmune disease
Brutons X linked hypogammaglobulinaemia
Failure to produce mature B cells
No circulating B cells
No plasma cells
No circulating antibody after the first 6 months.
Severe IgA deficiency
2/3rds are asymptomatic
1/3rd have recurrent respiratory tract infections
No known cause
Common variable immune deficiency
low IgG, IgA and IgE
Recurrent bacterial infection
Often with severe end organ damage.
Management of B cell deficiencies
Aggressive treatment of infections
Immunoglobulin replacement (derived from pooled plasma of donors). Administered IV every 3-4 weeks
Stem cell transplantation
Investigations into B cell deficiencies
First line- Total WCC
Serum and urine protein electrophoresis
Second line- Quantitation of B and T lymphocytes
Specific antibody responses to pathogen.
Roles of the liver
First destination of nutrients absorbed by the GI tract
Elimination of unwanted molecules
Secretion of plasma proteins
Storage of important molecules.
Functions of plasma proteins
Maintenance of oncotic osmotic pressure- prevents loss of plasma proteins
Transport of hydrophobic substances- steroid hormones, free fatty acids, bilirubin, cholesterol
pH buffering- amino acid side chains can carry net charges
Enzymatic- blood clotting
Most abundant plasma protein
Small, negatively charged and water soluble
Main determinant of plasma oncotic pressure
Insulin stimulates its production
Levels are low in liver disease
Starvation/low protein diet causes decrease in levels
Transport lipoproteins, lipids, hormones and bilirubin
Some also transport dietary metals
Retinal binding protien transports vitamin A- deficiency causes visual impairment
Transferrin- transports Fe3+
indicator of iron deficiency
Fibrinogen- inactive form of fibrin- clotting of blood.
Transport functions of albumin
Multiple binding sites for hydrophobic molecules
Low affinity but high capacity
Hydrophobic clefts in glomerular domain
Transports endogenous lipophillic substances e.g. fatty acids, bilirubin and thyroid hormone.
Transports exogenous substances e.g. aspirin
Transported as ferric ion (fe3+)- component of haemoglobin, myoglobin, cytochromes
Transported bound to transferrin
Stored in cells bound to ferritin
Transported in the blood attached to ceruloplasmin
Deficiency in ceruloplasmin- Wilson's disease- copper accumulation in the tissues.
Hormone transport in the blood
Steroid hormones (derived from cholesterol) and the T3/T4 thyroid hormones are hydrophobic.
Transported in circulation bound to specific transport molecules
Thyroxine bound to thyroid hormone
Cortisol bound to cortisol binding hormone
Core of hydrophobic lipids- cholesterol esters, triglycerides. Surrounded by a shell.
Free cholesterol dispersed throughout.
Function of lipoproteins
Transport fat between organs and tissues
Where are chylomicrons made and what is their function?
Made in the intestine. Transport exogenous fat to liver
Where are VLDL made and what is their function
Made in the liver. Transport endogenous fat to peripheral cells.
Where is LDL made and what is its function?
Made by IDL which is produced by VLDL which is made by the liver.
Cholesterol transport to peripheral tissues.
Where is IDL made and what is its function?
Made by VLDL. LDL precursor
Where is HDL made and what is its function?
Made by intestine and liver. Reverse transport of cholesterol.
Reverse transport of cholesterol
Removes excess cholesterol from cells.
Cholesterol is esterified with fatty acids
Transported back to the liver
Excreted as bile salts via biliary system or faeces.
Essential component of cell membranes
Precursor for bile acids, vitamin D and steroid hormones.
Transport and storage of cholesterol.
Majority of cholesterol is esterified to long chain fatty acids.
Incorporated into lipoprotiens
Stored in lipid droplets.
Synthesis of cholesterol
Virtually all cells can synthesise cholesterol.
Main site is the liver.
Requires a carbon source, a reducing agent and energy
HMG CoA reductase
Essential step in formation of cholesterol. Catalyses irreversible formation of metalonic acid. Target for STATINS.
Three groups of steroid hormones
Corticosteroids - produced by cerebral cortex
How much of vitamin A, vitamin D and vitamin B12 does the liver have?
Vitamin A- 10 months
Vitamin D- 3 weeks worth
Vitamin B12- few years worth.
Functions of the placenta
Acid base balance
Waste product transport
Transport of IgG
Lungs before birth
Fluid filled and non-expanded
Describe the circulation of the neonate
The foetal heart pumps blood to the placenta via the umbilical arteries. Oxygenated, nutrient rich blood from the placenta returns to the feotus via the umbilical veins.
Three foetal shunts
Ductus venosus- connects umbilical vein to IVC
Foramen Ovale- connects RA to LA
Ductus Arteriosus- Connects pulmonary arteries to decending aorta.
Why does the circulation bypass the liver?
Blood from the placenta doesnt need further processing.
Allows oxygenated blood from the RA to enter the LA
Bypasses the lungs to the descending aorta. Patency maintained by prostaglandin E2 produced by the placenta
Circulatory changes in the first few minutes of birth
First breath- lungs open. PO2 increases and causes pulmonary vasodilation. Decrease in resistance to the lungs.
Cord clamping- large, low resistance vascular bed removed. Systemic vascular resistnace increases.
Baby going pink- more blood circulating to the lungs. Gradually increasing Po2.
Foramen ovale shunt
As placental venous return decreases and systemic venous return increases. The left atrial pressure exceeds right atrial pressure causing the flap to close.
Ductus arteriosus closure.
Fall in pulmonary vascular pressure reduced blood flow through the duct.
Rising O2 tension has a direct effect on the duct smooth muscle contraction.
The loss of prostaglandin E2
Functional closure occurs within hours.
Anatomical closure takes up to 10 days.
Ends up as a fibrous ligament- ligamentum arteriosum