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Review posters 20/05/2016 Flashcards

1
Q

Exocrine pancreatic cancer

A

Adenocarcinoma

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2
Q

Endocrine pancreatic cancer

A

Insulinoma, gastrinoma, glucagonoma

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3
Q

Insulinoma

A

Produces insulin- causing the body to store sugar rather than burn it

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4
Q

Gastrinoma

A

Produces gastrin causing increase stomach acid

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5
Q

Glucagonoma

A

Produces glucagon- increaseing blood sugar levels

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6
Q

Symptoms of pancreatic cancer

A

Jaundice, back pain, weight loss (anorexia, nausea and vomiting)

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7
Q

Risk factors for pancreatic cancer

A

SMOKING
charred meat
Obesity and physical inactivity
Diabetes

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8
Q

Investigations into pancreatic cancer

A

CT scan- first
ERCP
Ultrasound
Blood tests

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9
Q

Staging of pancreatic cancer

A

TNM staging
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

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10
Q

Treatment of pancreatic cancer

A 
If resectable- 
Whipples resection- attach the bile duct straight to the duodenum
Total pancreatomy- remove whole pancreas
Distal pancreatomy
Midsegment pancreatomy

If not resectable-
Biliary bypass
Gastric bypass
Double bypass

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11
Q

Where do T cells stem from?

A

Haematopoeitic stem cells

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12
Q

What occurs in the thymus?

A

Immature T cells undergo selection (only 10% survive)

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13
Q

Reticular dysgenesis

A

Failure to make neutrophils, macrophages, lymphocytes, platelets

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14
Q

Severe combined immunodeficiency

A

Failure to produce lymphocytes.

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15
Q

Clinical findings of severe combined immunodeficiency

A 
Unwell by 3 months
Persistent diarrhoea
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
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16
Q

What immunoglobulin is transported to the child across the placenta?

A

IgG

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17
Q

What immunoglobulin is in breast milk?

A

IgA

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18
Q

Causes of severe combined immunodeficiency

A

Deficiency of cytokine receptors
Deficiency of signalling molecules
Metabolic defects

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19
Q

Treatment of SCID

A 
Prophylactic- avoidance
Prophylactic antibiotics
Prophylactic antifungals
NO VACCINES
Aggressive treatment of existing infections
Antibody replacement (IV immunoglobulin)

Definitive treatment
Stem cell transplantation
Gene therapy

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20
Q

Commonest form of SCID

A

X- linked
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

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21
Q

DiGeorge syndrome

A

Funny looking child, low down folded ears. Small mouth, high forehead, cleft palate.
Hypocalcaemia
Oesophageal atresia (top of the oesophagus doesn’t connect to the bottom)
Complex congenital heart disease
T cell lymphopenia- low T cell count

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22
Q

Genetics of DiGeorge syndrome

A

Caused by chromosomal deletion- 22q11- cumulative effect of deletion of several genes.
Results in T cell immunodeficiency

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23
Q

Infections and DiGeorge syndrome

A

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

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24
Q

Lab investigations into DiGeorge syndrome

A

Absent/decreased T cells
Increased/normal B cells- however poor antibody response.
Normal NK cells

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25
Management of DiGeorge syndrome
``` Correct cardiac abnormalities Prophylactic antibiotics Early and aggressive treatment of infection Immunoglobulin replacement T cell function improves with age. ```
26
Disorders of T cell effector function
IL 12 receptor of gamma interferon production Cytokine production Cytotoxicity T- B cell communication
27
Clinical features of T cell deficiencies
Recurrent infections-viral, bacterial, fungal, intracellular pathogens, opportunistic infections Malignancies Autoimmune disease
28
Investigation into T cell deficiencies
First line- Total WCC Serum immunoglobulins Protein electrophoresis Quantitation of lymphocyte subpopulations Second line: Functional tests of T cell Activation and proliferation HIV TEST
29
B cell deficiencies
Upper and lower resp tract and GI infections. Often by common organisms Viral infections less common but could occur
30
Clinical features of B cell deficiencies
Recurrent infections Opportunistic infections Antibody mediated autoimmune disease
31
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.
32
Severe IgA deficiency
Relatively common 2/3rds are asymptomatic 1/3rd have recurrent respiratory tract infections No known cause
33
Common variable immune deficiency
low IgG, IgA and IgE Recurrent bacterial infection Often with severe end organ damage.
34
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
35
Investigations into B cell deficiencies
First line- Total WCC Serum immunoglobulins Serum and urine protein electrophoresis Second line- Quantitation of B and T lymphocytes Specific antibody responses to pathogen.
36
Roles of the liver
``` Bile production First destination of nutrients absorbed by the GI tract Elimination of unwanted molecules Secretion of plasma proteins Storage of important molecules. ```
37
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 Immunity
38
Albumin
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
39
Alpha globulins
Transport lipoproteins, lipids, hormones and bilirubin Some also transport dietary metals Retinal binding protien transports vitamin A- deficiency causes visual impairment
40
Beta globulins
Transferrin- transports Fe3+ indicator of iron deficiency Fibrinogen- inactive form of fibrin- clotting of blood.
41
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
42
Iron transport
Transported as ferric ion (fe3+)- component of haemoglobin, myoglobin, cytochromes Transported bound to transferrin Stored in cells bound to ferritin
43
Copper transport
Transported in the blood attached to ceruloplasmin | Deficiency in ceruloplasmin- Wilson's disease- copper accumulation in the tissues.
44
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
45
Lipoproteins
Core of hydrophobic lipids- cholesterol esters, triglycerides. Surrounded by a shell. Free cholesterol dispersed throughout.
46
Function of lipoproteins
Transport fat between organs and tissues
47
Where are chylomicrons made and what is their function?
Made in the intestine. Transport exogenous fat to liver
48
Where are VLDL made and what is their function
Made in the liver. Transport endogenous fat to peripheral cells.
49
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.
50
Where is IDL made and what is its function?
Made by VLDL. LDL precursor
51
Where is HDL made and what is its function?
Made by intestine and liver. Reverse transport of cholesterol.
52
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.
53
Cholesterol
Essential component of cell membranes | Precursor for bile acids, vitamin D and steroid hormones.
54
Transport and storage of cholesterol.
Majority of cholesterol is esterified to long chain fatty acids. Incorporated into lipoprotiens Stored in lipid droplets.
55
Synthesis of cholesterol
Virtually all cells can synthesise cholesterol. Main site is the liver. Requires a carbon source, a reducing agent and energy
56
HMG CoA reductase
Essential step in formation of cholesterol. Catalyses irreversible formation of metalonic acid. Target for STATINS.
57
Three groups of steroid hormones
Corticosteroids - produced by cerebral cortex Adrogens- testis Estrogens- ovaries.
58
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.
59
Functions of the placenta
``` Fetal homeostasis Gas exchange Acid base balance Nutrient transport Waste product transport Hormone production Transport of IgG ```
60
Lungs before birth
Fluid filled and non-expanded
61
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.
62
Three foetal shunts
Ductus venosus- connects umbilical vein to IVC Foramen Ovale- connects RA to LA Ductus Arteriosus- Connects pulmonary arteries to decending aorta.
63
Why does the circulation bypass the liver?
Blood from the placenta doesnt need further processing.
64
Foramen ovale
Allows oxygenated blood from the RA to enter the LA
65
Ductus arteriosus
Bypasses the lungs to the descending aorta. Patency maintained by prostaglandin E2 produced by the placenta
66
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.
67
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.
68
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
69
Persistent pulmonary hypertension of the newborn
Lung resistance fails to fall. Therefore shunts remain Right to left at the patent foramen ovale Right to left at the patent ductus arteriosus. Baby will appear blue and need ventilation.

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