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Posters > Review posters 20/05/2016 > Flashcards

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
Q

Management of DiGeorge syndrome

A 
Correct cardiac abnormalities
Prophylactic antibiotics 
Early and aggressive treatment of infection
Immunoglobulin replacement
T cell function improves with age.
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26
Q

Disorders of T cell effector function

A

IL 12 receptor of gamma interferon production
Cytokine production
Cytotoxicity
T- B cell communication

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27
Q

Clinical features of T cell deficiencies

A

Recurrent infections-viral, bacterial, fungal, intracellular pathogens, opportunistic infections
Malignancies
Autoimmune disease

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28
Q

Investigation into T cell deficiencies

A

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
Q

B cell deficiencies

A

Upper and lower resp tract and GI infections. Often by common organisms
Viral infections less common but could occur

30
Q

Clinical features of B cell deficiencies

A

Recurrent infections
Opportunistic infections
Antibody mediated autoimmune disease

31
Q

Brutons X linked hypogammaglobulinaemia

A

Failure to produce mature B cells
No circulating B cells
No plasma cells
No circulating antibody after the first 6 months.

32
Q

Severe IgA deficiency

A

Relatively common
2/3rds are asymptomatic
1/3rd have recurrent respiratory tract infections
No known cause

33
Q

Common variable immune deficiency

A

low IgG, IgA and IgE
Recurrent bacterial infection
Often with severe end organ damage.

34
Q

Management of B cell deficiencies

A

Aggressive treatment of infections
Immunoglobulin replacement (derived from pooled plasma of donors). Administered IV every 3-4 weeks
Stem cell transplantation

35
Q

Investigations into B cell deficiencies

A

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
Q

Roles of the liver

A 
Bile production
First destination of nutrients absorbed by the GI tract
Elimination of unwanted molecules
Secretion of plasma proteins
Storage of important molecules.
37
Q

Functions of plasma proteins

A

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
Q

Albumin

A

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
Q

Alpha globulins

A

Transport lipoproteins, lipids, hormones and bilirubin
Some also transport dietary metals
Retinal binding protien transports vitamin A- deficiency causes visual impairment

40
Q

Beta globulins

A

Transferrin- transports Fe3+
indicator of iron deficiency
Fibrinogen- inactive form of fibrin- clotting of blood.

41
Q

Transport functions of albumin

A

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
Q

Iron transport

A

Transported as ferric ion (fe3+)- component of haemoglobin, myoglobin, cytochromes
Transported bound to transferrin
Stored in cells bound to ferritin

43
Q

Copper transport

A

Transported in the blood attached to ceruloplasmin

Deficiency in ceruloplasmin- Wilson’s disease- copper accumulation in the tissues.

44
Q

Hormone transport in the blood

A

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
Q

Lipoproteins

A

Core of hydrophobic lipids- cholesterol esters, triglycerides. Surrounded by a shell.
Free cholesterol dispersed throughout.

46
Q

Function of lipoproteins

A

Transport fat between organs and tissues

47
Q

Where are chylomicrons made and what is their function?

A

Made in the intestine. Transport exogenous fat to liver

48
Q

Where are VLDL made and what is their function

A

Made in the liver. Transport endogenous fat to peripheral cells.

49
Q

Where is LDL made and what is its function?

A

Made by IDL which is produced by VLDL which is made by the liver.
Cholesterol transport to peripheral tissues.

50
Q

Where is IDL made and what is its function?

A

Made by VLDL. LDL precursor

51
Q

Where is HDL made and what is its function?

A

Made by intestine and liver. Reverse transport of cholesterol.

52
Q

Reverse transport of cholesterol

A

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
Q

Cholesterol

A

Essential component of cell membranes

Precursor for bile acids, vitamin D and steroid hormones.

54
Q

Transport and storage of cholesterol.

A

Majority of cholesterol is esterified to long chain fatty acids.
Incorporated into lipoprotiens
Stored in lipid droplets.

55
Q

Synthesis of cholesterol

A

Virtually all cells can synthesise cholesterol.
Main site is the liver.
Requires a carbon source, a reducing agent and energy

56
Q

HMG CoA reductase

A

Essential step in formation of cholesterol. Catalyses irreversible formation of metalonic acid. Target for STATINS.

57
Q

Three groups of steroid hormones

A

Corticosteroids - produced by cerebral cortex
Adrogens- testis
Estrogens- ovaries.

58
Q

How much of vitamin A, vitamin D and vitamin B12 does the liver have?

A

Vitamin A- 10 months
Vitamin D- 3 weeks worth
Vitamin B12- few years worth.

59
Q

Functions of the placenta

A 
Fetal homeostasis
Gas exchange
Acid base balance
Nutrient transport
Waste product transport
Hormone production
Transport of IgG
60
Q

Lungs before birth

A

Fluid filled and non-expanded

61
Q

Describe the circulation of the neonate

A

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
Q

Three foetal shunts

A

Ductus venosus- connects umbilical vein to IVC
Foramen Ovale- connects RA to LA
Ductus Arteriosus- Connects pulmonary arteries to decending aorta.

63
Q

Why does the circulation bypass the liver?

A

Blood from the placenta doesnt need further processing.

64
Q

Foramen ovale

A

Allows oxygenated blood from the RA to enter the LA

65
Q

Ductus arteriosus

A

Bypasses the lungs to the descending aorta. Patency maintained by prostaglandin E2 produced by the placenta

66
Q

Circulatory changes in the first few minutes of birth

A

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
Q

Foramen ovale shunt

A

As placental venous return decreases and systemic venous return increases. The left atrial pressure exceeds right atrial pressure causing the flap to close.

68
Q

Ductus arteriosus closure.

A

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
Q

Persistent pulmonary hypertension of the newborn

A

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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