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mpharm year 3 sem 1 > MP322 week 9 > Flashcards

MP322 week 9 Flashcards

1
Q

acute diarrhoea treatment

A

adsorbant and bulk forming
- kaolin, light (adsorbent & bulk forming)

anti motility
- diphenoxylate and atropine (co-phenotrope)
- codiene (phosphate)
- morphine (with kaolin)
- loperamide (HCl)
- racecadotril

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2
Q

anti motility drugs morphine and codeine phosphate

A

mu opioid receptors on neuronal varicosities agonised decreases ACh release decreasing peristaltic activity

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3
Q

anti motility drugs diphenoxylate and atropine

A

atropine inversely agonises the mAChR receptors
diphenoxylate similar to codeine

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4
Q

anti motility drugs racecadotril and thiorphan

A
  • activation of gama opioid receptors decreases the cellular cAMP levels reducing water and electrolyte secretion
  • ## prodrug to give thiorphan
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5
Q

antimotility drugs loperamide

A
  • acts similar to morphine, codeine, diphenoxylate
  • also evidence of non selective calcium channel blocking
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6
Q

constipation treatment

A
  • linaclotide
  • lubiprostone
  • relatively new drugs
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7
Q

constipation treatment - linaclotide

A
  • guanylate cyclase activator
  • increase water/ electrolyte secretion
  • cyclic peptide
  • MWt= 1526
  • ## polar molecule
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8
Q

constipation treatment - lubiprostone

A
  • a prostone class of molecule
  • CIC-2 calcium channel activator
  • increase water/ electrolyte
  • given as capsules
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9
Q

what is malabsorption

A
  • inadequate absorption nutrients from the GIT- most absorption is through the small intestine
  • macronutrients- carbohydrate, fat, protein
  • micronutrients- vitamins and minerals
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10
Q

Crohn’s disease

A
  • mucosal
  • malabsorption linked to inflammation (+/- surgical resection)
  • iron deficiency anaemia
  • B12/ folate deficiency
  • vitamin D and calcium deficiency- osteoporosis/ osteomalacia- supplementation
  • also note- steroid use in IBD; effect on bones
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11
Q

coeliac disease

A
  • mucosal
  • an autoimmune condition - glutens activate an abnormal mucosal response chronic inflammation and damage- villous atrophy
  • fatigue, gastrointestinal symptoms, weight loss- diagnosed via serological testing
  • common complications include anaemia, osteoporosis (malabsorption of vitamin D/ calcium)
  • treatment elimination of gluten from the diet
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12
Q

short bowel syndrome

A
  • mucosal
  • usually secondary to surgery, but can be congenital
  • may require parenteral nutrition
  • less surface area available for absorption
  • osteoporosis and vitamin deficiencies are potential risks- supplementation of calcium +/- vitamins and minerals
  • levothyroxine, warfarin, oral contraceptives and digoxin- higher doses may be required
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13
Q

chronic pancreatitis

A
  • pre-mucosal
  • chronic inflammation leads to impaired function
  • affects males more than females
  • decrease pancreatic enzymes
  • strong association with long term alcohol
  • tests include faecal elastase (available tests only confirm severe pancreatic insufficiency)
  • also lets for fat-soluble vitamin deficiencies
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14
Q

cystic fibrosis

A
  • pre-mucosal
  • inherited, decreases chloride secretion, increased sodium absorption= thick mucous
  • pancreatic insufficiency (in 85%)
  • steatorrhoea
  • osteoporosis- multifactorial
  • malnutrition, weight loss
  • pancreatic enzyme supplementation, fat soluble vitamin supplementation, calorie replacement
  • intestinal obstruction
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15
Q

lactase deficiency

A
  • pre mucosal
  • primary, secondary, congenital or development
  • reduce or eliminate dietary lactose intake
  • alternative calcium source may be required
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16
Q

bacterial overgrowth

A
  • both mucosal and pre mucosal
  • incidence increases with age
  • chronic pancreatitis and motility disorders commonest causes
  • reduced gastric acid
  • impaired motility
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17
Q

fat malabsorption

A
  • problem with digestion (insufficient enzymes, bile) or absorption
  • malabsorption more common in coeliac, Crohn’s
  • deficiencies of fat-soluble vitamins (A, D, E, K)
  • steatorrhoea - excess fat is lost in the stools, making them float, appear pale and bulky and smell offensive
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18
Q

vitamin malabsorption

A
  • Poor fat absorption will impact the absorption of vitamins A, D, E and K
  • Vitamin D – osteomalacia(rickets)/osteoporosis - risk assessment +/- supplementation
  • Vitamin K – clotting problems
19
Q

Carbohydrate, protein, fat malabsorption - treatment options

A
  • Supplementation of pancreatic enzymes: lipase, amylase and protease ( Creon)
  • Pancreatitis, CF – where there are deficiencies of pancreatic enzymes. Reduce steatorrhoea, boost nutritional status
  • Cautions…local irritation. Take during or just after a meal. Timing is important!! Often need many capsules per day
  • Nb: derived from pork
20
Q

Iron malabsorption

A

Iron deficiency anaemia commonly seen with coeliac, Crohn’s, small bowel resection – impaired absorption

Note also…potential blood loss with Crohn’s, ulcerative colitis etc.

Oral iron replacement

Folate/B12 deficiency covered in detail next lecture

21
Q

Gluten free diets

A

patients referred by dietitian/ gp

22
Q

classification of vitamins

A

water soluble
- B complexes
- c or ascorbic acid

fat soluble
- A or retinol
- D or cholecalciferol
- E or tocopherol
- K

23
Q

sources of B12

A

Vitamin B12 (cobalamin)
Vitamin B12 is synthesised solely by microorganisms
Ruminants obtain vitamin B12 from the foregut, but the only source for humans is food of animal origin e.g. meat, fish, and dairy products
Vegetables, fruits, and other foods of non-animal origin are free from vitamin B12, unless they are contaminated by bacteria
Strict vegetarians are at risk of developing vitamin B12 deficiency (more likely to occur in vegans)

24
Q

dietary requirements of vitamin B12

A

RDA 1-2.5 microgram/day

Western daily diet contains 5-30 microgram of vitamin B12
Body stores are of the order 2-5 milligram
Adult daily losses (mainly in the urine and faeces) are between 1 and 3 microgram (~0.1% of body stores)
Sufficient stores of vitamin B12 for 2-5 years if the supply is completely cut off

25
Q

absorption of vitamin B12

A

Two mechanisms exist for vitamin B12 absorption
Passive absorption
Through buccal, duodenal and ileal mucosa
Rapid but extremely inefficient
<1% of an oral dose is absorbed
Active transport
Normal physiological mechanism is active transport
Occurs through the ileum
Mediated by gastric intrinsic factor
~70% of ingested amount is absorbed
Vitamin B12 is released from food and bound to haptocorrin (transcobalamin I)
Haptocorrin is produced by the salivary glands
Intrinsic factor (glycoprotein) is secreted by parietal cells
On reaching the duodenum haptocorrin is degraded releasing vitamin B12
Vitamin B12 is captured by intrinsic factor
Intrinsic factor-bound vitamin B12 passes along intestine
In the terminal ileum, intrinsic factor-bound vitamin B12 is endocytosed by cubam
Inside the enterocyte, intrinsic factor is degraded releasing vitamin B12
An ABC transporter releases vitamin B12 into the blood
Vitamin B12 binds to transcobalamin II

26
Q

Plasma transport of vitamin B12 and cellular uptake

A

Vitamin B12 is transported inthe plasma bound totranscobalamin I, II, or III
Vitamin B12 bound totranscobalamin II is mostimportant for cellular uptake
Internalisation occurs incomplex with transcobalaminreceptor (CD320) via endocytosis
The transcobalamin is degraded, yielding vitamin B12
Excess vitamin B12 is sent to liver for storage

27
Q

Plasma transport of vitamin B12 and cellular uptake

A

Vitamin B12 is transported inthe plasma bound totranscobalamin I, II, or III
Vitamin B12 bound totranscobalamin II is mostimportant for cellular uptake
Internalisation occurs incomplex with transcobalaminreceptor (CD320) via endocytosis
The transcobalamin is degraded, yielding vitamin B12
Excess vitamin B12 is sent to liver for storage

28
Q

cellular role of vitamin B12

A

Essential co-enzyme for 2 enzymes in the body:

29
Q

Role of intrinsic factor in absorption

A

Intrinsic factor is produced in the parietal cells and its secretion parallels that of acid
In the absence of intrinsic factor inadequate amounts of vitamin B12 are absorbed
Results in megaloblasticanaemia
When it is due to absenceof intrinsic factor, it is knownas pernicious anaemia
1934 Nobel prize to George Minot, George Whipple andWilliam Murphy

30
Q

pernicious anaemia

A
  • autoimmune atrophic gastritis (pernicious anaemia)
  • destruction of gastric parietal cells and the associated lack of intrinsic factor
  • immune response is directed against H+/K+ ATPase
  • also causes achlorhydria (production of gastric acid is low or absent)
  • can also be caused by antibodies directed against intrinsic factor
31
Q

aetiology of vitamin B12 deficiency

A
  • inadequate dietary intake
  • loss of gastric parietal cells or intrinsic factor
  • functionally abnormal intrinsic factor
  • bacterial overgrowth in intestine (stagnant loop syndrome)
  • disorders of ileal mucosa ( resection, absence of receptor on ileal cells)
  • disorders of plasma transport (eg transcobalamin II deficiency)
  • dysfunctional uptake and sue of vitamin B12 by cells
32
Q

drug induced vitamin B12 deficiency

A
  • PPI and H2 antagonists (reduction in stomach acid reduces separation of vitamin B12 from food)
  • oral contraceptives and hormone replacement therapy (thought to be due to a reduction in the B12 carrier transcobalamin)
  • metformin (reduces vitamin B12 absorption)
  • cholchocine (impairs or inhibits receptors in terminal ileum0
33
Q

consequences of vitamin B12 deficiency

A
  • normal serum concentration of vitamin B12 is 115-1000 pool/L
  • megaloblastic anaemia is the hallmark of symptomatic vitamin B12 deficiency
  • in advances cases, the anaemia may be severe, with haematocrit as low as 10-15% (normal 40% for woman and 45% for men)
  • may be accompanied by leucopaenia and thrombocytopaenia and hypersegmented neutrophils

neurological symptoms
- paresthesia ( pins and needles) in hands and feet
- sensory loss
- gait ataxia
- weakness in legs

subacute combined degeneration (SCD) of the spinal cord (also affects Brian and peripheral nerves)

digestive
- hunter’s glossitis

cardiovascular
- angina
- venous thromboebolic disease

gynaecological
- infertility

34
Q

vitamin B12 derivatives

A

Human serum has:
0-10% Cyanocobalamin (synthetic vitamin B12)
8-15% Hydroxocobalamin
22-39% Deoxyadenosylcobalamin
36-62% Methylcobalamin

deoyadenosylcobalamin and methylcobalamin are the active forms of the vitamins in humans (other cobalamins are converted to the active forms)

35
Q

treatment of vitamin B12 deficiency

A
  • oral (cyanocobalamin) or parenteral (hydroxycoblamain) cobalamin
  • mist be parenteral in the case of gastric intrinsic factor deficiency (pernicious anaemia) or total gastrectomy
  • lifelong treatment is necessary
36
Q

sources of vitamin B9

A
  • Vitamin B9 (folate, folic acid)
  • Dark green vegetables (e.g. broccoli, lettuce, Brussel sprouts, and spinach) and dried legumes (e.g. beans, lentils and chickpeas)
  • Fruits and fruit juices
  • Meat, seafood, poultry and eggs
  • Fortified cereals and bread
  • RDA 200 microgram/day
  • 400 microgram/day supplement in pregnancy
37
Q

absorption of folate

A
  • natural folates are conjugated t a polyglutamyl chain
  • folates are absorbed in the monoglutamate form
  • hydrolysed by folypoly-y-glutamate carboxypeptidase
  • N5-methyltetrahydorfolate (5-MTHF) is main dietary folate
  • most absorption occurs in proximal small intestine (duodenum and jejunum) some absorption in colon
  • folate is absorbed from the lumen by a proton-coupled folate transporter (PCFT)
  • absorption is also via a reduced folate carrier (RFC), with folate being exchanged for organic phosphate (OP)
  • enterocytes also have folate receptors (binds folate and internalises it by receptor mediated endocytosis)
  • folate can be exported without further metabolism, or reduced to 5-MTHF
  • both forms of folate are exported from enterocyte by an organic anion transporter (OAT)
38
Q

plasma transport of folate and cellular uptake

A
  • most is transported as mono-glutamyl derivative
  • most folate circulates free in the blood (some is bound to albumin)
  • plasma concentration is 10-30 mol/L
  • cellular uptake is by the same three mechanisms as for enterocytes (PCFT, RFC and folate receptor)
  • intracellular folates exist primarily (75%) as polyglutamate conjugates
39
Q

cellular requirements for folate

A

folate is crucial for the transfer on one carbon units to amino acids, nucleotides, and other biomolecules

40
Q

aetiology of folate deficiency

A
  • inadequate dietary intake
  • congenital defects in the uptake system
  • intestinal disease (eg coeliac disease, inflammatory bowel disease, tropical sprue)
  • drug interaction (eg cholestyramine, sulfasalazine, trimethoprim, methotrexate, metformin)
  • chronic alcohol use
  • increased cellular requirement (eg pregnancy)
41
Q

symptoms of folate deficiency

A
  • sore tongue (glossitis) and pain upon swallowing
  • GI symptoms (nausea, vomiting, abdominal pain, diarrhoea, especially after meals)
  • neurological (cognitive impairment, dementia and depression)
  • when severe it results in megaloblastic anaemia
42
Q

consequences of folate deficiency

A
  • neural tube defects
43
Q

treatment of folate deficiency

A
  • oral folic acid for 1-4 months
  • oral route is sufficient even in those with malabsorption
  • treated until haematological recovery occurs

mpharm year 3 sem 1 (10 decks)

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