Malabsorption And Malnutrition Flashcards

1
Q

What is malnutrition?

A

Insufficient dietary intake to meet metabolic requirements.

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2
Q

What is malabsorption?

A

Disorder of digestive tract which results in an inability to utilise a nutrient.

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3
Q

What are the macronutrients?

A

Carbohydrates, fats and proteins.

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4
Q

What is protein energy malnutrition?

A

Common childhood disorder characterised by stunting height and deficiency of energy and nutrients. A subtype of this is Kwashiorkor.

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5
Q

What is Kwashiorkor?

A

Insufficient dietary intake of protein which leads to childhood stunted growth. There are characteristic features like distended belly, round face and swelling of legs and feet

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6
Q

What is Marasmus?

A

Insufficient caloric intake with deficiency of all macronutrients that leads to wasting, with loss of body fat and muscle causing anorexic appearance.

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7
Q

What is anorexia?

A

Suppression of appetite which indicates:
Malignancy due to cytokine release
Infection with TB or AIDs
Anorexia nervosa: mental behavioural condition

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8
Q

What are the causes of malnutrition?

A

Anorexia
Increased metabolic demand
Dysphagia
Neglect

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9
Q

Why does increased metabolic demand occur?

A

Thyrotoxicosis which leads to hyperthyroidism, causing weight loss, tremors and irregular heartbeat.

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10
Q

What are causes of neglect?

A

Neurological issues
Elderly ‘tea and toast’ syndrome where they restrict food intake due to financial or physical issues with food preparation

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11
Q

What are the consequences of iron deficiency?

A

Microcytic hyperchromatic anaemia- this typically occurs in vegans/vegetarians or menstruating women.

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12
Q

What are the consequences of Vitamin B6 deficiency?

A

Neuropathy

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13
Q

What are the consequences of Vitamin B1 deficiency?

A

Cardiomyopathy and Encephalopathy

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14
Q

What are the consequences of Vitamin B2 deficiency?

A

Stomatitis: this is inflammation of the oral mucosa that leads to pain and difficulty talking.

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15
Q

What are the consequences of folic acid deficiency?

A

Megaloblastic anaemia and spinal defects in pregnancy.

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16
Q

What are the consequences of Vitamin D deficiency?

A

Bone osteomalacia which is common in India and those unexposed to UV.

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17
Q

What are the consequences of Vitamin B12 deficiency?

A

Megaloblastic anaemia
Ataxia
Dementia
Neuropathy
Subacute combined degeneration of spinal cord

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18
Q

What is the consequence of Vitamin C deficiency?

A

Scurvy

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19
Q

What is the consequence of Vitamin K deficiency?

A

Coagulopathy.

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20
Q

How are simple carbohydrate metabolism occur?

A

Begins in the mouth with the action of salivary amylase. In the descending duodenum, the hepatopancreatic ampulla allows entry of pancreatic amylase to break down carbohydrates further, and bicarbonate secretions reduce levels of gastric acid.

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21
Q

How does complex carbohydrate metabolism occur?

A

Brush border enzymes on the enterocytes are a-dextrose, maltase, lactase and sucrase cause the breakdown of oligosaccharides and disaccharides into glucose, fructose and lactose which are taken up by the portal vein to the liver.

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22
Q

What is the location of protein absorption?

A

Duodenum and jejunum.

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23
Q

Where does protein digestion begin?

A

In the stomach. Chief cells of the stomach release pepsinogen which is cleaved into pepsin by the low pH of the stomach, due to gastric acid secretion by parietal cells. In the small intestine, the pancreatic enzymes trypsinogen, chymotrypsinogen and procarboxypeptidase are activated by enterokinase/enteropeptidase which is secreted by brush border enzymes.

24
Q

Which protease activates majority of other proteases?

A

Trypsin, a pancreatic enzyme which is activated by enteropeptidase, a brush border enzyme.

25
Q

How does fat metabolism occur?

A

Begins in the mouth by lingual lipase to break down triglycerides ; emulsification into droplets in the stomach at 37 degrees by churning to increase the SA for action by bile salts from the liver. Bile salts coat them and prevent re-aggregation to cause micelle formation which have a hydrophobic exterior for uptake into the enterocytes. Fats are repackaged in enterocytes into chylomicrons.

26
Q

What are chylomicrons?

A

When micelles enter enterocytes, the free fatty acids undergo re-esterifciation and addition of apolipoproteins E to form chylomicrons. This is taken up by the lacteals duct and travel along the thoracic duct for direct access into the bloodstream.

27
Q

What are apolipoproteins?

A

Proteins important for fat transfer in the blood

28
Q

Which salivary gland produces the most saliva?

A

Submandibular gland.

29
Q

Which salivary gland produces the least saliva?

A

Sublingual gland.

30
Q

What are the regions of the stomach?

A

Cardiac
Fundus
Body
Pylorum

31
Q

What cell type is common in the fundus?

A

Goblet cells.

32
Q

Which cells produce pepsinogen?

A

Chief cells in the stomach. They also produce gastric lipase for fat digestion.

33
Q

Where is HCO3- produced in the stomach?

A

Surface mucosal cells to neutralise gastric acid and prevent damage to stomach surface.

34
Q

What is the role of parietal cells?

A

Produces intrinsic factor and HCL-.

35
Q

What is the role of G cells?

A

Located in the pyloric antrum which produces gastrin. This increases motility of stomach smooth muscle and the production of gastric acid from parietal cells. It stimulates histamine release from D cells.

36
Q

How does gastric acid secretion occur?

A

G cells produce gastrin which act on CCK2 receptors on:
Parietal cells for HCL- production
Enterochromaffin-like cells to release histamine that acts on H2 receptors on parietal cells.

This causes increase in action of K+/H+ ATPase pump.

37
Q

What is the cephalon stage of digestion?

A

Sight or smell of food stimulates vagus nerve to produce acetylcholine that acts on M3 receptors on parietal cells for gastric acid secretion.

38
Q

Which cells neutralise gastric acid in the stomach?

A

D cells in the pylorum which produce somatostatin in response to acid. This downregulates histamine release from ECL cells for gastric acid secretion.

39
Q

What is the role of enterochromaffin cells?

A

Produces histamine for acting on h2 receptors on parietal cells for gastric acid secretion.

40
Q

What is the role of S cells?

A

S cells in duodenum produce secretin in response to carbohydrates to increase:
-> HCO3- production from liver and pancreas
-> Bile salt production from liver

41
Q

What is the role of i cells?

A

The i cells in the duodenum produce cholecystokinin in response to presence of fat.
-> It inhibits gastric motility
-> Increases HCO3- production
-> Increases pancreatic release of amylase and protease
-> Bile salt production

42
Q

Where does the majority of digestion and absorption occur in the small intestine?

A

Duodenum

43
Q

What is the role of the jejunum?

A

Majority of absorption occurs here, out of the entire small intestine.

44
Q

What is the role of the ileum?

A

Absorption of B12 and bile salts action and reabsorption.

45
Q

Which enzymes does the pancreas produce?

A

Lipase, amylase and protease which are released into the descending portion of the duodenum at the hepatopancreatic ampulla.

46
Q

How are bile acids synthesised?

A

Synthesised in the liver from cholesterol. It undergoes conjugation with glycine and taurine to form bile salts for fat emulsification into micelles for uptake into enterocytes.

47
Q

What stimulates bile salt entry?

A

The i cells in the duodenum produce cholecystokinin which stimulates bile entry containing bile slats and acids into D2.

48
Q

What are the features of the enterocytes in the small intestine?

A

Polarised cells with apical cells and bass lateral membrane that has an electrochemical gradient. It contains intercellular junctions for the entry of glucose and amino acids via facilitated diffusion.

49
Q

Which diseases of the small intestine damage the mucosal surface?

A

Crohn’s disease
Coeliac’s disease

50
Q

What is the cause of luminal disease of the small intestine?

A

Infections and bacterial overgrowth

51
Q

What are the post-mucosal issues of the small intestine?

A

Lymphangeiactasia, which is dilation of the lymphatic vessels caused by scarring or obstruction to flow.

52
Q

What is the pathophysiology of giardiasis infection?

A

Parasitic infection caused by ingestion of cysts of giardiasis via Faeco-oral transmission. They adhere to mucosal surfaces in the duodenum and jejunum for replication and become infective in the large intestine. They cause shortening of the microvilli, decreasing brush border enzymes that leads to malabsorption. They disrupt commensal bacteria and cause intestinal inflammation.

Leads to vomiting, watery steatorrhea and retching.

53
Q

What is bacterial overgrowth?

A

High amounts of bacteria in the small intestine due to contamination typically from the large intestine that leads to loss of B12, iron and bile. It can also cause malabsorption and lead to chronic diarrhoea.

Typically caused by surgery to intestines or decreased gastric acids secretion.

54
Q

Which vitamin deficiency is present in Coeliac’s disease?

A

Folate deficiency
Iron deficiency, leading to anaemia.
Vitamin D and Calcium, leading to osteomalacia

55
Q

What is the cause of chronic pancreatitis?

A

Alcoholism

56
Q

What is Zollinger-Ellisson syndrome?

A

Pancreatic carcinoma which secretes gastrin and results in high gastric acid, peptic ulcers in the stomach and small intestine and epigastric gnawing pain.