malabsoprtion

Question 1

A broad clinical term which refers to the impaired absorption of nutrients (fats,carbohydrates, protein, vitamins, electrolytes, minerals and water) at any point wherenutrient absorption takes place. Often presents as —
Three steps are required for normal nutrient absorption:
1- — processing
2-Absorption into the —
3-Transport into the —
Malabsorption can result from defects in any of these three phases

Answer 1

chronic diahorrhea
luminal
intestinal mucosa
circulation

Question 2

Malabsorption is a complication of many disease processes.
Classification systems include:

1-Global malabsorption– due to disease that affects the — or causes reduced — area. This leads to nutrients not being adequately absorbed. Eg — disease
2-Partial malabsorption – — disease that interferes with absorption of specific nutrients, eg B12 deficiency in —
3- Selectivemalabsorption– specific deficiency eg. — deficiency.

OR
-Primary, or — malabsorption– due to congenital defects in the membrane— systems.
-Acquired, or — malabsorption– Malabsorption results from acquired defects (eg, — disease, — disease, or after extensive — resection or intestinal bypass operations) in the epithelial absorptive surface.

Answer 2

mucosa
reduced absorption
coeliac
localised
pernicious anemia
primary lactase
congenital
transport
secondary
crohns , coeliac , surgical

Question 3

causes of fat malabsorption :
Small intestinal disease/resection:
Small bowel disease
Resection
Impairment of the enterohepatic circulationof bilesalts
Small intestinal bacterial overgrowth
Deconjugation of bile acids by bacteria
Pancreatic exocrine insufficiency–
Impaired production of pancreaticenzymes
Due to chronic pancreatitis, or cystic fibrosis
Disorders of bile acid metabolism
Inadequate synthesis (eg. cirrhosis)
Inadequate secretion of bile salts (eg. cholestasis)
Inadequate deliver of bile (eg. Biliary obstruction- tumour, stone)
Other causes–
Abetalipoproteinemia: Rare inherited disorder, inadequate synthesis ordefective structure of apoproteinsnecessary for the packaging ofchylomicrons,impairs their secretion into the lymphatics
Abnormalities in lymphatic flow (eg,intestinal lymphangiectasia, TB tuberculous lymphadenitis, lymphoma)
- cardinal symptoms :
—- : pale, greasy, foul smelling, frothy or foamy, bulky stools that are difficult to flush due to increased fat content

Answer 3

STEATORRHOEA

Question 4

protein :
Mechanism of protein digestion andabsorption​:
Protein digestion begins in thestomach by the action of gastricpepsins.​
Amino acids released from gastricdigestion results in the release ofcholecystokinin (CCK) from duodenaland jejunal endocrine epithelial cells.This stimulates the release ofpancreatic enzymes responsible forthe digestion of all threemacronutrients.​
In the duodenum, several proteasesact together to digest proteins intoamino acids, or dipeptides andtripeptides.​
Amino acids, dipeptides, andtripeptides can be absorbed at thebrush border membrane. Differentclasses of amino acid transportersexist on the brush border.

Causes of protein malabsorption​:
Impaired pancreatic — and — secretion eg pancreatic insufficiency due to— or chronic —.
Impairedactivity of enzymes.​
Reduced intestinalabsorptive surface.

Answer 4

bicarbonate and protease
cystic fibrosis and chronic pancreatitis

Question 5

carbs:
Mechanism of carbohydratedigestion and absorption​
Dietary starch and disaccharidesmust be broken down into theirconstituent monosaccharidesprior toabsorption​
Both salivary and pancreaticamylase contribute to theirdigestion.​
At the brush border enzymeshydrolyze and broken-downnutrients areabsorbed.​
Carbohydrates that are notdigested and absorbed in the — undergo bacterialdegradation in the – .

Causesofcarbohydrate
malabsorption:
Deficiency in pancreatic amylase​ (pancreatitis, CF)
Reduced disaccharidase activity inthesmall intestinal epithelium​
Decreased absorptive intestinalsurfacearea (eg. coeliac disease)​
Unabsorbable carbohydrates (eg — )​
Congenital; lactase deficiency andsucrase-isomaltasedeficiency.

Answer 5

small intestine
colon
sarbtol
Symptoms: flatulence, abdominal cramps and pain, diarrhoea

Question 6

Vitamins, minerals, trace element:
Mechanism
The proximal half of the — is thepredominant site for the absorption of mostvitamins andminerals.​
Vitamin B12 is absorbed in the —-​
Calcium, iron and folate (vitamin B9) arepredominantly absorbed in the —-

Causesofmalabsorption​:
Proximalsmall bowelresections.​
Distalsmall bowel resections; typically, distal ileumwill result invitamin B12deficiency.​
Distalsmall intestinal and colonic disease cancausehypomagnesemia​
Fat-soluble vitamins– The fat-soluble vitamins (A,D, E, and K).Factors that impact fat absorption willusually affect absorption ofthesevitamins​
Theexcess fatty acids present in the intestinallumen of patientswith untreated fat malabsorptionbind to divalent cations, such ascalcium andmagnesium, causing malabsorption of theseminerals. Calcium depletion in this setting is furthermagnifiedif vitamin D deficiency is alsopresent.​
VitaminB12– Extensive ileal disease or resectiondecreases B12absorption and often leads to adeficiency state. Eg Crohn’s disease. Diminished — leads to reduced absorption of B12 eg pernicious anaemia.

Answer 6

small intestine
ileum
upper small intestine
intrinsic factor

Question 7

coeliac disease:
Glutenis the water- — protein mass present in wheat, rye and barley and is used widely in food processing to add flavours and improve texture.
Pathophysiology: Immune disorder triggered by an environmental agent (gluten) in genetically predisposed individuals.(HLA DR3-DQ2 and/or DR4-DQ8)​
Immune response to gliadin (gluten fraction) promotes an inflammatory reaction, characterized by infiltration of the — and epithelium with chronic inflammatory cells, ultimately causing destruction of — , seen microscopically as villous — and — of the crypts of Lieberkuhn.

Answer 7

insoluble
lamina proper
villi
atrophy
hyperplasia

Question 8

coeliac disease:
Prevalence: High rates in European populations, however now becoming increasingly more prevalent inNorthern Africa, the Middle East, India, and Northern China.
Other individuals at increased risk for coeliac disease include (among several other autoimmune diseases): —- , —-

Symptoms:
Classically: Diarrhoea, signs and symptoms of malabsorption (eg, steatorrhea, weight loss, iron deficiency anaemia, other signs ofnutrient or vitamin deficiency eg ADEK vitamins), and resolution of symptoms upon withdrawal of gluten-containing foods, usually within a few weeks to months.
— : – common among patients with coeliac disease, multiple intensely pruritic papules and vesicles that occur in grouped (“herpetiform”) arrangements, particularly over elbows, dorsal forearms, knees, scalp, back, and buttocks.

Diagnosis: —- antibody positive is supportive, gold standard for diagnosis is — with D2 — showing villous atrophy.

Tissue — , an enzyme which deamidates gluten peptides, increases their —. Tissue transglutaminase is released by inflammatory and endothelial cells and fibroblasts in response to — irritation or — .

Answer 8

Type 1 diabetes,Autoimmune thyroiditis
dermatitis herptiformis
anti-TTG
OGD
d2 biopsy
transglutaminase
immunogenicity
mechanical irritation
inflammation

Question 9

Pancreatic exocrine insufficiency:
-Pathophysiology: The pancreas secretes approximately — liters of alkaline, enzyme-rich fluid every day for the digestion of fats, starch, and protein. Issues can be due to failure of gland to produce fluid, blockage of ducts which can lead to — , reduced—/—stimulus, — impairment.
-Symptoms: Maldigestion of fat leads to —- , maldigestion of protein leads to weight loss, bloating, flatulence,cramping.
Deficiency of fat-soluble vitamins A,D,E,K.

Differentials:
Chronic pancreatitis:Most common cause of pancreatic exocrine insufficiency in adults, prolonged inflammation and scarring results in permanent structural damage and an inability to produce pancreatic fluid.
Pancreatitis presents as severe pain in LUQ/epigastrium, improved by leaning forward.
Elevated —.
Low faecal elastase

Answer 9

1.5
auto digestion
cck/secretin
nerve impairment
steatorrhea
amylase

Question 10

more differential diagnosis of pancreatic exocrine insuffinecy :
Differentials continued:
Cystic fibrosis:CFTR mutation leads to inappropriate transport of chloride and water across endothelial cell membranes in the lungs and exocrine glands. Approximately 80 percent of patients with cystic fibrosis develop progressive pancreatic damage due to the blockage of ductuleswith thickened pancreatic secretions.
Gastric, pancreatic, or small bowel resection: loss of sites ofsecretin and CCK synthesis and inadequate mixing of chyme with pancreatic enzymes due to rapid gastric emptying. Total or a partial resection of the pancreas or postoperative pancreatic duct occlusion. Extensive denervation following lymph node dissection can result in decreased pancreatic stimulation.
Rare: Hereditary hemochromatosis can cause progressive iron deposition in the pancreas. Gastrinoma (Zollinger-Ellison syndrome) can cause inactivation of pancreatic enzymes by excessive gastric acid. Small bowel mucosal disease (eg. coeliac disease) can result in decreased CCK release.

Treatment:
Address underlying cause
Pancreatic enzyme replacement: —
Taken with meals

Answer 10

creon

Question 11

symptoms:
Diarrhoea: 3 or more loose or liquid stools per day.

Steatorrhoea: Excessive faecal fat causing bulky, frothy, greasy, yellow or clay-coloured stools. Foul-smelling, difficult to flush. Think the biliary system

Chronic malabsorption:
Weight loss
Anorexia
Abdominal distention
Borborygmi
Muscle wasting
Failure to thrive

Answer 11

Consequences
Anaemia (iron, pyroxidine, folate, B12)
Bleeding (vit K deficiency)
Osteoporosis (calcium, magnesium, vit D deficiency)
Oedema (protein deficiency)
Nervous system (B12 deficiency): peripheral neuropathy/Subacute combined degeneration of cord

Question 12

presenting complaint:
The aetiology and type of malabsorption can often be obtained from a history.
The history should include:
The duration of the symptoms
Character of the stool
Timing of bowel motions in relation to meals
Exacerbating factors
Presence of associated symptoms (eg, abdominal pain, bloating, distension)
Description of stools: STEATORRHOEA
Excess flatus, and bloating are common when carbohydrate malabsorption predominates (eg, lactose malabsorption)
Symptoms due to carbohydrate malabsorption typically occur within 90 minutes of carbohydrate ingestion.

Answer 12

Important medical history/ risk factors: history of chronic intestinal disease, intestinalresection, bariatric surgery or other surgical interventions or radiation treatments to theabdomen
Risk factors for coeliac disease;eg. type 1 diabetes mellitus, family history of coeliacdisease, ethnic background.
Looking at risk factors for pancreaticinsufficiency: history of excessive alcoholconsumption, acute/chronic pancreatitis, or pancreatic surgery.
Recurrent peptic ulcer disease may be indicative of either agastrinomaormastocytosis,each of which can cause malabsorption.

Question 13

signs:

Answer 13

cachexia
koilnyochia; spoon shaped nails
angular stomatitis

Question 14

investigation:
In patients withpositive coeliacserologies (Anti-TTG), weperform an—- withmultiple mucosal — of the — and —portions oftheduodenum.

In individuals with ahistory of pancreatitisor excessivealcoholuse or a low fecalelastase, investigations include;
Faecal ===
Imaging ofthepancreas withmagneticresonancecholangiopancreatography (MRCP)
Endoscopicultrasoundevaluation.

Answer 14

upper endoscopy
biopsies
2nd and 3rd
elastase

Question 15

investigation:
If the patient has predisposing risk factors for bacterial overgrowth, (eg. strictures or adhesions, small bowel diverticulosis, blind intestinal loops), can perform breath test for small bacterial overgrowth.

In patients without an identifiable cause/risk factors:
Upper endoscopy and colonoscopy with multiple mucosal biopsies (eg.To out rule — disease)
Imaging of the small bowel with computed tomography (CT) or magnetic resonance (MR) enterography.
D-xylose test can help establish a diagnosis of malabsorption and distinguish mucosal disease from conditions that cause maldigestion.

Answer 15

crohns

Question 16

Other infrequently performed tests
●Dxyloseabsorptiontestforsmallbowelmucosaldisease– used to determine whetherdefects in theintestinal mucosa are responsible formalabsorption
●Proteinmalabsorption– Testing for proteinmalabsorption israrely performed in the clinical setting,intestinal protein loss ismore commonly a result ofprotein-losing gastroenteropathy,which can bedemonstrated by measurement of the faecal alpha-1antitrypsin.

Answer 16

●Bile acid malabsorption
Evaluation of bile acidabsorptionwith aSeHCATtest can differentiate bile aciddiarrhoea fromdiarrhoea due to fat malabsorption.
SeHCAT: Stands for 75-Selenium Homocholic Acid Taurine. It is a nuclear medicine test which tests the absorption of bile acids. A capsule containing radioactive bile acids (75 selenium as a gamma emitter and a synthetic bile acid tauroselcholic acid) acting as a tracer is swallowed, and the patient returns later for a scan. Low levels of SeHCAT remaining in the body at the second scan indicates bile acid diarrhoea.

In theabsence of an objectivetest, patients with diarrhoea duetocholorrhoea (excessive secretion of bile)can undergo atherapeutic trial with a bileacid-binding resin such ascholestyramine, resolutionofsymptoms supports the diagnosis ofcholorrhoea.Cholestyraminecan make the fat malabsorptionworse.

Question 17

Loperamide/ imodium
Synthetic anti-diarrhoeal/ anti-motility agent:
Mechanism of Action:
Binds to — receptors in bowel wall,inhibits the release of — and — , thereby reducing propulsive — , and increasing intestinal — time.
Reduces daily faecal volume, increases the viscosity and bulk density, and diminishes the loss of fluid and electrolytes.
Loperamide increases the tone of the anal sphincter, thereby reducing incontinence and urgency.
Tolerance to the antidiarrhoeal effect has not been observed.

Metabolism: CYP450, CYP3A4

Side Effects:
Common: Gastro-intestinal disorders, nausea, headache, constipation.
Rare: CNS toxicity leading to dizziness, impaired consciousness, coordination impairment, increased muscle tone, urinary retention, angioedema.
QTc prolongation, torsades de pointes, cardiac arrest with higher than normal doses.

Interactions:
Class 1A (e.g., quinidine, procainamide) or Class III (e.g., amiodarone, sotalol) antiarrhythmics, antipsychotics (e.g., chlorpromazine, haloperidol), antibiotics (e.g., moxifloxacin, ciprofloxacin), or any other drug known to prolong the QT interval (e.g., pentamidine, levomethadyl acetate, methadone).

Contra-indications: Due to the risk of significant sequelae including ileus, megacolon and toxic megacolon
Patients with acute dysentery, which is characterized by blood in stools and high fever.
Patients with acute ulcerative colitis.
Patients with bacterial enterocolitis caused by invasive organisms including Salmonella, Shigella, and Campylobacter.
Patients with pseudomembranous colitis (e.g., Clostridium difficile) associated with the use of broad-spectrum antibiotics.

Cautions:
Risk of abuse, dependency due to its’ action as a mu-opioid agonist.
Overdose: Life threatening cardiac, respiratory and CNS implications

Answer 17

opiate
ach + prostagladins
peristalsis
trasnit