Malnutrition Flashcards

1
Q

What BMI should be considered for treating malnutrition?

A

BMI less than 18.5 or BMI less than 20 with unintentional weight loss greater than 5% in the last 3 to 6 months.

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2
Q

What are the types of nutritional support for reduced oral intake?

A

enteral tube feeding
Parenterally nutrition
Oral nutrition suppot

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3
Q

What is oral nutrition support?

A

Fortified food, additional snacks, and high-calorie drinks.

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4
Q

What is enteral tube feeding?

A

Feeding directly into the gut through a nasogastric or oro gastric tube. aThe GI tract should be accessible and functional, therefore avoid in malabsorptive diseases, diverticular disease, GI bleeding and bowel obstruction.

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5
Q

What are some contraindications for enteral tube feeding?

A

Malabsorptive diseases, diverticular disease, GI bleeding, bowel obstruction, and haemodynamic instability.

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6
Q

Why should enteral tube feeding be avoided in haemodynamic instability?

A

Haemodynamically instability will be worsened with enteric feeding due to poor end-organ perfusion and diversion of blood away from vital areas.

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7
Q

What risks are associated with enteral tube feeding?

A

Obstruction, dislodgement, bleeding, pneumothorax, and refeeding syndrome.

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8
Q

What is parenteral nutrition?

A

Nutrition delivered through a central vein for those with a non-functioning GI system.

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9
Q

What components are included in parenteral nutrition?

A

Lipid emulsions, protein, carbohydrates, sodium, magnesium, calcium, and potassium.

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10
Q

What are the risks with parenterally nutrition?

A

There is risk of pneumothorax from air embolism, central line associated infection or re feeding syndrome, Wernicke’s encephalopathy and parenteral-associated cholestasis. They should be monitored daily but there is risk of hyperglycaemia and lipid excess causing hepatic toxicity

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11
Q

What is the contraindication for parenterally nutrition?

A

Wernicke’s encephalopathy and parenteral-associated cholestasis.

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12
Q

What is the suggested nutritional prescription for energy?

A

25 to 35 kcal/kg per day. with 0.8 to 1.5g per kilogram in protein and 30 to 35 ml fluid per kilogram. The fluid should account for losses from drains and fistula and input from other sources like intravenous drugs

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13
Q

How should low food amounts in the last 5 days be provided with t nutritional support for reduced?

A

nutrition support should be 50% of requirements in first 2 days before increasing the feed rates.

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14
Q

What is refeeding syndrome?

A

A complication caused by sudden reversal of starvation, leading to loss of electrolytes. loss of potassium, phosphate, magnesium and calcium in starvation. The sudden reversal causes increased uptake of these ions and loss of sodium and water out of the cell which the kidney cannot handle.

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15
Q

What are key markers of refeeding syndrome?

A

Hypophosphatemia, which can cause rhabdomyolysis, cardiac failure, muscular weakness and sziure. This is more common with enteral feeding.

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16
Q

Who is at risk for refeeding syndrome?

A

Chronic alcoholics and patients nil-by-mouth for more than 7-10 days.

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17
Q

What causes malnutrition?

A

Deficiency in nutrient intake causing adverse effects on body composition or function.

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18
Q

What are some malabsorption disorders?

A
  • Coeliac disease
  • IBS/IBD
  • Cystic fibrosis
  • Whipple disease
  • Chronic pancreatitis
  • Bacterial overgrowth
  • Parasitic diseases
  • HIV infection
  • Hyperthyroidism
  • Lactose deficiency
  • Zollinger-Ellison syndrome
  • Liver disease.
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19
Q

What is bacterial overgrowth?

A

Presence of excess colonic bacteria in the small intestine, causing epithelial injury. This is typically E.Coli, kliebsella and aeromans, anaerobes which produce enterotoxins and cause direct epithelial injury.

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20
Q

What factors regulate bacteria levels in the small intestine?

A
  • Gastric acid secretion
  • Intestinal motility
  • Intact ileocecal valve
  • IgA levels.
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21
Q

What cases loss of gastric acid secretion?

A

h.pyrloi infection, antacids, pernicious anaemia and Sjögren’s syndrome

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22
Q

What reduces intestinal motility

A

IBS
Hypothyroidism
Type 2 diabetes

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23
Q

What reduces the function of the ileocecal valve?

A

diverticulosis
Bowel strictures
Ileocacecal resection

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24
Q

How does bacterial overgrowth present?

A

This can result in abdominal pain, bloating, watery diarrhoea and malabsorption. Fat malabsorption causes weight loss, diarrhoea and vitamin A (vision) D (bones) and K (coagulopathy) and E (muscle co-ordination) deficiencies.

There is typically Bitamin B12 deficiency and B1 and B3 deficiencies occur from utilisation from bacteria. Ataxia may be present and paraesthesia and sensory ataxia from B12 deficiency

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25
Q

What are symptoms of fat malabsorption?

A

Weight loss, diarrhoea, and deficiencies in vitamins A, D, K, and E.

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26
Q

Which conditions increase the risk of bacterial overgrowth?

A

Bacterial overgrowth is associated with liver disease, pancreatic enzyme insufficiency, kidney disease and immunodeficiency disorders.

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27
Q

How is bacterial overgrowth diagnosed?

A

Bacterial overgrowth is diagnosed with aspirate culture, carbohydrates breath test as bacteria will produce hydrogen or methane, hwoever results may be falsely positive in patients with short bowel syndrome

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28
Q

What is the treatment for bacterial overgrowth?

A

Antibiotic therapy for 2 weeks, tailored to the type of bacteria present.

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29
Q

How is methane dominant bacterial overgrowth treated?

A

neomycin and rifaximin

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30
Q

How is methane dominant bacterial overgrowth treated?

A

Rifaximin

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31
Q

What is a complication from bacterial overgrowth?

A

D-lactose’s is a complication which can rise from bacterial overgrowth. Excess ammonia production can occur which can lead to hepatic encephalopathy precipitate may develop.

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32
Q

What is Whipple disease?

A

A systemic disease caused by Tropheryma whipplei, results in disruption of normal villus function leading to malabsorption.

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33
Q

What is trophyeryma whipplei?

A

Gram positive bacteria found in soil and. Diagnosis is made through endoscopy and biopsy of the intestine with positive results for PAS-positive foamy macrophages.

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34
Q

What is the treatment of whipped disease?

A

ceftriaxone (cephalosporin) for 2 weeks followed by trimethoprim, sulphamethoxazole

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35
Q

What are clinical features of malabsorption?

A
  • Chronic diarrhoea
  • Weight loss
  • Flatulence
  • Chronic fatigue
  • Steatorrhoea
  • Dry hair
  • Fluid retention
  • Anaemia.
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36
Q

What is Zollinger-Ellison syndrome?

A

Gastrin-secreting tumors causing destruction of pancreatic enzymes and peptic ulcers which results in peptic ulcers and interferes with absorptive action. It is associated with nausea, vomiting, weight loss, abdominal pain, heartburn and intestinal bleeding. It is treated with PPIs.

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37
Q

What is lactase deficiency?

A

A condition causing abdominal pain, loose stools, and bloating due to lactose intolerance. Lactase peaks shortly after birth and declines gradually and presents with abdominal pain, loose stools, nausea, flatulaence and borborygmi (rumbling noise produced by morement of fluid/gas in the intestines

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38
Q

What tests are used for malabsorption?

A
  • Faecal tests for Sudan III fat
  • Breath test for glucose or lactulose indicating small itnestne bacterial overgrowth
  • CT for pancreatitis
  • ERCP for pancreatic insufficiency
  • Endoscopy with biopsy.
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39
Q

How does B12 deficiency resent?

A

paraesthesia , fatigue, jaundice, gloss it is, diarrhoea, peripheral neuropathy, headaches and neuropsychiatric disturbances. There may be ataxia and loss of propioception.

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40
Q

What is coeliac disease?

A

An inflammatory disorder due to intolerance of gliadin peptide in gluten. causing intestinal cells to disassemble their titre junctions and it activates T cells in the lamina propia, resulting in inflammatory cel production and antibodies of anti-gliadin and anti-tissue transglutaminase antibodies. Tissue transglutaminase is an enzyme in the extracellular space of the subepithelial region or at the brush border. There is a greater risk factor in individuals with the HLA-DQ2 and HLA-DQ8

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41
Q

What is the presentation of coeliac’s disease?

A

Classical presentation between 6 to 18 months of age after introduction of weaning foods, with histology showing villous atrophy
Atypical form, with the absence of extra-intestinal symptoms and few or nog Astro intestinal symptoms. Usually found in older children and adults and features of absorption are absent
Silent coeliac is asymptomatic but having hisotlogical abnormalities.
There is a peak in presentation in childhood less than 6 years old and those in their 40-50s

42
Q

What are the clinical symptoms of coeliac disease?

A
  • Gastrointestinal symptoms Of malabsorption diarrhoea and failure to thrive, abdominal pain, steatorrhoea, bloating and constipation. Nutritional deficiency may occur with iron, folate and Vtmain D and Vitamin K. This results in iron deficiency or Macrocytic anaemia, rickets, hypocalcaemia and coagulaopathy. Chidlren will have a short stature and delayed puberty. Deficiency in Vitamin A can cause ocular issues with difficulty seeing in the dark, and Vitamin E deficiency can result in ataxia and impaired reflexes.
  • Extra-intestinal symptoms (e.g., dermatitis herpetiformis where diffuse symmetrical lesions of erythema, blisters with hyperpigmentations and execrations appears o the extensor areas. It commonly appears in the 30’s
    infertility, ataxia, epilepsy
43
Q

What is the importance of serological testing in coeliac disease diagnosis?

A

Identifies antibodies indicating gluten intolerance.

Testing for IgA and IgA tissue transglutaminase
-> IgA endomysial antibodies is a confirmatory test
IgA deficiency is total IgA less than 0.07g PE litre.
IgG endomysial antibody, IgG deaminated gliadin peptide or IgG titssue transglutaminase
HLA DQ2/DQ8 should only be used in specialist settings
Anti-gliadin antibodies are not reccomended expect in younger children

44
Q

What is the treatment for coeliac disease?

A

Lifelong gluten-free diet and dietary management with calcium and vitamin D.

45
Q

What is diverticular disease?

A

Outpouching forming in the colon, commonly in the sigmoid colon which is the narrowest part of the colon with the greatest pressure. They form due to increases in the intraluminal pressure which causes the mucosa to herniate outwards. The outpouches contain a mucosa and submucosa.

46
Q

What is the cause of diverticular disease?

A

Diverticular disease commonly occurs due to low dietary fibre intake, low intestinal motility and structural abnromalities in the colon where weakening of circular muscle allows out-pouches to form.

47
Q

What is true divertiuclosis?

A

True diverticulosis where there is an outpouches of all layers of intestinal walls, typically a congenital issue.

48
Q

What is false diverticulosis?

A

False diverticulosis involves only the mucosa and submucosa and is acquired, generally in adult population

49
Q

What causes diverticulitis?

A

Inflammation of diverticular outpouches due to obstruction which builds up the back pressure and causes the diverticula to distention, resulting in oedema and distention of the bowel containing faecal content, mucus and fluid and compresses arteries and venous congestion which increases the risk of bacterial colonisation

50
Q

What is the presentation of diverticulitis?

A

presents with left lower quadrant pain, and there is a fever and raised WBC. T

51
Q

What are complications of diverticulitis?

A
  • Abscess
  • Fistulas
  • Perforation.from distention causing compression of arteries, resulting in ischaemia and mean air leaks out, called pneumoperitoneum.
52
Q

What is the most common cause of large colonic blood loss?

A

Diverticular bleeding.

53
Q

Where is colon all weakest?

A

Colon wall is weakest between the mesenteric and anti mesenteric tendinae where vasa recta penates the muscle.

54
Q

What are signs of colonovesicular fistula?

A

Bubbling in urine and frequent UTI.

55
Q

How does peritonitis present?

A

Peritonitis findings are common in diverticulitis with extreme abdominal pain, rigidity of abdomen, rebound tenderness and increased QBC and fever.

56
Q

What are the diagnostic tools for diverticular disease?

A
  • Colonoscopy
  • CT abdomen and pelvis.
57
Q

What sign indicates a colonovesicular fistula?

A

Bubbling in urine and frequent UTI

58
Q

What is the initial diagnostic tool for diverticular disease?

A

Colonoscopy unless patient is excessively bleeding and haemodynamically unstable

59
Q

What imaging is indicated for signs of diverticulitis?

A

Abdominal X-ray

60
Q

What complications can be assessed with a CT scan in diverticular disease?

A

Pockets of colon, bowel wall thickening, inflammation, pericolic collections, or enterovesocolic fistula

61
Q

What is the treatment for diverticulosis?

A

High fibre diet and treat bleeding guided by colonoscopy with thermal coagulation with adrenaline injection

62
Q

What antibiotics are used for uncomplicated diverticulitis?

A

Cefuroxime or ciprofloxacin for gram positives
metronidazole for anaerobes

63
Q

What is the treatment for perforated diverticulitis?

A

Emergency surgery with Hartmann’s procedure

Fistulas will be treated with surgical repiar

64
Q

How is diverticular bleeding managed?

A

Colonoscopy and thermal coagulation with adrenaline

65
Q

What are hemorrhoids?

A

Normal vascular cushions aiding in fecal continence that become symptomatic when irritated or displaced with venous dilatation, vascular thrombosis and rupture of anal subepithelial muscle.

peak prevalence of haemorrhoids between 45-65 years old

66
Q

What are the locations of internal and external hemorrhoids?

A

Internal above the dentate line; external below the dentate line

67
Q

What is the peak prevalence age for hemorrhoids?

A

45-65 years old

68
Q

What are the degrees of hemorrhoids?

A
  • First degree: bleeds
  • Second degree: bleeding and prolapse on straining but reduces spontaneously
  • Third degree: prolapse through anus on straining requiring manual replacement
  • Fourth degree: irreducibly prolapsed
69
Q

What are common features of hemorrhoids?

A
  • Bright red blood at end of bowel movement
  • Sensation of fullness in rectum
  • Mucus discharge At end of bowel movement or in toilet paper
  • Incontinence
  • Pruritus
70
Q

What are the features of external haemorrhoids?

A

External haemorrhoids features include a perianal mass/swelling that is visible which is firm and purple and tender to touch. Bleeding is a major risk from ulcerated external haemorrhoid which is darker blood with clots and there is typically very painful due to thrombosis of vessels. Painless external skin tags may be present which may be a sin of previous haemorrhoidal or fissure disease

71
Q

What are the risk factors for hemorrhoids?

A
  • Constipation
  • Pregnancy
  • Obesity
  • Portal hypertension
  • Heavy lifting
72
Q

What is the treatment for hemorrhoids?

A
  • High fibre diet
  • Sitz bath ( warm shallow bath to cleanse the perineum)
  • Steroid cream
  • Pramoxine (anaesthetic and anti-priuretic)
  • Rubber band ligation or photocoagulation
  • Stapled hemorrhoidopexy
73
Q

What is an anal fissure?

A

A superficial tear in the skin below the pectinate line. The most common location of anal fissure is the posterior midline which receives the lowest perfusion of the canal. As sphincter pressure increases, canal perfusion decreases.

74
Q

What are common causes of anal fissures?

A
  • Constipation
  • Sexual intercourse
  • Childbearing
  • STDs
  • Cancer
75
Q

What are the symptoms of anal fissures?

A
  • Anal pain worse with defecation
  • Blood with defecation
  • Tenderness on palpation
76
Q

What distinguishes acute from chronic anal fissures?

A

Acute is less than 6 weeks; chronic is more than 6 weeks

77
Q

What is the most common location for anal fissures?

A

Posterior midline

78
Q

What is the treatment for anal fissures?

A
  • Stool softeners
  • Sitz baths
  • High fibre diet
  • Topical analgesics like lidocaine
  • Nifedipine to reduce sphincter tone
79
Q

What are the complications of hemorrhoidectomy?

A

haemorrhoidectomy is a very painful operation, so patients should eat high fibre diet and take stool softeners prior to this.

  • Anal stricture
  • Blood clots
  • Incontinence
  • Urinary retention
  • Stroke
80
Q

What genetic conditions are commonly associated with colorectal cancer?

81
Q

What is the mean age of onset for colorectal cancer?

A

70 years old and has he second highest mortality rate after lung cancer.

82
Q

What are common risk factors for colorectal cancer?

A
  • Older age above 50
  • Family history
  • History of IBD
  • Low fibre diet high in processed foods
  • Smoking
  • Alcohol consumption
  • High BMI
83
Q

What is the most common type of colorectal cancer?

A

Adenocarcinoma

84
Q

What are the common presentations of colorectal cancer?

A
  • Asymptomatic
  • Abdominal pain
  • Stool changes With alternating constipation anddiarrhoea
  • Weight loss
  • Melena/haematochezia
85
Q

What is the typical screening method for colorectal cancer?

A

Fecal immunochemical test

86
Q

When does screening for colorectal cancer begin?

A

age 50
-> Fhx of colorectal cancer means screening is from 40

87
Q

What is the staging system used for colorectal cancer?

A

TNM system

88
Q

What is FAP?

A

Family adenomatous polyposis is an autosomal dominant condition caused by a mutation of APC tumour suppressor gene resulting in many polyps forming and more polyps are more likely to form an adenocarcinoma and all patients with this will develop colorectal cancer, therefore prophylactic colectomy is essential.

89
Q

What are the subtypes of FAP?

A

Turcot syndrome is where tumours from in the CNS and Gardner syndrome is tumours in the gut and soft tissue and osteomas of mandible and skull(bones like jaw).

90
Q

What is the presentation of FAP?

A

They present with non specific symptoms like diarrhoea, aomdinal discomfort and rectal bleeding.

91
Q

What is the treatment for Family Adenomatous Polyposis (FAP)?

A

definitive management is removing the entire colon and rectal issue at risk, with ideal pouch-anal anastomosis which removes the entire colon and rectum.

92
Q

What syndrome is characterized by CNS tumors and is associated with FAP?

A

Turcot syndrome

93
Q

What is Lynch syndrome also known as?

A

HNPCC is more common and 80% of patients will develop colon cancer. HNPCC is caused by a DNA mismatch repair with microsatellite (nucleotide repair) instability, typically associated with a BRAF mutation and absence of polyps and there is a high risk of accelerated tumour formation

94
Q

How is Lynch syndrome diagnosed?

A

PCR reaction
immunohistochemical staining for mismatch repair proteins and general genetic testing.

95
Q

What is the typical management for patients with Lynch syndrome?

A
  • Daily aspirin
  • Regular colonoscopy
    From 20-25 years old, there will be 2 yearly colonoscopy until 75 years old
96
Q

What are the clinical features of colorectal cancer?

A
  • Change in bowel habit
  • Obstruction symptoms
  • Bleeding
  • Local invasion pain

Obstruction from tumour causes constipation, distention, pain, nausea and vomiting this is more common in sigmoid/descending/transverse colon. As the tumours enlarge, they can narrow the bowel lumen and cause diarrhoea but ectal tumours can lead to tenesmus. Bleeding is occult and presents as iron-deficiency anaemia in the right colon but left sided or rectal tumours appear as bright red. Local invasion of tumour produces pain and invovles bladder invasion, ureteric obstruction or malignant fistulasaion Cachexia, particularly of subcutaneous

97
Q

What urgent treatment is required for unstable rectal bleeding?

A

Packed RBCs or endoscopic hemostasis methods

98
Q

What surgical treatments may be indicated for ongoing lower GI bleeding?

A
  • Rubber band ligation
  • Inferior mesenteric vein occlusion
  • Portocaval shunting
99
Q

Which chronic diseases cause malnutrition?

A

Chronic kidney disease
Heart failure
COPD