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HHD 2 > The GI system and Diseases > Flashcards

The GI system and Diseases Flashcards

1
Q

Describe the difference between first and second pass

A

If drugs are taken unmetabolised it won’t go to the liver straight away but will on the second pass when it has entered the blood stream.

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2
Q

What are the benefits of first pass

A

It provides a stronger and quicker effect

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3
Q

What are 4 alcohol related diseases?

A

Acute alcoholic hep,pancreatitis, coma, chronic liver disease

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4
Q

What does alcohol mean in dentistry?

A

People are more susceptible to erosion from sugar and vomiting, at risk of halitosis, tooth. Staining, oral cancer, dental trauma, poor OH

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5
Q

What is chronic liver disease caused by?

A

Continuous or repetitive injury to the liver which results in inflammation.

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6
Q

What are some causes of Chronic liver disease?

A

Alcohol, obesity, viral hep.

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7
Q

What does alcohol, obesity and viral hepatitis lead to?

A

The accumulation of fatty deposits in the liver to host immunity causing inflammation.

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8
Q

What is the acute liver disease presentation?

A

Abdominal pain, weight loss/gain, malnutrition, anorexia, fatigue and a build up of fluid in the peritoneal cavity.

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9
Q

What are the signs of liver disease?

A

Leukaemia, palmar erythema, spide naevi, finger dubbing

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10
Q

What are some conditions relating to liver disease?

A

Portal hypotension and jaundice.

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11
Q

Acute liver disease diagnosis

A

Raised ASD/ALT, normal or elevated ALP, ultrasound

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12
Q

Management of ALD

A

First line is alcohol abstinence with alcohol withdrawal and management. Weight reduction and nutritional support

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13
Q

Dental considerations of liver disease

A

May withdraw over night, may be resistant to sedation and benzodiazepines.

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14
Q

NAFLD pathophysiology

A

Stenosis,causes inflammation or NASH with the end result being cirrhosis and scarring.

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15
Q

End stage NAFLD solutions

A

transplant, bypass jugular system so it isn’t connected to the portal system

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16
Q

How is Hep A transmitted?

A

Through faeco-oral and causes acute infection (VACCINE)

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17
Q

What is Hep B?

A

Transmitted via sexual contact, blood. Ca come in acute and chronic forms (VACCINE)

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18
Q

What is Hep C?

A

Transmitted via blood and is 80% chronic with acute rarely being symptomatic (NO VACCINE)

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19
Q

Explain the management of Hep B

A

Monitoring when in low risk phase. Treatment with interferon to regain immune control

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20
Q

What are the stages of Cirrhosis?

A

compensated and decompensated.

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21
Q

Explain the compensated stage of cirrhosis

A

Biochemical, radiological or histological findings consistent diagnosis of cirrhosis

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22
Q

Explain the decompensated stage of cirrhosis.

A

Reduced hepatic synthetic unction and portal hypertension.

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23
Q

What are some complication of cirrhosis?

A

Jaundice, coagulotherapy, portal hypertension, hepatocellular carcinoma, malnutrition, susceptibility to infection

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24
Q

Dental consideration of compensated cirrhosis

A

Check FBC andINR prior to procedures, reduction of paracetamol, may be sensitive to opiates, alcohol dependence.

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25
Q

Dental considerations of decompensated cirrhosis

A

Thrombocytopenia and cogulotherapy are likely to be issues, give vit K prior to procedures if INR is raised.

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26
Q

DEntal considerations post transplant

A

Poor dentition pre transplant is common, immunosuppressants, opportunistic infection, long term steroids can reduce bone density.

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27
Q

What are the functions of the stomach?

A

Storage, absorption, mechanical breakdown, digestion, sterilisation, neuroendocrine

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28
Q

What are the functions of the small intestine?

A

Motility, absorption, immunological, mixing and chemical digestion.

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29
Q

functions of the large intestine

A

Motility and expulsion, micro biome, absorption and storage.

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30
Q

what is inflammatory bowel disease?

A

A group of autoimmune diseases causing inflammation of the GI tract.

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31
Q

Explain the aetiology of IBD

A

It is unknown but it is likely to be an interaction between a genetic predisposition, environmental factors and the hosts immune response.

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32
Q

What genetic factors increase IBD?

A

First degree relatives

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33
Q

What are environmental factors that affect IBD?

A

Smoking, the pill, measles, mycobacterium Adium paratuberculosis

34
Q

What is the histology of ulcerative Colitis?

A

Distortion of crypt architecture, ulceration confined to submucosa, abscesses, pseudopolyps andinflammtory cells in lamina propria.

35
Q

Histology of Chrons Disease

A

Fistulation, ulceration, granulomata, ship lesions, cobblestone.

36
Q

What is the distribution of Chrons disease?

A

Anywhere from the mouth to the anus and can healthy patches in between ship lesions.

37
Q

What is the clinical presentation of Chrons disease?

A

Abdominal pain, bloody stools, weight loss, prolonged diarrhoea, fatigue and extra GI manifestations.

38
Q

what is a fistula?

A

an abnormal connection between two epithelial is surfaces.

39
Q

What are some Oral manifestations in Chrons

A

Persistent enlargement of the lips, full width gingivitis and gingival enlargement, fissuring of the tong.

40
Q

How can you diagnose Chrons?

A

Rio tudie, stool samples, CT, faecal cal protein and lactoprotein

41
Q

Complications of inflammatory bowel disease

A

Stenosis and obstruction, nutritional inadequacy, short bowel spasms and osteoporosis.

42
Q

Management of Chrons

A

Smoking cessation, surgical, nutritional, steroids, psychological.

43
Q

What is gastro-oesophageal reflux disease?

A

It is symptom or complications resulting from the reflux of gastric contents into the oesophagus . The lower oesophageal sphincter relaxation causes reflux of gastric contents into the oesophagus.

44
Q

How does gastro-oesophageal reflux disease present?

A

With dysphasia

45
Q

What are the risk factors of GORD

A

Obesity, alcohol, smoking, pregnancy, coffee, fatty foods and calcium channel blockers

46
Q

What is the management of GORD?

A

A trial of proton pump inhibitors

47
Q

What are some complications of GORD?

A

Oesophageal ulcer, haemorrhage or perforations, Barrett’s oesophagus

48
Q

What is Barret’s Oesophagus?

A

A change is squamous epithelium of the oesophagus to columnar epithelium.

49
Q

What is a peptic ulcer?

A

A break in the mucosal lining of the stomach or duodenum more than 5mm in diameter with depth to the submucosa.

50
Q

What is the presentation of a peptic ulcer?

A

Abdominal pain, epigastric tenderness and weight loss

51
Q

If a patient with a peptic ulcer is actively bleeding, what should you do?

A

ABCD resuscitation

52
Q

What is helicabacter pylori?

A

It is a gram negative bacteria found i the stomach

53
Q

How does H pylori infect a person?

A

It penetrates the mucous innings of the stomach to find a less acidic region. Urease breaks down urea to CO2 an ammonia which is toxic to cells.

54
Q

What is oesophageal cancer?

A

A squamous cell carcinoma caused by alcohol and smoking and GORD

55
Q

What are the stages of cancer?

A

0- in situ
1 - localised
2 - early locally advanced
3 - late early advanced
4 - metastasised

56
Q

Where are the kidneys?

A

They sit at T12-13

57
Q

How are the kidneys supplied?

A

they are supplied by the renal artery, it flows out of the renal vein

58
Q

What are some unusual anatomies of the kidneys?

A

Some sit over the midline also known as horseshoe kidneys. And sometimes one may be found in the pelvis due to a transplant.

59
Q

Detail the micro anatomy of the kidneys

A

Blood is brought in by an afferent arteriolar which forms itself into a knotted structure known as a glomerulus ad then the blood is taken away by a efferent arteriole and blood goes into the vein.

60
Q

What is the corpuscle?

A

Where blood is brought into the glomerus and allows the loss of material out of the discerning membrane.

61
Q

Why is the glomerus knotted?

A

To increase the surface area and the pressure in the system.

62
Q

What is glomerular filtration rate (GFR)?

A

The volume of blood passing through the glomeruli/minute.

63
Q

What is tubular reabsorption?

A

Where the body decides what should or shouldn’t be reabsorbed through the renal tubule.

64
Q

What is the collecting duct?

A

It connects nephrons to the renal pelvis and it collects urine.

65
Q

What is the Renin-angiotensin System?

A

It is a system in place for when blood pressure drops.

66
Q

What occurs when blood pressure drops?

A

The glomerus alerts the low pressure and renin is released into the blood. It turns into angiotensin which increases the blood pressure.

67
Q

What is the antidiuretic hormone?

A

It causes a rise in plasma osmolality and it is what moves water out of the duct when water is absorbed.

68
Q

What are some renal function tests?

A

GFR, measuring urea and blood, urine dip tests.

68
Q

What are some renal function tests?

A

GFR, measuring urea and blood, urine dip tests.

69
Q

What is acute renal injury?

A

Where there is an acute decline in GFR.

70
Q

What are the three types of renal injury?

A

Pre, renal and post

71
Q

What is the presentation of acute renal failure?

A

Reduced urine output, dizziness, vomiting, hypotension and tachycardia.

72
Q

What are the risk factors of acute renal failure?

A

Age, chronic renal disease and diabetes.

73
Q

Management of acute renal injury?

A

volume expression and tretment of underlying causes.

74
Q

What is Chronic renal disease?

A

A pathological abnormality of the kidney. Reduction in GFR for more than 3 months.

75
Q

Risk factors of chronic renal diease?

A

Age and diabetes

76
Q

What is the aetiology of chronic renal disease?

A

It affects more people with diabetes and hypertension

77
Q

What is the presentation of chronic renal disease?

A

Fatigue, oedema, nausea, pruitus, anorexia, hyperplasia and bleeding tendency.

78
Q

Dentlal considerations for renal disease?

A

Best treated the day after dialysis, can be predisposed to blood borne viruses.

79
Q

Transplant considerations to be made?

A

They are immunosuppressed for life. Cyclosporine can cause gingival hyperplasia.

HHD 2 (5 decks)

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