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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
Dental considerations of decompensated cirrhosis
Thrombocytopenia and cogulotherapy are likely to be issues, give vit K prior to procedures if INR is raised.
26
DEntal considerations post transplant
Poor dentition pre transplant is common, immunosuppressants, opportunistic infection, long term steroids can reduce bone density.
27
What are the functions of the stomach?
Storage, absorption, mechanical breakdown, digestion, sterilisation, neuroendocrine
28
What are the functions of the small intestine?
Motility, absorption, immunological, mixing and chemical digestion.
29
functions of the large intestine
Motility and expulsion, micro biome, absorption and storage.
30
what is inflammatory bowel disease?
A group of autoimmune diseases causing inflammation of the GI tract.
31
Explain the aetiology of IBD
It is unknown but it is likely to be an interaction between a genetic predisposition, environmental factors and the hosts immune response.
32
What genetic factors increase IBD?
First degree relatives
33
What are environmental factors that affect IBD?
Smoking, the pill, measles, mycobacterium Adium paratuberculosis
34
What is the histology of ulcerative Colitis?
Distortion of crypt architecture, ulceration confined to submucosa, abscesses, pseudopolyps andinflammtory cells in lamina propria.
35
Histology of Chrons Disease
Fistulation, ulceration, granulomata, ship lesions, cobblestone.
36
What is the distribution of Chrons disease?
Anywhere from the mouth to the anus and can healthy patches in between ship lesions.
37
What is the clinical presentation of Chrons disease?
Abdominal pain, bloody stools, weight loss, prolonged diarrhoea, fatigue and extra GI manifestations.
38
what is a fistula?
an abnormal connection between two epithelial is surfaces.
39
What are some Oral manifestations in Chrons
Persistent enlargement of the lips, full width gingivitis and gingival enlargement, fissuring of the tong.
40
How can you diagnose Chrons?
Rio tudie, stool samples, CT, faecal cal protein and lactoprotein
41
Complications of inflammatory bowel disease
Stenosis and obstruction, nutritional inadequacy, short bowel spasms and osteoporosis.
42
Management of Chrons
Smoking cessation, surgical, nutritional, steroids, psychological.
43
What is gastro-oesophageal reflux disease?
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
How does gastro-oesophageal reflux disease present?
With dysphasia
45
What are the risk factors of GORD
Obesity, alcohol, smoking, pregnancy, coffee, fatty foods and calcium channel blockers
46
What is the management of GORD?
A trial of proton pump inhibitors
47
What are some complications of GORD?
Oesophageal ulcer, haemorrhage or perforations, Barrett’s oesophagus
48
What is Barret’s Oesophagus?
A change is squamous epithelium of the oesophagus to columnar epithelium.
49
What is a peptic ulcer?
A break in the mucosal lining of the stomach or duodenum more than 5mm in diameter with depth to the submucosa.
50
What is the presentation of a peptic ulcer?
Abdominal pain, epigastric tenderness and weight loss
51
If a patient with a peptic ulcer is actively bleeding, what should you do?
ABCD resuscitation
52
What is helicabacter pylori?
It is a gram negative bacteria found i the stomach
53
How does H pylori infect a person?
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
What is oesophageal cancer?
A squamous cell carcinoma caused by alcohol and smoking and GORD
55
What are the stages of cancer?
0- in situ 1 - localised 2 - early locally advanced 3 - late early advanced 4 - metastasised
56
Where are the kidneys?
They sit at T12-13
57
How are the kidneys supplied?
they are supplied by the renal artery, it flows out of the renal vein
58
What are some unusual anatomies of the kidneys?
Some sit over the midline also known as horseshoe kidneys. And sometimes one may be found in the pelvis due to a transplant.
59
Detail the micro anatomy of the kidneys
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
What is the corpuscle?
Where blood is brought into the glomerus and allows the loss of material out of the discerning membrane.
61
Why is the glomerus knotted?
To increase the surface area and the pressure in the system.
62
What is glomerular filtration rate (GFR)?
The volume of blood passing through the glomeruli/minute.
63
What is tubular reabsorption?
Where the body decides what should or shouldn't be reabsorbed through the renal tubule.
64
What is the collecting duct?
It connects nephrons to the renal pelvis and it collects urine.
65
What is the Renin-angiotensin System?
It is a system in place for when blood pressure drops.
66
What occurs when blood pressure drops?
The glomerus alerts the low pressure and renin is released into the blood. It turns into angiotensin which increases the blood pressure.
67
What is the antidiuretic hormone?
It causes a rise in plasma osmolality and it is what moves water out of the duct when water is absorbed.
68
What are some renal function tests?
GFR, measuring urea and blood, urine dip tests.
68
What are some renal function tests?
GFR, measuring urea and blood, urine dip tests.
69
What is acute renal injury?
Where there is an acute decline in GFR.
70
What are the three types of renal injury?
Pre, renal and post
71
What is the presentation of acute renal failure?
Reduced urine output, dizziness, vomiting, hypotension and tachycardia.
72
What are the risk factors of acute renal failure?
Age, chronic renal disease and diabetes.
73
Management of acute renal injury?
volume expression and tretment of underlying causes.
74
What is Chronic renal disease?
A pathological abnormality of the kidney. Reduction in GFR for more than 3 months.
75
Risk factors of chronic renal diease?
Age and diabetes
76
What is the aetiology of chronic renal disease?
It affects more people with diabetes and hypertension
77
What is the presentation of chronic renal disease?
Fatigue, oedema, nausea, pruitus, anorexia, hyperplasia and bleeding tendency.
78
Dentlal considerations for renal disease?
Best treated the day after dialysis, can be predisposed to blood borne viruses.
79
Transplant considerations to be made?
They are immunosuppressed for life. Cyclosporine can cause gingival hyperplasia.

HHD 2 (5 decks)

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