Digestive Disorders Flashcards

GORD, Peptic Ulcer Disease, Chronic Inflammatory Bowel Disease, Bowel Cancer, Hepatobiliary Disease, Diabetes Mellitus

1
Q

Gastro-Oseophageal Reflux Disease (GORD): Aetiology and pathophysiology

A

dysfunction of lower osephageal sphincter (type of muscle) -> results in tonic contraction failure
-> leads to regurgitation of gastric contents into the osephagus
Sphincter dysfunction is due to altered neuromuscular control -> which means the osephagus will not be clear of contents -> increases mucosal damage

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2
Q

Gastro-Oseophageal Reflux Disease (GORD): contributing factors

A

the capability of nervous system innervation and gastrointestinal motility (movement of food down GI tract) are contributing factors in GORD development
other contributing factors: gastric and abdominal distension (swelling/bloating), delayed gastric emptying, increased secretion of pro-inflammatory mediators (these tend to cause inflammation), increased intragastric and abdominal pressure, poor posture, obesity and smoking
genetic link suggested by higher rate of symptoms in relatives of affected individuals

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3
Q

Gastro-Oseophageal Reflux Disease (GORD): Clinical Manifestations

A

Symptoms:
Adults: heartburn, regurgitation, epigastric (upper abdominal region), nausea, flatulence (fart), chronic cough, hoarseness, and ear ache.
Infants: difficult to distinguish from normal gastro-oseophageal reflux, characterised regurgitation.

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4
Q

Gastro-Oseophageal Reflux Disease (GORD): Diagnosis and Management

A

Diagnosis and Management:
gastroscopy: visualises mucosa, monitors osephagitis severity, confirms or excludes other dieases
lifestyle modifications are essential, including weight management to prevent obesity
decrease gastric secretion: avoid large meals and wait several hours after eating before lying down.
Mild intermittent symptoms: initial treatment with antacids
persistent symptoms: use drugs that reduce gastric secretion

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5
Q

Peptic Ulcer Disease: Aetiology and Pathophysiology

A

Peptic Ulcer: erosive injury to the mucosa layer of digestive organs
exposes underlying smooth muscle, blood vessels, and sensory nerves to GI contents
typically develops in the stomach or small intestine, occasionally in the oseophagus
Two primary mechanisms for mucosal damage:
1) aggressive action of gastric juices (stomach acid and pepsin) on the mucosa
2) weakened mucosa protection
Inflammatory processes trigger both mechanisms

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6
Q

Peptic Ulcer Disease: Clinical Manifestations

A

Common symptoms: pain, nausea, vomiting, bloating, weight loss, and loss of appetite
Pain is epigastric, burning, and occurs when the stomach is empty (before meals and overnight).

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7
Q

Peptic Ulcer Disease: Diagnosis and Management

A

Diagnosis and Management:
Hematology and biochemistry values help identify associated issues but does not confirm diagnosis
stopping non-steroid anti-inflammatory drugs and smoking is crucial
eliminating infection promotes healing and prevents relapse and recurrent bleeding

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8
Q

Ulcerative colitis: Aetiology and Pathophysiology

A

involves abnormal immune activation causing inflammation of large intestine epithelium
inflammation typically starts in the rectum and progresses proximally
usually restricted to the epithelial tissue layer

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9
Q

Ulcerative colitis: Clinical manifestations

A

Symptoms: include rectal bleeding, diarrhea, and ineffective straining to defecate
may experience cramping and weight loss
severe cases cause systemic symptoms like fever, tachycardia, and hypotension due to volume depletion

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10
Q

Ulcerative colitis: Diagnosis and Management

A

Diagnosis and management:
diagnosis involves a Full blood examination and relevant chemical pathology tests, often revealing anemia and electrolyte imbalance
stool analysis helps confirms or rule out other causes of symptoms
colonoscopy is the best imaging technique, allowing direct visualisation and biopsy of affected tissues
anti-inflammatory drugs are commonly used to reduce bowel inflammation

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11
Q

Crohn’s disease: Aetiology and Pathophysiology

A

linked to factors such as immune disorders, infections, allergies and genetic influences
can occur anywhere in the digestive tract but is most common in the ileum
inflammation affects all four layers of the intestinal wall

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12
Q

Crohn’s Disease: Clinical Manifestations

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Symptoms are highly variable and may include malaise, lethargy, anorexia, abdominal pain, fever, malabsorption, nutritional deficiency, diarrhea, bowel obstruction, abscesses (painful pocket of pus), fitsulas (abnormal connections between organs)
disease follows a pattern of remission and relapse but is lifelong

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13
Q

Crohn’s Disease: Diagnosis and Management

A

X-rays help assess severity and extent of the disease.
Colonoscopy allows for biopsy and direct observation of epithelium and lesions.
Other imaging techniques like CT, MRI, and ultrasonography may also be useful.
Anti-inflammatory and immunosuppressive drugs are used for treatment.
Symptom relief includes anti-diarrheal agents and antispasmodics (drugs that help relax the smooth muscles of like digestive organs) for abdominal cramping pain.

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14
Q

Bowel Cancer: Aetiology and Pathophysiology

A

most frequent malignancy of the digestive tract
almost always occurs in the large intestine, with tumour growth in the small intestine being rare
tumours in the proximal colon extend along one wall
Distal colon tumours grow as a ring causing bowel constriction and obstruction
Most colon cancers are adenocarcinomas (glandular like) located in the rectum and sigmoid colon
risk factors include age (60-70 years, and chronic inflammatory conditions like ulcerative colitis
continuous regeneration of intestinal epithelial cells –> increases the likelihood of spontaneous mutations

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15
Q

Bowel Cancer: Clinical Manifestations

A

early stage colon cancer is often asymptomatic and can grow for years before diagnosis
symptoms in advanced stages include abdominal discomfort, bowel habits, pain, fatigue, anorexia, and weight loss
Acute symptoms like nausea, vomiting, pain and fever may arise from obstruction or perforation
symptoms vary based on tumour location

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16
Q

Bowel Cancer: Diagnosis

A

Diagnosis typically begins with a physical examination to detect swellings or lumps.
Colonoscopy is the primary diagnostic tool, allowing for biopsies to identify cancer type, differentiation, and staging.
Additional imaging techniques like CT, PET, and MRI scans are used to stage the cancer and identify metastases.
The stage of cancer at diagnosis determines the management approach.
Surgery, such as colectomy or colostomy, may be indicated based on the extent of the cancer.
Chemotherapy is a principal treatment used in almost all stages of colon cancer, both pre- and post-surgery.
Immunomodifying agents are becoming more common, and radiotherapy may be used for rectal cancer but is not standard for colon cancer.

17
Q

Bowel Cancer: Management

A

Diet high in fresh fruits, vegetables, and white meat is preferable to one rich in red meat and highly processed foods.
Reducing smoking and alcohol intake and maintaining a healthy waist-to-hip ratio may also be beneficial.

18
Q

Hepatobiliary Diseases

A

cause major function alterations:
- damage or death of liver cells and reduced liver function
fibrosis and scarring
portal hypotension
impaired bile excretion and pain

19
Q

Viral Hepatitis: Aetiology and Pathophysiology

A

Hepatitis is liver inflammation associated with hepatocyte damage
causes: microbial agents or chemical toxicity
Hepatitis viruses are significant pathogens
–> Hepatitis A and E spread through fectal-oral route
–> Hepatitis B,C, D and G are transmitted through blood and bodily fluids

20
Q

Viral Hepatitis: Clinical Manifestations, Diagnosis and Management

A

Symptoms: pain, fever, anorexia, nausea, vomiting, Jaundice
symptoms may be absent in some cases
Diagnosis and Management:
diagnosed through serological testing revealing elevated liver enzymes and possibly reduced albumin levels
no specific treatment for acute viral hepatitis; management focuses on hydration and symptom relief
Prevention is crucial

21
Q

Fatty liver disease: Aetiology and Pathophysiology

A

Associated with alcohol abuse or excessive fat and monosaccharide intake
two forms: alcoholic liver intake, and non-alcoholic fatty liver disease
risk factors: type 2 diabetes, obesity, older age, metabolic syndrome
similar to viral hepatitis

22
Q

Fatty Liver Disease: Clinical Manifestations, Diagnosis and Management

A

early stages may be asymptomatic
symptoms: GI malaise (discomfort), mild fever, serious manifestations over time
Diagnosis and Management:
comprehensive history of alcohol intake
liver function tests, possibly liver biopsy
restraining from alcohol in order to manage alcoholic liver disease
nutritional support and dietary supplements of micro-nutrients are important
corticosteroid anti-inflammatory agents may reduce inflammation

23
Q

Gallstones: Aetiology and Pathophysiology

A

Risk factors: age, female sex, pregnancy, obesity, metabolic syndrome, genetic predisposition, low physical activity
cholesterol in bile may suddenly turn into crystals forming gallstones
gallstones usually form in the gallbladder, less commonly in bile ducts

24
Q

Gallstones: Clinical Manifestations, Diagnosis, and Management

A

may be asymptomatic
problems arise when stones start to block bile and pancreatic ducts -> causes upper abdominal pain and acute gallbladder inflammation
Diagnosis and Management:
ultrasound is preferred
CT scan identifies the precise location of the stones and assesses the extent/severity of the stones.

25
Q

Diabetes Mellitus

A

metabolic disorder characterised by abdominal insulin secretion and/or action
leads to hyperglycemia which is a defining feature
patients may exhibit features of multiple forms or switch types overtime
severe imbalance between insulin supply and demand leads to similar metabolic effect and complications
Commonality: insulin dysfunction and hyperglycemia.

26
Q

Type 1 Diabetes Mellitus: Aetiology and Pathophysiology

A

extensive damage to insulin-producing cells in the pancreas
caused by an autoimmune attack from the immune system
insulin production decreases, leading to insulin deficiency
can develop at any age, peak diagnosis age 10-19 years
develops slowly over several years or rapidly

27
Q

Type 2 Diabetes Mellitus: Aetiology and Pathophysiology

A

patient can produce insulin, but release is dysfunctional
characterised by reduced insulin sensitivity in muscle, adipose tissue and liver –> results from decreased insulin receptors or problems with cell signaling
pancreatic cells cannot compensate, leading to hyperglycemia
influenced by genetic predisposition and lifestyle factos e.g. diet, activity levels
strongly associated with obesity, especially central fat deposits
more prevalent than other diabetes forms

28
Q

Hyperglycemia

A

causes dehydration and increased thirst (polydipsia)
increased blood volume leads to frequent urination (polyuria)
kidneys cannot absorb glucose, so it excretes excess glucose into urine

29
Q

Hypoglycemia

A

blood glucose levels drop due to an imbalance between eating, activity levels, and medication
missing meals, excessive exercise, overdosing medication can lead to hypogylcemic state
disrupts brain function, rapid development, triggers SNS
Symptoms: concentration lapses, headaches, irritability, tremors, clammy skin, HR and BP changes
advanced hypoglycemia can cause seizures, coma and even death

30
Q

Acute complications of Diabetes Mellitus

A

Normal BGL: 4-8mmol/L
Hyperglycemia: >11 mmol/L after meals
Hypoglycemia: <3 mmol/l

31
Q

Chronic complications of Diabetes Mellitus

A

poor glucose control and chronic hyperglycemia affect cardiovascular, renal, nervous and visual systems
chronic issues: HT, coronary heart disease, stroke, peripheral vascular disease, renal impairment/failure, ANS impairments etc.

32
Q

Diabetes: Diagnosis and Management

A

Diagnosis: through clinical manifestation, patient history, and blood glucose testing

obesity in T2 diabetes: measuring body fat aids diagnosis
oral glucose tolerance teat (OGTT) and glycosylated hemoglobin (HbA1c) levels are important diagnostic measures
treatment goals: normal BGL, minimise acute complications rise, prevent chronic complications, improve QOL
Patient education on risk factors, disease processes, and management
Good meal planning and exercise to align BGL with insulin action
T1 Diabetes: insulin replacement therapy
T2 Diabetes: some patients may require oral hypo-glycemic agents