Respiratory, GI and Liver Revision Flashcards

1
Q

What is the normal blood pH range?

A

7.35-7.45. Above 7.45= alkalosis. Below 7.35= Acidosis. Outside 6.8 and 7.7=cell death

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2
Q

What are the possible causes of respiratory acidosis (hypoventilation Pco2 >45mmHg; pH <7.35).

A

Impaired lung function such as chronic bronchitis, CF, emphysema= impaired gas exchange or alveolar ventilation.

Impaired ventilator movement: paralysed respiratory muscles, chest injury, extreme obesity.

Narcotic or barbiturate overdose or injury to brain stem: depression of respiratory centres, resulting in hypoventilation and respiratory arrest.

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3
Q

What are the possible causes of respiratory alkalosis (hypoventilation PCo2 <35mmHg, pH >7.45))

A

Strong emotions- pain, fear, panic attack.
Hypoxemia: Asthma, pneumonia, high altitude, represents efforts to raise P02 at the expense of excessive Co2 excretion
Brain tumour or injury: abnormal respiratory controls

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4
Q

What are the possible causes of metabolic acidosis? (HCO2 <22, PH <7.35)

A

Severe diarrhoea: bicarb rich intestinal and pancreatic secretions rushed through the digestive tract before their solutes can be reabsorbed; bicarbonate ions are replaced by renal mechanisms that generate new bicarb ions.

Renal disease: failure of kidneys to rid body of acids formed by normal metabolic processes

Untreated diabetes mellitus: lack of insulin or inability of tissue cells to respond to insulin, resulting in inability to use glucose; fats are used as primary energy fuel, and KA occurs

Starvation: lack of dietary nutrients for cellular fuels; body proteins and fat reserves are used for energy- both yield acidic metabolites as they are broken down for energy

Excess alcohol ingestion: results in excess acids in blood

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5
Q

Metabolic alkalosis (HCo2 >26, pH >7.45).

A

Vomiting or gastric suctioning: loss of stomach HCL requires that H- be withdrawn from blood to replace stomach acid: thus H+ decreases and HC02 increases.

Selected diuretics: K+ depletion and H20 loss. Low K+ directly stimulates tubule cells to secrete H+. Reduced blood volume elicits the renin-angiotensin-aldosterone mechanism, which stimulates Na+ reabsorption and H+ secretion.

Ingestion of excessive sodium bicarb (antacid): bicarb moves easily into ECF, where it enhances natural alkaline reserve

Excess aldosterone (eg adrenal tumours)- promotes excessive reabsorption of Na+, which pulls increased amount of H+ into urine. Hypovolemia promotes the same relative effect because aldosterone secretion is increased to enhance Na+ and H20 reabsorption.

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6
Q

What are restrictive defects?

A

Those that decrease compliance of the lungs or chest wall

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7
Q

What are obstructive defects?

A

Those that block the exchange of air to and from the lungs

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8
Q

What are some ventilator function tests?

A

Spirometer; FEv1 (the forced expiratory volume in one second- the normal value for this is 80%); Forced Vital Capacity- the maximal amount of air that can be expired

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9
Q

What is COPD?

A

Chronic Obstructive Pulmonary Disease- recurrent chronic productive cough for min of 3 months over the past 2 years; characterised by progressive development of airflow limitation, that is not fully reversible and destruction of the lung parenchyma. Airflow limitation is progressive and associated with an inflammatory response of the lung to noxious particles or gases

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10
Q

What is asthma?

A

A chronic inflammatory disorder of the airways characterised by reversible airflow obstruction and resulting in cough, wheeze, chest tightness and SOB

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11
Q

What is emphysema?

A

Decrease of elastic recall, destruction of alveolar walls produce dilated air spaces, less surface area for gas exchange, unsupported airways tend to collapse on expiration, obstruction small bronchioles, air trapping, exertion dyspnoea, weight loss, accessory muscle breathing

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12
Q

What happens during an asthma attack?

A

Bronchial hyperactivity (abnormal sensitivity to normal stimuli by an antigen). The smooth muscle cells in the bronchi constricts, the airways become inflamed (oedema) and swollen, increase in mucous production to produce mucus plugs. Breathing becomes difficult (dyspnoea), turbulent air produces a wheeze, SOB, chest tightness, dry, irritating cough

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13
Q

What is the management of obstructive lung disorder?

A

Nutritional intervention- chronic resp disease increases calorie required due to WOB; drugs- bronchodilators (short and long-acting), corticosteroids, antibiotics for infections, flu vac; pressured metered dose inhalers, nebs, ventilators, o2 therapy, self-management

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14
Q

What are the acquired GI disorders?

A

Gastritis, peptic ulcers, oesophageal ulcers, gastric ulcers, duodenal ulcers, ulcerative colitis, diverticulitis, polyps, cancer, adhesions, hernias

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15
Q

What is gastritis?

A

Inflammation of the gastric mucosa. May be acute or chronic, erosive or non-erosive. Erosive does not cause significant inflammation but can wear away the stomach lining- bleeding, erosions, ulcers.

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16
Q

What is the most common cause of erosive gastritis?

A

NSAIDS- eg aspirin and ibuprofen. Other agents include alcohol, cocaine, radiation, burns, major surgery or critical illness (stress induced).

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17
Q

What is the most common cause of non-erosive gastritis?

A

Helicobacter pylori (H.pylori) infection- infect the stomach lining.

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18
Q

What are the diagnostic tests for gastritis?

A

Endoscopy with a biopsy of the stomach. Other tests may include upper GI series: barium, xray to show changes in the stomach lining such as erosions of ulcers; Blood tests: anemia may be a sign of chronic bleeding in the stomach; stool test: presence of blood in the stool (melena); tests for H.pylori infection

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19
Q

What does the treatment for Gastritis include?

A

Medications that reduce the amount of stomach acid or treat cause including: Antacids, H2 Blockers, proton pump inhibitors, reduce dose of NSAIDs/switch to other class of pain meds, treat H.pylori infection.

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20
Q

What is a peptic ulcer?

A

A lesion in the gut lining of the stomach, duodenum or esophagus, which occurs when the lining of these organs is corroded by the acidic digestive juices that are secreted by the stomach cells. A peptic ulcer of the stomach= gastric

21
Q

What is the most common type of ulcer?

A

Duodenal- hypersecretion of acid and pepsin from stomach, which enters duodenum. Decreased bicarb production by pancreas may also contribute

22
Q

Why is the onset of oesophageal ulcer relatively fast?

A

Lining of oesophagus does not have same protection as stomach and duodenum; however least common type of peptic ulcer

23
Q

What is pancreatitis?

A

Inflammation, haemorrhage, fat necrosis of pancreatic fat , pancreatic necrosis

24
Q

Why does pancreatitis occur?

A

Due to local effect of proteolytic enzymes being inappropriately activated prior to leaving the pancreas and leaking into the interstitial space.
Acute- usually due to gallstones blocking the common duct or alcohol abuse; serum amylase and serum lipase levels elevated; inflammation and oedema in the retroperitoneum, can become systemic- 5% mortality
Chronic: mainly due to chronic alcoholism with calcification of pancreatic ducts, mild abdominal pain, diarrhoea, weight loss

25
Q

What are two inflammatory bowel diseases?

A

Crohn’s disease and ulcerative colitis.

26
Q

What is ulcerative colitis?

A

A type of inflammatory bowel disease that affects the lining of the large intestine (colon) and rectum; unknown cause. Begins in rectum and proceeds to entire colon.

27
Q

What are the symptoms ulcerative colitis?

A

Inflammation, ulceration, abscesses and denudation of mucosa; bloody diarrhoea, lower abdominal pain, fever
Normal mucosa is surrounding ulcerated “humps” to give appearance to pseudopolyps)
Loss of haustra (pipe-like appearance).

28
Q

What is Crohn’s diesase?

A

Inflammation of the submucosa lymphatics resulting in oedema, abscesses and ulcerations, which can affect any part of the GI tract (usually colon or distal ileum); cause unknown. Appearance of mucosa is the “cobblestone effect” due to areas of ulcers surrounding inflamed mucosa.

29
Q

What are the signs and symptoms of Crohn’s?

A

Mild pain, anorexia, fever but if severe: persistant pain, abdominal tenderness, diarrhoea, fistula formation, malnutrition, perianal disease (fissure, fistulas, abscesses).

30
Q

What is diverticulosis?

A

The process in which pockets or pouches are formed on the outside of the colon and large intestines. These pocket hernias are referred to as diverticula. The diverticula build up bacteria and infection causing diverticulitis.

31
Q

What are polyps?

A

Benign mucosal tumours that may be found along the length of the intestine. Colon cancer typically develops when benign colon polyps become cancerous (malignant), damaging intestinal tissues

32
Q

What are adhesions?

A

Bands of scar tissue between and around organs.

33
Q

What can cause adhesions?

A

Infection, surgery or trauma can cause adhesions to form within the body.

34
Q

What can adhesions cause?

A

Abdo pain and intestinal obstruction.

35
Q

How do hernias occur?

A

One part of the body protrudes through a gap, tear or opening into another part. There are two types that can cause digestive system disorders- Hiatal and Inguinal

36
Q

What is an hiatal hernia?

A

Forms at the opening in the diaphragm, where the oesophagus joins the stomach. Can allow food and acid to go back up into the oesophagus causing heartburn, chest pain, nausea.

37
Q

What is an Inguinal Hernia?

A

When soft tissue, often part of the intestine, protrudes through a weak point or tear in the lower abdominal wall. Inguinal hernias may occur as a result of muscle weakness, strenuous physical activity, excessive weight or excessive coughing.

38
Q

What are the two types of intestinal obstruction?

A

Mechanical- simple (luminal obstruction) or strangulated (luminal obstruction with ischaemia).
Non-mechanical/ functional- neurogenic (post-op).

39
Q

What is the pathophysiology behind intestinal obstruction?

A

Build up of fluid in lumen. Results in proximal distension to obstruction and distal collapse.

40
Q

What are the signs and symptoms of intestinal obstruction?

A

Anorexia: constipation/liquid stools/diarrhoea; Pain- severe (volvulus, perforation) or collicky pain (due to peristalsis); abdo tenderness of palpitation; rebound tenderness, sometimes guarding; nausea and vomiting.

41
Q

What are some complications associated with intestinal obstruction?

A

Perforation (acute emergency); peritonitis- infection of peritoneal cavity due to perforation or transduction of toxic intestinal contents.

42
Q

What are the main functions of the liver?

A

Elimination of bilirubin; production of bile salts; metabolism of drugs; metabolism of alcohol; metabolism of steroid hormones; metabolism carbs, fats, proteins; storage of minerals and vitamins; synthesis of plasma proteins and clotting factors.

43
Q

What are the metabolic functions of the liver?

A

Glucose- stored as glycogen, converted to glucose, used to make fats, formed from amino acids and other substrates.

Lipids- oxidised for energy, synthesised, packaged into lipoproteins

Proteins- synthesised from amino acids, transamination and deamination (ammonia made into urea).

44
Q

What is hepatitis?

A

Inflammation of the liver, if persists- fibrosis- cirrhosis. Often caused by viral infection (hepatitis virus) an alcoholism

45
Q

What is cholestasis?

A

A reduction or stoppage of bile flow leading to accumulation of bile, causing pruritus (severe itching of the skin), damage to liver cells, release of Alkaline phosphate (diagnostic blood marker) into blood.

46
Q

What are the consequences of liver damage?

A

Hepatocellular: injury to hepatocytes leads to cell necrosis. This causes decreased synthetic/metabolic activity and the release of intracellular contents (eg liver enzymes used in diagnosis).

Cholestasis: impaired bile formation by hepatocytes or impaired bile flow by blockage of the bile ducts/ductules causes a build-up in the blood of substances that are normally excreted in the bile (e.g. bilirubin and bile acids) and the synthesis and release of proteins from the apical membrane of duct cells (eg ALP).

47
Q

What is bilirubin?

A

Hemoglobin from old red blood cells becomes unconjugated bilirubin. The liver links unconjugated bilirubin in blood to glucuronide- conjugated bilirubin- bile.

Liver disease= excess unconjugated bilirubin in the blood- bilirubinemia- jaundice

48
Q

What are the three types of Jaundice?

A

Pre-hepatic (hemolytic): increased rate of breakdown of RBCs- eg haemolytic anemias, blood transfusion reactions, incompatible Rh factor in neonates.

Intrahepatic: damage to liver cells stop conjugation of bilirubin and/or its secretion; failure to process or secrete bile.

Posthepatic: bile flow is obstructed between the liver and intestines. Due to strictures of bile duct, gallstones, tumours of bile duct or pancreas etc.