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Year 2 Medicine @ Lancaster Uni > 2.04 - Upper GI disorders and Shock > Flashcards

2.04 - Upper GI disorders and Shock Flashcards

1
Q

From where does the upper GI tract run from and to?

A
  • From the mouth to the duodenal-jejunal junction
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2
Q

What are the main functions of the GI tract?

A
  1. Digestion
  2. Motility
  3. Secretion
  4. Absorption
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3
Q

What are the different layers of the GI tract?

A
  1. Mucosa
  2. Submucosa
  3. Muscularis externa
  4. Serosa
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4
Q

What is the structure and the function of the mucosa?

A
  • Made up of epithelium, lamina propia, muscularis mucosa
  • Provides important absorpative surface for nutrients that are ingested
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5
Q

What is the type of epithelium found in the mouth, oesophagus and pharynx?

A
  • Stratified squamous
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6
Q

What is the type of epithelium found in the stomach and duodenum?

A
  • Simple columnar
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7
Q

Where is smooth muscle found in the upper GIT?

A
  • All below 1/3 of oesophagus
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8
Q

Where is skeletal muscle found in the upper GIT?

A
  • Pharynx
  • Upper 1/3 of the oesophagus
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9
Q

What is the structure and fucntion of the submuscosa?

A
  • Thick layer of connective tissue that contains major blood/lymphatic vessels
  • Provides a key supportive function
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10
Q

What is the structure and function of the muscularis externa?

A
  • Responsible for the contraction of the GIT
  • Inner layer = circular
  • Outer layer = longitudinal
  • Contains the myenteric plexus
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11
Q

What is the structure and function of the serosa?

A
  • Thin layer of areola connective tissue with an outer covering of simple squamous epithelium
  • Forms outer covering of GIT and is continuous with visceral peritoneum
  • Secretes a serous fluid to prevent friction
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12
Q

What are the 4 ways in which the GIT is controlled?

A
  1. Pacemaker cells
  2. Enteric nervous system
  3. Autonomic nervous system
  4. Hormonal control
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13
Q

How do pacemaker cells help to control the GIT?

A
  • Found in smooth muscle cells
  • Propagate slow-wave potentials to allow for constant movement
  • Found in interstital cells of Cajal
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14
Q

How does the enteric nervous system control the GIT?

A
  • Allows for local control of the GIT
  • Important for control of gland secretion/hormone secretion
  • Hirschsprung’s disease
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15
Q

How does the autonomic nervous system control the GIT?

A
  • Parasympathetic - Vagus nerve
  • Sympathetic - Splanchnic nerve
  • Sympathetic = Inhibitory
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16
Q

What is the normal stomach capacity in an adult?

A
  • 1.5L
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17
Q

What are the digestive functions of the stomach?

A
  • Helps to digest carbs and proteins
  • Begins to produce chyme
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18
Q

What are the motility functions of the stomach?

A
  • Mixing contents to produce chyme
  • Storage purposes
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19
Q

What are the secretion functions of the stomach?

A
  • Responsible for both exocrine and endocrine secretions to help with digestion
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20
Q

What are the absorbative functions of the stomach?

A
  • Mininal nutritional absorption
  • Ethanol and aspirin are absorbed in the stomach
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21
Q

What are the different parts of the stomach?

A
  • Cardia
  • Fundus
  • Body
  • Antrum
  • Pylorus
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22
Q

What do surface mucous cells secrete?

A
  • Mucous
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23
Q

What do mucous neck cells secrete?

A
  • Mucous
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24
Q

What do parietal cells secrete?

A
  • HCl and intrinsic factor
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25
Q

What do chief cells secrete?

A
  • Pepsinogen and lipase
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26
Q

What do G cells secrete?

A
  • Gastrin
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27
Q

Where is CCK released from?

A
  • Enteroendocrine cells in the small intestine
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28
Q

What do D cells secrete?

A
  • Somatostatin
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29
Q

What are the two parts of the pancreas?

A
  • Endocrine (2%)
  • Exocrine (98%)
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30
Q

What are the endocrine functions of the pancreas?

A
  • Organised into islets of langerhans
  • Alpha cells = secrete glucagon
  • Beta cells = secrete insulin
  • Delta cells = secrte somatostatin
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31
Q

What is the function of glucagon?

A
  • Acts to oppose the action of insulin
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32
Q

What is the function of insulin?

A
  • Works to reduce blood sugar levels
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33
Q

What are the exocrine functions of the pancreas?

A
  • Organised into secretory sacs called acini
  • Secrete bicarb rich, alkaline solution which helps to neutralise stomach acid
  • 1L-2L of secretions a day
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34
Q

What are the main exocrine pancreas secretions?

A
  • P. Amylase - Carbohydrates
  • P. Lipase - Fats
  • P. Proteolytic enzymes
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35
Q

What are the three main pancreatic proteolytic enzymes?

A
  • Trypsinogen
  • Chymotrypsinogen
  • Procarboxypeptidase
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36
Q

What are the main functions of the gallbladder?

A
  • Storage and concentration of bile which is produced by the bile
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37
Q

What is the primary function of bile?

A
  • Emulsification of fats in the GI tract
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38
Q

What is the responsible for blood supply to the oesophagus?

A
  • Upper 1/3 = inf. thyroid
  • Middle 1/3 = branches of thoracic aorta
  • Lower 1/3 = branches of left gastric and left phrenic
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39
Q

What is responsible for the innervation of the oesophagus?

A
  • Vagus nerve (CNX)
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40
Q

What is responsible for the blood supply to the stomach?

A
  • Coeliac artery -> L. gastric, common hepatic, splenic arteries
  • L/R gastric = Lesser curvature
  • L/R gastroepiploic = Greater curvature
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41
Q

What is reponsible for innervation of the stomach?

A
  • Parasympathetic = Vagus nerve
  • Sympathetic = Coeliac ganglia
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42
Q

What is responsible for blood supply to the duodenum?

A
  • Superior mesenteric + superior pancreatoduodenal = 1st part
  • Superior mesenteric = 2nd part
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43
Q

What is responsible for the innervation of the duodenum?

A
  • Parasympathetic = Vagus nerve
  • Sympathetic = Coeliac/Sup. mesenteric plexus
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44
Q

What is an upper GI bleed?

A
  • Any bleeding that occurs in the GI tract that is above the suspensory ligament of the duodenum
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45
Q

What are some oesophageal causes of UGIBs?

A
  • Oesophagitis
  • Varicies
  • Malignancy
  • GORD
  • Mallory-Weiss tear
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46
Q

What are some gastric causes of UGIBs?

A
  • Peptic ulcers
  • Varicies
  • Gastritis
  • Malignancy
  • Mallory-Weiss tear
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47
Q

What are some duodenal causes of UGIBs?

A
  • Peptic ulcer
  • Diverticulum
  • Fistula
  • Duodenitis
  • Excess acid production
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48
Q

What are some factors that can increase the risk of an UGB?

A
  • NSAID’s
  • Anti-coagulants
  • Alcohol abuse
  • Chronic liver disease
  • CKD
  • Increasing age
  • Previous peptic ulcer
  • Previous H. Pylori infection
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49
Q

What is the immediate management used for an UGIB?

A

A - ABCDE approach to resus
B - Blood
A - Access - Two large bore cannulas
T - Transfuse - Blood products and clotting factors
E - Endoscopy
D - Drugs - STOP anti-coagulants + NSAID’s

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50
Q

In variceal bleeding which drug is given to reduce portal HTN and therefore reduce volume of blood?

A
  • Terlipressin
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51
Q

How is endoscopy used in the management of an UGIB?

A
  • Can be used for both diagnostic and investigative purposes
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52
Q

What are the signs of an UGIB?

A
  • Dehydration
  • Pallor
  • Confusion
  • Tachy and hypotensive
  • Abdominal tenderness
  • Melaena
  • Haematochezia
  • Stigmata of liver disease
  • Telangiectasia (small bundles of capillaries)
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53
Q

What clincal signs are seen in someone with an UGIB?

A
  • Haematemesis
  • Dizziness
  • Syncope
  • Weakness
  • Abdominal pain
  • Dyspepsia
  • Heartburn
  • Melaena
  • Haematochezia
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54
Q

What are some complications associated with an UGIB?

A
  • Respiratory distress
  • MI
  • Infection
  • Shock
  • Death
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55
Q

What is GORD?

A
  • Gastro-oesphageal reflux disorder
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56
Q

What happens in GORD?

A
  • The lower oesophageal sphincter relaxes inappropriately which allows the stomach’s contents to flow back up into oesophagus
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57
Q

What histological features would be seen in someone with GORD?

A
  • Basal zone hyperplasia
  • Elongation of lamina propia papillae
  • Eosinophil/Neutrophil release
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58
Q

What is the pathological process involved with the development of GORD?

A
  • ANS controls the sphincter but VIP and NO neurotransmitters of PNS become disrupted
  • This leads to decreased oesophageal pressure and increased gastric pressure
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59
Q

What are the symptoms seen in GORD?

A
  • Regurgitation
  • Substernal pain
  • Odynophagia
  • Dysphagia
  • Cough
  • Wheezing
  • Nausea/Vomiting
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60
Q

What are the oesophageal signs seen in GORD?

A
  • Typical reflux syndrome
  • Reflux chest pain syndrome
  • Reflux oesophagitits
  • Barrett’s oesophagus (Metaplasia from squamous)
  • Oesophageal adenocarcinoma
  • Strictures
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61
Q

What are the extra-oesophageal signs see in GORD?

A
  • Reflux cough syndrome
  • Reflux laryngitis syndrome
  • Reflux asthma syndrome
  • Reflux dental erosion syndrome
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62
Q

What are the risk factors relating to the development of GORD?

A

A - Alcohol
F - Fatty diet
C - Caffeine
O - Obesity
P - Pregnancy
S - Smokinh
H - Hiatal hernia

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63
Q

What are some factors that can exacerbate GORD symptoms?

A
  • After meals
  • Lying down
  • Bending forward
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64
Q

What are some red flag symptoms that could be seen in GORD?

A
  • Anaemia
  • Anorexia
  • Loss of weight
  • New onset
  • Haematemesis
  • Dysphagia
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65
Q

What are the two key investigations used in the diagnosis of GORD?

A
  1. pH monitoring (Either 24hr or wireless)
  2. Endoscopy/Gastroscopy
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66
Q

What are the conservative management options for GORD?

A
  • Lifestyle changes such as weight loss, smoking cessation and dietary management
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67
Q

What are the pharmacological management options used in GORD?

A
  • Histamine (H2) antagonists and PPI’s used to inhibit acid production
  • Alginates, Sucralfate, Antacids help to neutralise already present stomach acid
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68
Q

What are the surgical management options available for GORD?

A
  • Nissen fundoplication
  • Involves wrapping the fundus of the stomach around the lower oesophagus
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69
Q

What is a complication related to GORD?

A
  • Barrett’s oesophagus
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70
Q

What happens in Barrett’s oesophagus?

A
  • Metaplasia of the distal oesophagus
  • Squamous epithelium -> Columnar epithelium
  • Pale pink -> Red
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71
Q

What can Barrett’s oesophagus lead to?

A

Can lead to the development of malignancy such as adenocarcinoma

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72
Q

What three ways can be Barrett’s oesophagus be classified?

A
  1. Long segment = >3cm
  2. Short segment = 1cm-3cm
  3. Ultra-short segment = <1cm
    - This classification is based on the length of the metaplasia
73
Q

What are the two types of oesophagel cancer?

A
  • Adenocarcinoma
  • Squamous cell carcinoma
74
Q

Where is squamous cell carcinoma usually found?

A
  • Mainly found in upper 2/3 of oesophagus
75
Q

Where is adenocarcinoma usaually found?

A
  • Mainly found in the lower 1/3 of the oesophagus
76
Q

What is the definition of peptic ulcer disease?

A
  • An umbrella term for gastric and duodenal ulcers
  • An ulcer is a deep break through the full thickness of the epithelium/mucosal surface
77
Q

What are the three main causes of peptic ulcer disease?

A
  • H. Pylori
  • Medications
  • Other
78
Q

What medications can lead to the development of PUD?

A
  • NSAID’s
  • Corticosteroids
  • Alcohol
79
Q

What are the other causes of PUD?

A
  • Zollinger-Ellison syndrome
  • Acute stress
  • Malignancy
  • Inflammatory disease (Crohns, colitis)
80
Q

What proportion of PUD is caused by a H. Pylori infection?

A
  • Associated with 95% of DU
  • Associated with 70%-80% of GU
81
Q

Where does H. Pylori usually colonise?

A
  • Predominantly colonises the antrum of the stomach
82
Q

What type of bacteria is H.Pylori?

A
  • Gram positive
  • Curved bacilli
83
Q

How does H. Pylori survive in the stomach?

A
  • Urease able to buffer H2 and survive in the stomach
  • Releases CagA which inhibits mucosal production = no protection to stomach
84
Q

How do NSAID’s contribute to the development of PUD?

A
  • Inhibit COX-1 which reduces prostagladin production that stimulate the epithelium to produce mucous and HCO3-
85
Q

What are the symptoms associated with PUD?

A
  • Epigastric pain
  • Dyspepsia
  • Distension/Bloating
  • Heartburn
  • Nausea
  • Vomiting
86
Q

What are the acute presentation signs of PUD?

A
  • UGIB
  • Haematemesis
  • ?Malaena
  • Features of shock
87
Q

What are the signs associated with a perforation caused by PUD?

A
  • Acute, severe abdominal pain + tenderness
  • Localised or general guarding
  • Features of shock
88
Q

A cancer of which cells can contribute to the development of PUD?

A
  • G cells
  • Causes excess gastrin release
89
Q

What are some risk factors that can increase the chance of developing PUD?

A
  • Alcohol
  • Acute stress
  • Drugs
90
Q

What invasive investigations are undertaken in suspected cases of PUD?

A
  • H. Pylori testing but must be off PPI’s for two weeks prior
  • Rapid urease test
  • Cultures of biopsies
  • Histology sampling
91
Q

What non-invasive investigations can be undertaken in suspected cases of PUD?

A
  • Urease breath test by using C13 urea which is then converted into O2
  • Serological test which will show IgG in the blood
  • Stool antigen test
92
Q

What are the lifestyle management strategies for PUD?

A
  • Avoid triggers such as caffeine or spicy foods
  • Weight loss
  • Smoking cessation
  • Alcohol reduction
93
Q

What is the first line treatment for a H. Pylori infection?

A
  • Eradication therapy = PPI + 2x antibiotics
  • PPI = Omeprazole
  • Amoxicillin or clarithromycin if allergic to penicllin
  • Clarithromycin or Metronidazole if no alcohol consumption
94
Q

What is the first line for NSAID associated PUD?

A
  • 2 months of PPI
  • Then eradication therapy
95
Q

What is the second line treatment for someoen with PUD who has a penicillin allergy?

A
  • Omeprazole
  • Metronidazole
  • Levofloxacin/tetracycline
  • Bismuth
96
Q

What is the treatment for PUD that is not associated with a H. Pylori infection?

A
  • 4-8 weeks of PPI treatment
97
Q

What are some complications associated with PUD?

A
  • Perforation -> Peritonitis
  • Haemorrhage
  • Gastric outlet obstruction
98
Q

How is H. Pylori adapted to survive?

A
  1. Contain urea-converting enzymes
  2. Has a flagellum that allows tight adherance to gastric epithelium
  3. Releases cytokine CagA
  4. Destroys D cells -> Less somatostatin release
  5. Increases pH which causes more HCL release
99
Q

What is Zollinger-Ellison syndrome?

A
  • Occurs secondary to a hyper-secreting gastrinoma within the pancreas
  • High levels of gastrin (hypergastrinaemia) -> Multiple gastric ulcers
100
Q

What are the clincal features associated with Zollinger-Ellison syndrome?

A
  • Epigastric pain
  • Dyspepsia
  • Heartburn
  • Nausea
  • Vomiting
101
Q

What is the definitive diagnostic tool for PUD?

A
  • Upper GI endoscopy
102
Q

What triggers the intrinsic pathway of the coagulation cascade?

A
  • Internal damage to vessel wall
103
Q

What triggers the extrinsic pathway of the coagulation cascade?

A
  • Caused by external trauma
104
Q

Which proteins help to regulate the coagualtion cascade?

A
  • Protein C
  • Protein S
  • Antithrombin
105
Q

What are the vitamin K dependant clotting factors?

A
  • Factors 2,7,9,10
106
Q

Before a blood transfusion occurs, what two tests are undertaken?

A
  • Cross-match
  • Group and save
107
Q

What is a cross-match in blood screening?

A
  • Blood is tested for antibodies
  • This is then saved and matched to specific units of blood, platelets or other products
108
Q

What is a group and save in blood screening?

A
  • Patients blood is typed and saved but NOT matched
  • Only valid for 7 days
  • Used when there is low risk of needing blood products
109
Q

How do PPI’s work?

A
  • Reduce acid secretion to protect gastric lining
  • Inhibit H+ ATPase on parietal cells
  • Inhibit carbonic anhydrase in mucosal lining
110
Q

What are some side effects related to taking PPI’s?

A
  • GI upset
  • Increased fracture risk
  • Increased GI infection risk
  • Can mask cancer symptoms
  • Hyponatraemia
111
Q

How do histamine H2 antagonists work?

A
  • Competitively inhibit histamine action at all H2 receptors
  • Inhibits histamine/gastrin stimulated acid secretion
112
Q

What are some side effects of histamine H2 antagonists?

A
  • Diarrhoea
  • Dizziness
  • Muscles pains
  • Alopecia
113
Q

How do alginates work?

A
  • Neutralise stomach acid
  • Form a ‘raft’ on top of stomach acid to prevent reflux
114
Q

How do antacids work?

A
  • Neutralise stomach acid
  • Oppose acidity of stomach
  • Aluminimum based - constipation
  • Magnesium based - laxative
115
Q

How do sulcrafates work?

A
  • Neutralise stomach acid
  • Work by binding to proteins in ulcerated tissue and forms a protective layer
116
Q

How do 5-HT3 anatagonists work?

A
  • Blocks serotonin stimulation centrally and peripherally to reduce vomiting stimulation
117
Q

How do dopamine receptor antagonists work?

A
  • Blocks dopaminergic receptors in the brain
  • Metroclopramide and domperidone both promote gastric emptying
118
Q

What are the different types of laxatives?

A
  • Osmotic
  • Stimulant
  • Softeners
  • Bulk forming
119
Q

What is shock?

A
  • A life threatning form of acute circulatory failure that results in inadequate organ perfusion and tissue hypoxia
  • Reduction in cardiac output
120
Q

What is hypovolemic shocK?

A
  • Shock caused by a reduction in intravascular volume
121
Q

What is the pathophysiology around hypovolemic shock?

A
  • Reduced venous return -> Reduced preload -> Reduced cardiac output -> Hypotension -> Perfusion failure
122
Q

What are the symptoms seen in hypovolemic shock?

A
  • Thirst
  • Postural dizziness
  • Nausea/Vomiting
  • Palpitations
123
Q

What are the intial signs seen in hypovolemic shock?

A
  • Tachycardic
  • BP maintained
  • Cold extremities (Peripheral vasoconstriction)
  • Oliguria
  • Lowered JVP
124
Q

What are the signs seen later in hypovolemic shock?

A
  • Raised HR
  • Low BP
  • Cold extremities
  • Dysuria
  • Lowered JVP
125
Q

What are causes of hypovolemic shock?

A
  • Blood loss
  • Fluid loss
  • Diarrhoea/Vomiting
  • Burns
  • Sweating
126
Q

What are some risk factors associated with the precipitation of hypovolemic shock?

A
  • DKA
  • Peritonitis
  • Ascites
  • Cholera
127
Q

What investigations are performed when hypovolemic shock is suspected?

A
  • ECG
  • Obs
  • ABCDE assessment
  • Bloods -> FBC
  • Coag screen
  • Blood gases
  • Urine output
128
Q

What management used in hypovolemic shock?

A
  • ABCDE
  • Oxygen
  • 2x large bore cannulas
  • Fluid resus
  • Replacing what was lost
  • Clingfilm burns etc.
129
Q

What is the main complication associated with hypovolemic shock?

A
  • Organ failure
130
Q

What is cardiogenic shock?

A
  • Primary impairement of cardiac function (Essentially heart failure)
  • Can be either mechanical or electrical
131
Q

What are some symptoms associated with cardiogenic shock?

A
  • Tachycardia
  • SOB
  • Tachypnoea
  • Weak pulse
  • Sweating
  • Cold extremities
  • Hypotension
132
Q

What are the clinical signs seen in the cardiogenic shock?

A
  • Cardiac dysfunction
  • Arrythmias
  • MI
  • Peripheral vasocontriction
133
Q

What is the most common cause of cardiogenic shock?

A
  • Serious heart attack (MI)
134
Q

What are the risk factors associated with the precipitation of cardiogenic shock?

A
  • Carries the same risk factors that are associated with MI’s
135
Q

What are the investigations undertaken when cardiogenic shock is suspected?

A
  • ABCDE
  • ECG
  • Obs
  • Bloods ->
  • U&E
  • Blood gases etc.
  • Coag screen
136
Q

What is the emergency management used in cardiogenic shock?

A
  • Clot-busting drugs such as tPA to dissolve coronary artery clots
  • Anticlotting medicines such as aspirin
  • Drugs to increase pumping ability of heart such as dobutamine
  • GTN to help relax and widen blood vessels
  • Drugs that help to decrease the hearts workload
137
Q

What is the long term management for cardiogenic shock?

A
  • Treat arrhythmias
  • PCI for thrombus
  • Inotropes
138
Q

What are some complications associated with cardiogenic shock?

A
  • Permanent damage to liver, kidneys and other organs due to hypoperfusion
139
Q

What is obstructive shock?

A
  • A blockage of the heart or a greater vessel results in inadequate cardiac output
140
Q

What is the pathological process related to obstuctive?

A
  • A blockage causes a reduction in blood pressure this means less blood reaches organs leading to tissue hypoxia
141
Q

What are some symptoms associated with obstructive shock?

A
  • Skin rash
  • Tachy
  • Low BP
  • Warm arms and legs
  • Cold/clammy skin
  • Fever/Chills
  • Abdo pain
142
Q

What are the clinical signs seen in obstructive shock?

A
  • Hypotension
  • Tachycardia
143
Q

What are the different potential causes of obstructive shock?

A
  • Tension pneumothorax
  • PE
  • Cardiac tamponade
144
Q

What are the investigations performed when obstructive shock is suspected?

A
  • ABCDE
  • ECG
  • Obs
  • Bloods ->
  • U&E
  • Blood gases etc.
  • Coag screen
145
Q

What are the potential managment options for obstructive shock?

A
  • Requires treatment of underlying cause
  • Thrombolysis
  • Pericardiocentesis
146
Q

What is distributive shock?

A
  • A physical obstruction of blood circulation and inadequate blood oxygenation
147
Q

What are the three types of distibutive shock?

A
  • Septic
  • Neurogenic
  • Anaphylactic
148
Q

What is the pathophysiological process behind distributive shock?

A
  • Peripheral vasodilation leading to abnormal volume distribution and inadequate perfusion
  • Loss of blood volume by leaky capillaries
149
Q

What are the symptoms seen in distributive shock?

A
  • Tachypnoea
  • Altered consciousness
  • Very little urine output
  • Cool, clammy skin
  • Subcutaneous emphysema
  • Chest or abdominal pain
150
Q

What are the clincal signs seen in distributive shock?

A
  • Warm + flushed peripheries
  • Tachycardia
  • Bouncing pulse
151
Q

What are the potential causes of distributive shock?

A
  • Septic shock
  • Neurogenic shock
  • Anaphylactic shock
152
Q

What are the risk factors for the development of distributive shock?

A
  • Sepsis - Either bacterial or fungal
  • Neurogenic - Spinal cord injury, Guillan-barre
  • Anaphylactic - Allergies
153
Q

What investigations should be performed when distributive shock is suspected?

A
  • Blood tests to determine severity
  • History/Examination to identify the underlying cause of symptoms
154
Q

What is the management used for distributive shock?

A

Crucial to treat the underlying cause:
- Vasopressors
- Adrenaline - Anaphylactic
- Antibiotics - Septic

155
Q

What is septic shock?

A
  • The body’s overwhelming and life-threatening response to severe systemic infection
  • This causes chemicals to be released into the bloodstream to fight the infection however this causes inflammation
156
Q

What are the symptoms related to septic shock?

A
  • Clammy
  • Sweats and chills
  • Palpitations
  • Altered mental state
157
Q

What are the clincal signs seen in septic shock?

A
  • Low JVP
  • Tachy
  • Pyrexic
  • Oliguria
  • Warm extremities
  • Rashes or other signs of infection
158
Q

What are some potential causes of septic shock?

A
  • Meningitis
  • Pneumonia
  • Infection of any kind that gets into the bloodstream
159
Q

What investigations should be performed when septic shock is suspected?

A
  • ABCDE assessment
  • Bloods
  • Cultures
  • ECG
  • Monitor urine output
  • Clotting factors
160
Q

What is the management used for septic shock?

A
  • ABCDE
  • Oxygen
  • Fluid resus
161
Q

What can be given to patients who remain hypotensive despite fluid resus?

A
  • Vasopressors
162
Q

What is the first line catecholamine used in septic shock?

A
  • Noradrenaline
163
Q

What is the second line catecholamine used in septic shock?

A
  • Vasopressin + adrenaline
164
Q

What is used if a septic shock patient is still unstable following 1st/2nd line catecholamine treatments?

A
  • Dobutamine
165
Q

When are corticosteroids used in the treatment of spetic shock?

A
  • To aid in the maintenance of arterial pressure
  • Hydrocortisone
166
Q

What is anaphylactic shock?

A
  • Acute allergic reaction to an antigen which the body has become hypersensitive
167
Q

What are the clinical signs seen in anaphylatic shock?

A
  • Low JVP
  • Tachycardia
  • Tachypnoea
  • Warm clammy
  • Low BP
  • Dysuria
168
Q

What is the main cause of anaphylatic shock?

A
  • An allergy trigger
169
Q

What is the management plan used in anaphylactic shock?

A
  • ABCDE assessment
  • Oxygen
  • Fluid bolus
  • IM adrenaline
  • Antihistamines
170
Q

What medications can be given in the treatment of anaphylactic shock?

A
  • IM/IV chlorphenamine
  • IM/IV hydrocortisone
  • Nebulised salbutamol
  • IM adrenaline
  • Antihistamines
171
Q

What are some symptoms seen in anaphylactic shock?

A
  • Hypotension
  • Severe bronchospasm
  • Hypoxia
  • Hypercapnia
172
Q

What investigations are utilised in the diagnosis of anaphylaxis?

A
  • ABCDE assessment
  • Bloods
  • Cultures
  • ECG
  • Monitor urine output
  • Clotting factors
173
Q

What is neurogenic shock?

A
  • Loss of sympathetic tone + unopposed parasympathetic response
174
Q

What are some clinical features of neurogenic shock?

A
  • Hypotension
  • Bradycardia
  • Temperature dysregulation
175
Q

What is the usual cause of neurogenic shock?

A
  • Usually follows spinal transection or a brainstem injury
176
Q

What physiological derangement is seen in hypovolemic shock?

A
  • Low preload
177
Q

What physiological derangement is seen in distributive shock?

A
  • Low SVR
177
Q

What physiological derangement is seen in cardiogenic shock?

A
  • Low contractility
178
Q

What physiological derangement is seen in obstructive shock?

A
  • Low preload

Year 2 Medicine @ Lancaster Uni (15 decks)

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