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Year 1 NME > GIT Anatomy Revision > Flashcards

GIT Anatomy Revision Flashcards

1
Q

What are the 3 salivary glands in the oral cavity?

A

1 - sublinguinal glands

2 - submandibular glands

3 - parotid glands

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2
Q

What are the 3 salivary glands in the oral cavity?

A

1 - sublinguinal glands

2 - submandibular glands

3 - parotid glands

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3
Q

What % of salive do the the 3 salivary glands in the oral cavity contribute towards total saliva?

A

1 - sublinguinal glands - 5%

2 - submandibular glands - 70%

3 - parotid glands - 25%

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4
Q

Of the 3 salivary glands, sublinguinal glands, submandibular glands and parotid glands, which nerve innervates the parotid glands?

A
  • glossopharyngeal nerve
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5
Q

Of the 3 salivary glands, sublinguinal glands, submandibular glands and parotid glands, which nerve innervates the sublinguinal and submandibular glands?

A
  • facial nerves
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6
Q

What are the 3 phases of swallowing?

A

1 - oral phase

2 - pharyngeal phase

3 - oesophageal phase

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7
Q

Of the 3 phases of swallowing oral, pharyngeal and oesophageal phase, which is the only voluntary phase?

A
  • swallowing phase
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8
Q

What is the anatomical landmark used to determine the upper from lower aspects of the GIT?

A
  • suspensory muscle of the duodenum
  • also known as the ligament of Treitz
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9
Q

The suspensory muscle of the duodenum, also known as the ligament of Treitz is the anatomical landmark used to determine the upper from lower aspects of the GIT. Where does this attach and what is the importance of this muscle/ligament?

A
  • attaches at the duodenojejunal flexure and celiac artery
  • contracts and increases area for chyme movement helping motility
  • marks transition from foregut to the midgut
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10
Q

What are the 4 layers of the GIT?

A

1 - mucosa

2 - submucosa

3 - muscularis propria

4 - serous

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11
Q

The mucosa is the first layer of the GIT. What 3 makes up the mucosa?

A

1 - epithelium

2 - lamina propria

3 - muscularis mucosae

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12
Q

What are the 2 plexi of the GIT wall?

A

1 - submucosa plexus (secretions and blood flow)

2 - myenteric plexus (peristalsis)

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13
Q

What is the role of the sub muscularis?

A
  • contract and make mucosa fold
  • increases surface area of GIT
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14
Q

What is intrinsic and extrinsic regulation of motility in the GIT?

A
  • intrinsic = enteric nervous system
  • extrinsic = autonomic control
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15
Q

There are 2 types of motility in the small intestines, segmentation and peristalsis. Which is responsible for mixing and which is responsible for chyme motility?

A
  • segmentation = mixing
  • peristalsis = motility
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16
Q

In the GIT what does bi-directional flux refer to?

A
  • fluid and secretions being released into the GIT
  • then reabsorbed by the GIT (aprox 99%)
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17
Q

Which exocrine cells in the gastric pits of the stomach are responsible for secretion of HCl and intrinsic factor (B12 binding)?

A
  • parietal cells
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18
Q

Which exocrine cells in the gastric pits of the stomach are responsible for secretion of gastric enzymes pepsinogen and gastric lipase?

A
  • chief cells
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19
Q

Which endocrine cells in the gastric pits of the stomach are responsible for secretion of gastrin?

A
  • G cells
  • G for Gastrin
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20
Q

Which endocrine cells in the gastric pits of the stomach are responsible for secretion of somatostatin?

A
  • D cells
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21
Q

Which endocrine cells in the gastric pits of the stomach are responsible for secretion of histamine?

A
  • enterochrommafin like cells
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22
Q

In the small intestines which cells secrete mucus?

A
  • goblet cells
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23
Q

In one cell in the small intestines is able to secrete cholecystakinin, secretin and glucose dependent insulinotropic peptide?

A
  • enteroendocrine cells
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24
Q

In the small intestines which cell differentiates from daughter cells and then migrates downwards below the stem cells? These cells also secrete antimicrobial lysosomes.

A
  • paneth cells
  • migrate down to protect the stem cells
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25
Q

In the small intestines there is a specific cell that is only found in the small intestines, what is responsible for secreting HCO3- and mucus, what is this cell called?

A
  • brunners gland
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26
Q

What are the 3 ways in which pareital cells can be stimulated to secrete HCl?

A

1 - gastrin

2 - histamine (stimulated by gastrin)

3 - ACh (stimulated by vagal nerve)

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27
Q

What secretion in the stomach is able to in hibit secretion of HCl by D cells?

A
  • somatostatin
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28
Q

The pancrease contains endocrine and exocrine clusters, what is the majority of the pancreas made of?

A
  • exocrine clusters
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29
Q

Where are the endocrine cells of the pancreas located within the pancreas?

A
  • in the islets of langerhans
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30
Q

Somatostatin can be released from D cells in the islets of langerhans. They act as inhibitors, what are the 2 things they they inhibit in the GIT?

A
  • HCl secretion in the stomach by parietal cells
  • inhibition of both glucagon and insulin
  • somatostain appears to inhib all secretions
  • remember STOP secretions for somatostatin
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31
Q

What is the main nerve that stimulates pancreatic secretions?

A
  • vagal nerve
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32
Q

A hormone is secreted in response to fat, carbohydrates and proteins being present in the duodenum. What is this hormone and what does it increase the secretion of from the pancreas?

A
  • cholocystekinin (CCK)
  • increases pancreatic enzyme rich secretions to digestion nutrients
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33
Q

A hormone is secreted in response to high level of H+ and a low pH being present in the duodenum. What is this hormone and what does it increase the secretion of from the pancreas?

A
  • secretin
  • increases HCO3- rich pancreatic secretions to neutrilise acidic chyme
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34
Q

There are 3 phases of pancreatic secretions, what are they and what % of the toal secretions does each one contribute?

A

1 - cephalic = 20% of secretions

2 - gastric = 10% of secretions

3 - intestinal = 70% of secretions

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35
Q

Which part of the stomach does the stretching signal gastric secretions

A
  • fundus
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36
Q

What are the 3 broad types of transport in enterocytes?

A

1 - passive (down electrochemical gradients)

2 - solvent drag (parracellular)

3 - active (Na+ / K+ ATPase, needs energy)

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37
Q

What is solvent drag?

A
  • H2O moves due to osmosis and balance concentrations
  • solutes are able to follow or be dragged (Na+. K+, Cl-)
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38
Q

Solvent drag is where H2O moves due to osmosis and balance concentrations. Solutes are able to follow or be dragged (Na+. K+, Cl-), but this only occurs paracelluarly between cells and tight junctions. Where in the small intestines does the majority of this occur?

A
  • proximally, so mainly in the duodenum
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39
Q

If enzymes from the pancrease were secreted in their active form they would digest the pancreas, such as proteases. How does the pancreas and small intestines get around this?

A
  • secretes inactive protein digesting enzymes called zymogens
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40
Q

To ensure enzymes from the pancrease do not digest the pancreas, such as proteases, the pancrease secretes inactive protein digesting enzymes called zymogens. How do these enzymes then become active?

A
  • enterokinase in the brush border
  • trypsinogen becomes trypsina and can they activate other enzymes
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41
Q

H2O is able to diffuse in a number of ways through osmosis to maintain equilibrium of ion concentrations (isotonic). H2O can be absorbed in 2 main ways in the GIT, what are they?

A
  • enterocytes contain aquaporins allow H2O to diffuse and maintain equilibrium
  • H2O can move paracelluarly via solvent drag and move electrolytes with it to maintain equilibrium
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42
Q

From the options belowe, which is not a risk factor for malnutrition?

  • Being 95 years old
  • Being a nursing home resident
  • Being male
  • Chronic Kidney Disease
  • Moderate dementia
A
  • being male
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43
Q

Which of the following information would be needed to calculate a patients MUST score?

  • MUAC score (Mid-humeral circumference)
  • His total body fat percentage
  • His ulnar length
  • Total weight lost unintentionally in the last 3-6 months.
  • Whether Colin is acutely unwell at this time OR unlikely to have any nutritional intake for 5 or more days
A
  • Total weight lost unintentionally in the last 3-6 months
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44
Q

To calculate a MUST score for malnutrition, what 3 thinsg are required, and what score determines if someone is malnourished?

A
  • score of _>_4
  • patients BMI
  • % weight lost unintentionally in last 3-6 months
  • if patient is acutely unwell and low nutritional intake for >5 days
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45
Q

What are some of the most common risk factors for colorectal cancer?

A
  • age (median age 71 years old)
  • genetics (family history)
  • smoking
  • processed meats and low fibre
  • long standing UC with PSC
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46
Q

Is smoking associated with crohns or UC?

A
  • Crohns disease
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47
Q

Which religous group has a higher risk of developing crohns disease?

A
  • Ashkenazi Jewish
48
Q

If a male with mitochondrial disease has a baby with a woman who does not have mitochondrial disease, what is the liklihood of their child having mitochondrial disease?

  • 0%-
  • 0.5%
  • 1.25%
  • 5%
  • 10%
A
  • 0%
  • mitochondrial genome is maternal, so only women can pass it on
49
Q

A patient with Von Gierke’s disease, a glycogen storage disorder that is inherited in an autosomal recessive pattern (needs 2 mutated genes from no sex chromosomes) has been having convulsions (seizures). Which of thes is the most likely cause?

  • Epilepsy
  • Hypoglycaemia
  • Hyperglycaemia
  • Lactic alkalosis
  • Poor feeding
A
  • hypoglycaemia = they have glycogen in liver but cannot leave due to lack of G-6-Phosphotase deficiency
  • brain relies on glucose, so no glucose it begins to shut down and cause convulsions/seizures
50
Q

A patient with Von Gierke’s disease, a glycogen storage disorder that is inherited in an autosomal recessive pattern (needs 2 mutated genes from no sex chromosomes) has hepatomegaly, why?

A
  • glycogen is broken down but cannot be converted from G-6-P due to lack of G-6-Phosphotase
  • glyclogen remains in liver and attracts waer, so becomes enlarged
51
Q

Von Gierke’s disease is a glycogen storage disorder that is inherited in an autosomal recessive pattern (needs 2 mutated genes from no sex chromosomes). These patients lack G-6-Phosphotase and cannot remove the phosphate, allowing glucose to enter the blood. However, can gluconeogenesis occur?

A
  • no
  • final stage of gluconeogenesis is converstion of G-6-P to glucose using G-6-Phosphotase
  • no glucose from glycogenolysis or gluconeogenesis
52
Q

Von Gierke’s disease is a glycogen storage disorder that is inherited in an autosomal recessive pattern (needs 2 mutated genes from no sex chromosomes). If a patient with this disease eats a high carbohydrate meal can this help with their energy levels?

A
  • may provide some glucose for muscles
  • BUT, if lots of glucose, means insulin released and activates glycogen synthase, which means more glycogen stroage and a bigger liver
53
Q

Von Gierke’s disease is a glycogen storage disorder that is inherited in an autosomal recessive pattern (needs 2 mutated genes from no sex chromosomes). In addition to the liver becoming enlarged, what else can happen to the liver due to so much glucose and glycogen storage?

A
  • fatty liver
54
Q

Von Gierke’s disease is a glycogen storage disorder that is inherited in an autosomal recessive pattern (needs 2 mutated genes from no sex chromosomes). In these patients nogastric feeding may be used to help with the patients energy levels and reduce the risk of hypoglycaemia. Why is nasogastric feeding a good choice in these patients?

A
  • provides bolus of glucose to help with energy levels
  • bolus of glucose also reduces the risk of hypoglycaemia
55
Q

We need to know about GLUT 1-4 receptors. Rank the GLUT transports from 1-4 in order of their affinity for glucose, with the highest affinity first.

A

1st = GLUT 1 and 3 - high affinty 1mmol/L

2nd = GLUT 4 - moderate affinity 5mmol/L

3rd = GLUT 2 - low affinity 15-20mmol/L

56
Q

If a patients has become hypoglycaemic at 3mmol/L, which GLUT transporters would continue to absorb glucose from the blood?

A
  • GLUT 1 and 3 as they have a high affinity of 1mmol/L
57
Q

The mnemonic Big Fat Boys can be used to remember where GLUT 1 receptors are located, which is where?

A
  • Big = Brain
  • Fat = Foetus
  • Boys = Blood Brain Barrier
58
Q

The mnemonic Kill Small Little Pansies can be used to remember where GLUT 2 receptors are located, which is where?

A
  • Kill = Kidneys
  • Small = Small Intesintes
  • Little = Liver
  • Pansies = Pancreas
59
Q

The mnemonic Producting Nervous Kids can be used to remember where GLUT 3 receptors are located, which is where?

A
  • Producting - Placenta
  • Nervous = Nerves
  • Kids = Kidneys
60
Q

The mnemonic Mad Fathers can be used to remember where GLUT 4 receptors are located, which is where?

A
  • Mad = Muscle
  • Fathers = Fat
61
Q

The presence of which of the following are most likely to indicate a urinary tract infection? (2 correct answers) and why?

  • Blood
  • Glucose
  • Nitrites
  • Leukocytes
  • Proteins
A
  • nitrities = bacteria convert nitrates into nitrites
  • leukocytes = infection increases immune cells at site of infection
62
Q

In a patient with Acute Kidney Injury (AKI), and urinary tract infection, what is likley to be found in the following tests?

  • Haemoglobin
  • White Blood Cells (WBC)
  • C-Reactive Protein (CRP)
  • Urea
  • Creatinine increase
  • Estimated Glomerular Filtration Rate (eGFR)
A
  • Haemoglobin = remains stable
  • White Blood Cells (WBC) = increase
  • C-Reactive Protein (CRP) = increase
  • Urea = increase
  • Creatinine = increase
  • Estimated Glomerular Filtration Rate (eGFR) = reduces
63
Q

If a patient with dementia presents with a renal problem, is this likley to be pre renal, renal or post renal?

A
  • pre renal
  • patients with dementia forget to drink so will be dehydrated
  • low H2O = low blood volume and low BP
  • low BP = hypoperfusion of the kidney
64
Q

If an 82 year old patient presents with diabetes presents with a renal problem, is this likley to be pre renal, renal or post renal?

A
  • renal
  • likely to already have some form of kidney disease, such as diabetes glomerulonephritis
65
Q

If an 82 year old patient presents with hypertension and has a renal problem, is this likley to be pre renal, renal or post renal?

A
  • renal
  • hypertension is the second most common cause of end stage renal disease
66
Q

If an 82 year old patient presents with benign prostatic hyperplasia (BPH) and a renal problem, is this likley to be pre renal, renal or post renal?

A
  • post renal
  • also likley to have bladder retention
67
Q

An 82-year-old patient is brought into the Emergency Department by his daughter as she is concerned that he has not been eating or drinking much over the past 3 days. On further questioning it is found that the patient has got a background of dementia, benign prostatic hyperplasia (BPH), hypertension, and type 2 diabetes. Taking into account all of his conditions, which of the following can be managed quickly to stop his condition from deteriorating?

  • Age
  • Benign prostatic hyperplasia
  • Diabetes
  • Fluid hydration
  • Hypertension
A
  • Benign prostatic hyperplasia can be quickly treated through catherisation
  • Fluid hydration will help with pre renal kidney problems
68
Q

How can dehydration contribute to acute kidney injury?

A
  • low H2O = low blood volume
  • low blood volume = low BP
  • low BP = hypoperfusion of kidney
  • GFR will reduce and nephron ischaemia
69
Q

What medication can contribute to pre renal injury?

A
  • ACE inhibitors
  • instead of vasocontraction of efferent arterioles to increase GFR, ACE inhibitors will vasodilate efferent arterioles also reducing GFR
70
Q

In diabetes glomerulonephritis how can glucose be filtered at the glomerula, when normally is doesnt?

A
  • high levels of glucose means glucose sticks to endothelial
  • glucose can then enter the glomerula
  • proteins also stick to glucose and pass through glomerula
71
Q

In diabetes glomerulonephritis glucose is able to get into the urine, and bind with proteins, which are also able to be filtered by the glomerula. In addition this protein bound glucose can damage the efferent arterioles, causing them to thicken and become stiff. If this continues, how can this damage the glomerula?

A
  • thickened efferent arterioles means reduced blood flow and GFR
  • afferent arterioles dilate to increase blood flow and GRF, whcih can be good
  • BUT this causes a back log of pressure in the glomerula and can lead to damage
72
Q

In diabetes glomerulonephritis glucose is able to get into the urine, and bind with proteins, which are also able to be filtered by the glomerula. In addition this protein bound glucose can damage the efferent arterioles, causing them to thicken and become stiff. This can lead to chronic pressure build up in the kidneys, and cause structural changes in the kidneys, specifically by the mesangial cells. This can lead to protein filled nodules building up within the mesangial cells. These can be detected on histology and only in diabetes, what are these called?

A
  • Kimmelstiel-Wilson nodules
73
Q

In diabetes glomerulonephritis the glomerula basement membrane increases in size and as it does, proteins are able to pass through the glomerula and into the filtrate, increasing protein in the blood. How can an enlargement of the glomerula basement membrane lead to more protein leaking out?

A
  • podocytes are stretched
  • filtration slits increase in size allowing molecules to pass through
74
Q

In diabetes glomerulonephritis the GFR continues as normal, but eventually as the glomerula increases in size and the glomerula basement membrane thickens what happens to GFR?

A
  • reduces
  • leading cause of end stage renal disease
75
Q

Although Ramipril (ACE inhibitor) is generally removed in patients with renal disease, why can Ramipril be useful in patients with diabetes glomerulonephritis?

A
  • reduces efferent arteriole resistance
  • reduced pressure in the glomerula
76
Q

Alport syndrome is a genetic disorder that affects the type 4 collagen that makes up the lamina of the glomerula basement membrane. What does this do to the golmerula?

A
  • reduces GFR
  • proteinuria and hematuria
77
Q

Is Alport syndrome classed as nephrotic or nephritic syndrome?

A
  • nephritic
  • due to prescence of hematuria
78
Q

What is Polycystic kidney disease?

A
  • genetic mutation called polycystin kidney disease- (PKD-1) that causes hundreds of cycts to form on kidneys
  • autosomal dominant meaning only 1 mutated gene on non sex chromosome is needed
79
Q

Polycystic kidney disease can lead to hundreds of cytes to form throughout the kidney, including the tubules. If cysts filled with fluid form on the tubules they can compress neighbouring blood vessels, which can cause hypoperfusion of that glomerula. What can this then activate in the kidney?

A
  • RAAS
  • causes hypertension and makes matters worse
80
Q

Polycystic kidney disease can lead to hundreds of cytes to form throughout the kidney, including the tubules and collecting ducts, such as the renal papilla and calyces, slowing or even stopping urine flow. What can this increase the risk of?

A
  • urinary stasis causes concentration of urine
  • this increases the risk of kidney stones
81
Q

What is systemic lupus erythematosus?

A
  • autoimmune disease
  • antigen-antibody complexes form and accumulate in glomerula
  • inflammation and glomerula damage follows
82
Q

Hepatitis is inflammation of the liver, what is the most common cause of this?

A
  • viral infections
83
Q

In hepatitis, why do plasma transaminase increase in concentration?

A
  • hepatocytes are damaged and leak enzymes out
84
Q

AST ansd ALT will be increased in viral hepatitis, but which one will be raised more?

A
  • ALT
  • also be the last enzyme to return to normal after treatment
85
Q

Why do patients with hepatitis get jaundice?

A
  • bile ducts and hepatocyes become damaged
  • conjugated and unconjugated biliruben leak out
86
Q

What is the definition of acute vs chronic hepatitis?

A
  • acute = <6 months
  • chronic = >6 months
87
Q

How is hepatitis A virus (HAV) and E (HEV) transmitted?

A
  • if it starts with a vowel it came from the bowel
  • dirty water, infected food, seen in travellers
88
Q

Does hepatitis A virus (HAV) and E (HEV) have a chronic phase?

89
Q

When diagnosing hepatitis A virus (HAV) and E (HEV), what 2 antibodies can be found in the blood?

A
  • HAV = IgM anti-HAV antibodies = active and IgG anti-HAV antibodies = recovery or vaccination
  • HEV = IgM anti-HEV antibodies = active and IgG anti-HEV antibodies = recovery
90
Q

How is Hepatitis C virus (HCV) transmitted?

A
  • HCV is in the circulation (semen, blood, childbirth)
91
Q

How is Hepatitis C virus (HCV) diagnosed?

A
  • HCV RNA PCr
92
Q

How is Hepatitis B virus (HBV) transmitted and does it always become chronic?

A
  • HBV is in bodily fluids (semen, blood, birth)
  • it can become chronic but only in 20%
93
Q

Out of all the hepatitis virus (A-E), which has the most liklihood of causing liver cancer?

94
Q

Hepatitis B virus (HBV) can be diagnosed by an antigen on the virus surface, what is this antigen called?

A
  • hepatitis B surface antigen (HBsA)
95
Q

In hepatitis B virus (HBV) the hepatitis B surface antigen (HBsA) can be detected. But there is another antigen that can also be detected that lies within the virus, what is this?

A
  • hepatic B virus core antigen (HBcA)
96
Q

In hepatitis B virus (HBV) the hepatitis B surface antigen (HBsA) and hepatic B virus core antigen (HBcA) can be detected. But there is another antigen that can be used to determine which of the 4 stages of the HBV a patient currently has. What is this virus?

A
  • hepatic B virus e antigen (HBeA)
  • secreted by infected cells, so is a good marker of active infection
97
Q

There are 4 phases of hepatitis B, what are they?

A

1 - immune tolerent (high VL but low ALT)

2 - immune active (high VL, high ALT and e antigen positive)

3 - inactive (low VL and ALT)

4 - immune active (low VL, high ALT and e antigen negative)

98
Q

Hepatitis D virus (HDV) requires the prescence of another hepatic virus, which is this?

99
Q

In saliva what is able to degrade bacteria?

A
  • lysosomes
  • secreted with saliva
100
Q

Where does the vagus nerve stop innervating the gastrointestinal tract?

A
  • midgut
  • hindgut then becomes pelvic nerve
101
Q

Pyoderma gangrenosum is an inflammatory skin condition, commonly presenting in what GIT disease?

A
  • ulcerative colitis
102
Q

Erythema nodosum is an inflammatory skin condition, commonly presenting in what GIT disease?

A
  • ulcerative colitis
103
Q

If a patient is suspected of having an appendicities, what is the area called that lies one-third of the distance laterally on a line drawn from the umbilicus to the right anterior superior iliac spine?

A
  • McBurney point
104
Q

What is the most common type of bladder cancer?

A
  • transitional cell bladder cancer
105
Q

Which hepatitis vaccine can be cured using anti-virals?

A
  • hepatitis C
106
Q

What is the superior border or the abdominal cavity?

A
  • diaphragm
  • xiphoid process
  • costal margins
107
Q

What is the most common cause of acute liver disease?

A
  • medication overdose (paracetamol)
108
Q

What is the mechanism of action of vancomyosin?

A
  • inhibits cell wall synthesis
  • binds to the D-Ala-D-Ala terminal of the growing peptide chain during cell wall synthesis meaning cell wall cannot form
109
Q

What is the mechanism of action of clarithromycin?

A
  • binds to 50S subunit of ribosome
  • inhibits protein translation
110
Q

What is the difference between bactercidal and bacteriostatic?

A
  • bactercidal = kills bacteria
  • bacteriostatic = inhibit the growth of bacteria
111
Q

What are couinaud liver segments?

A
  • liver can be divided into segments
  • in case surgery is required
112
Q

Where is the lesser sac within the Supra colic compartment of the peritoneal cavity?

A
  • posterior to the stomach and lesser omentum
  • functions by allowing the stomach to move freely against the structures posterior and inferior to it
113
Q

The greater and lesser sacs of the supra colic compartment are able to communicate via what?

A
  • epiploic foramen
114
Q

In addition to providing support and attaching organs to the posterior wall of the abdomen, what else does the mesentary create?

A
  • support ligaments for the stomach (gastrosplenic ligament)
  • support ligaments for the spleen (lienorenal ligament)
115
Q

To treat obesity the aim is to reduce calorie intake and increase energy expenditure, what are the 4 mains ways this can be achieved?

A
  • motivational interviewing and behaviour change
  • diets
  • drugs
  • bariatric surgery
116
Q

The NICE guidelines have identified how to assess and identify and manage patients with obesity based on their risk factors that encompass BMI, wasit circumference and co-morbidities. What are the 4 levels of the intervention plan?

A
  • level 1 = general advice healthy weight and lifestyle
  • level 2 = diet and physical health
  • level 3 = diet and physical activity, drugs
  • level 4 = diet and physical activity, drugs, surgery

Year 1 NME (61 decks)

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