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BLOCK 15 Flashcards

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1
Q

where is gastrin secreted from?

A

G cels in the antrum of the stomach

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2
Q

what stimulates secretion of gastrin?

A

distention of stomach
vagus nerves
luminal peptides

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3
Q

whats the function of gastrin?

A

increases acid secretion by parietal cells
pepsinogen and intrinsic factor secretion
increases gastric motility
stimulates parietal cell maturation

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4
Q

where is CCK secreted from?

A

I cells in upper small intestine

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5
Q

what stimulates CCK secretion?

A

partially digested proteins and triglycerides and fats

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6
Q

whats the function of CCK?

A

increases secretion of enzyme rich secretions from pancreas
contracts gallbladder and relaxes sphincter of oddi
decreases gastric emptying
trophic effect on pancreatic acinar cells
induces satiety

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7
Q

where is secretin released from

A

S cells in upper small intestine

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8
Q

what stimulates secretin release?

A

acidic chyme

fatty acids

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9
Q

what is secretin function?

A

bicarbonate rich fluid release from pancreas and hepatic duct cells
decreases gastric acid secretion
trophic effect on pancreatic acinar cells

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10
Q

where is vasoactive intestinal peptide secreted from?

A

small intestine and pancreas

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11
Q

whats the function f vasoactive intestinal peptide?

A

stimulates secretion by pancreas and intestines

inhibits acid secretion

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12
Q

where is somatostatin released from?

A

D cells in the pancreas and stomach

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13
Q

what triggers somatostatin release?

A

fat, bile salts, glucose in the intestinal lumen

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14
Q

whats the function of somatostatin?

A 
decreases gastrin secretion
decreases pancreatic enzyme secretion
decreases insulin and glucagon secretion
inhibits trophic effects of gastrin
stimulates gastric mucous production
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15
Q

where is pepsinogen secreted from?

A

gastric chief cells

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16
Q

how do crohns and UC affect goblet cell numbers?

A

crohns increases goblet cells

UC deplete goblet cells

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17
Q

what is chariots cholangitis triad?

A

fever, RUQ pain and jaundice

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18
Q

what is Reynolds pentad?

A

fever, jaundice, RUQ pain, confusion and sepsis

ascending cholangitis signs

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19
Q

what are some of cortisol’s functions?

A

increase bp by up-regulating alpha 1 receptors on arterioles
inhibits bone formation by decreasing osteoblasts, type 1 collagen, absorption of calcium from the gut and increases osteoclastic activity
increases insulin resistance
increases gluconeogenesis, lipolysis and proteolysis
inhibits inflammatory and immune responses
maintains function of skeletal and cardiac muscle

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20
Q

what is somatostatin effect on insulin?

A

it inhibits its secretion

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21
Q

what increases gut absorption of calcium?

A

1,25-dihydroxycholecalciferol

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22
Q

what is hyperthyroidism also known as?

A

thyrotoxicosis

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23
Q

outline the HPA axis of the thyroid hormones?

A

hypothalamus secretes thyrotropin releasing hormone
anterior pituitary secretes thyroid stimulating hormone
thyroid gland increases production of thyroxine (T4) and triiodothyronine (T3)

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24
Q

whats the most common cause of hypothyroidism?

A

hashimotos thyroiditis

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25
whats the most common cause of thyrotoxicosis?
graves disease
26
what is hashimotors thyroiditis?
an autoimmune disease associated with diabetes mellitus/addisons disease/pernicious anaemia
27
what is graves disease?
an autoimmune disease where your body attacks the thyroid gland causing overactivtaion
28
what will hormone levels look like in graves disease?
high free T4 | low TSH
29
what will hormones levels look ike in primary hypothyroidism?
high TSH | low free T4
30
what antibodies are usually present in those with Graves disease?
TSH receptor antibodies
31
what antibodies are usually present in Hashimotos thyroiditis?
anti-TPO antibodies
32
outline the relative glucocorticoid and mineralocorticoid activity of fludrocortisone?
minimal gluco | very high mineralo
33
outline the relative glucocorticoid and mineralocorticoid activity of hydrocortisone?
little gluco and high mineralo
34
outline the relative glucocorticoid and mineralocorticoid activity of prednisolone?
mostly gluco | low mineralo
35
outline the relative glucocorticoid and mineralocorticoid activity of dexamethasome?
very high gluco and minimal mineralo
36
outline the relative glucocorticoid and mineralocorticoid activity of betmethasone?
very high gluco and minimal mineralo
37
what are some adverse effects associated with excess glucocorticoids?
``` thinning of skin, osteonecrosis and osteoporosis immunosuppression hyperglycemia cushings syndrome adrenal suppression weight gain ```
38
whats the main cause of acute primary adrenal insufficiency?
massive adrenal haemorrhage
39
what are hormone levels lie in primary adrenal insufficiency?
low aldosterone and low cortisol
40
what are hormone levels like in secondary adrenal insufficiency?
``` cortisol low aldosterone normal (as not under ACTH control) ```
41
what are hormones levels like in tertiary adrenal insufficiency?
low cortisol | normal aldosterone
42
what are the common causes of tertiary adrenal insufficiency?
head trauma/intercranial tumours | sudden withdrawal of chronic glucocorticoid therapy and resolution of cushings syndrome
43
what is adrenal crisis?
acute adrenal insufficiency usually when the body is under stress e.g. illness/surgery, and the adrenal glands cant meet the increase demands of cortisol
44
how does acute adrenal insufficiency present?
``` hypotension/shock vomiting abdominal pain fever mental state changes ```
45
why can symptoms of chronic adrenal insufficiency often go unnoticed?
as the body can compensate for low cortisol and aldosterone
46
what are the main symptoms of chronic adrenal insufficiency?
fatigue anorexia abdominal pain muscle and joint pain
47
what are the main symptoms of chronic adrenal insufficiency?
fatigue anorexia abdominal pain muscle and joint pain
48
what are some symptoms specific to primary adrenal insufficiency?
hyperpigmentation (of oral mucosa, creases on hands etc) salt cravings hypotension
49
why do we see hyperpigmentation in primary adrenal insufficiency?
due to increased production of melanin proopiomelanocortin is the precursor for ACTh and melanostimulating hormone so when we get increased ACTH we get increase MSH
50
why do we see salt craving in primary adrenal insufficiency?
because cortisol is too low to regulate Salt so not enough is retained and we crave it
51
why do we see hypotension in primary adrenal insufficiency?
aldosterone levels being low means Na+ is not retained so we get Na+ loss and therefore volume loss
52
what is aldosterone effect on K+?
increases excretion of potassium by the kidneys
53
what are some symptoms specifically related to secondary and tertiary adrenal insufficiency?
headaches visual abnormalities features of hypopituitarism
54
what symptoms will those with secondary and tertiary adrenal insufficiency not have that primary do?
hyperpigmentation hyperkalaemia (as aldosterone levels are normal and np ACTH excess)
55
what is cosyntropin?
synthetic ACTH
56
what does it mean if cortisol is low before and after cosyntropin administration?
primary adrenal insufficiency
57
what does it mean if cortisol is low and then high once cosyntropin is given?
central adrenal insufficiency (secondary or tertiary)
58
how is adrenal insufficiency treated?
with glucocorticoids e.g. hydrocortisone | and mineralocorticoids in cases of primary with decreased aldosterone (e.g. fludrocortisone)
59
outline the steps of steroidogenesis that lead to aldosterone formation?
cholesterol is converted to pregnenolone by cholesteroldesmolase pregnenolone is converted to progesterone by 3-beta HSD progesterone Is converted to 11-deoxycorticosterone by 21-hydroxylase 11-deoxycorticosterone is converted to corticosterone by 11 beta hydroxylase corticosterone is converted to aldosterone by aldosterone synthase
60
outline the steps of steroidogenesis that lead to cortisol formation?
17 alpha hydroxylase turns pregnenolone into 17-OH pregnenolone and turns progesterone into 17-OH progesterone 3beta-HSD can turn 17-OH pregnenolone into 17-OH progesterone 17-OH progesterone can be converted to 11-deoxycortisol by 21 hydroxylase 11-deoxycortisol can be converted to cortisol by 11 beta hydroxylase
61
outline the steps of steroidogenesis that lead to testosterone formation?
17-OH progesterone and 17-OH pregnenolone can be converted to dehydroepiandrosterone and androstenedione by 17,20-lyase these can then be converted to testosterone
62
what symptoms appear in carcinoid syndrome?
diarrhoea, shortness of breath and flushing
63
whats the cause of carcinoid syndrome?
when a neuroendocrine tumour secretes large amounts of hormones which build up and cannot be broken down by the liver due to the dysfunction caused by metastasis to here
64
what is MEN?
multiple endocrine neoplasias | a group of inherited diseases which cause tumours to grow in endocrine glands
65
whats the cause of MEN type 1?
dominant mutations in MEN1 gene
66
whats the cause of MEN type 2a and 2b?
mutations in the RET gene
67
what are the 3 types of tumours in Men type 1?
pituitary parathyroid pancreatic
68
what is Zollinger-Ellison syndrome?
a condition in which a gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas causes overproduction of gastric acid, resulting in recurrent peptic ulcers.
69
what do men2a and 2b cause?
medullary thyroid cancer and pheochromocytoma
70
which drugs are CYP450s inducers?
``` carbemazepines rifampicin alcohol phenytoin griseofulvin phenobarbitone sulphonylureas ``` (CRAP GPs)
71
which drugs are CYP450 inhibitors?
``` sodium valproate isoniazid crimetidine ketoconazole fluconazole alcohol and grapefruit juice chloramphenicol erythromycin sulfonamides ciprofloxacin omeprazole metronidazole ``` (SICKFACES.COM)
72
what is a pheochromocytoma?
an adrenal medulla tumour which causes excess catecholamines to be secreted
73
what is Gilberts disease?
UGT gene variant results in decreased activity of bilirubin UGT enzyme so bilirubin is processed more slowly
74
what is Wilsons disease?
rare genetic disorder characterized by excess copper stored in liver/brain/corneas. Can lead to liver disease, CNS dysfunction and even death
75
what predisposes you to chronic pancreatitis?
heavy alcohol, autoimmune conditions, genetic mutations due to cystic fibrosis, blocked pancreatic or common bile duct, familial pancreatitis.
76
what is acute cholangitis?
acute inflammation and infection of biliary tree due to bile stasis or bacterial growth in bile.
77
what is primary biliary cirrhosis?
chronic disease affecting bile ducts which leads to blackage, causing a build up of bile within the liver, causing liver inflammation and scarring.
78
what is primary sclerosing cholangitis?
a chronic liver disease in which the bile ducts inside and outside the liver become inflamed and scarred, and eventually narrowed or blocked.

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