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REVISION EXTRAS > BLOCK 15 > Flashcards

BLOCK 15 Flashcards

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
Q

whats the most common cause of thyrotoxicosis?

A

graves disease

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26
Q

what is hashimotors thyroiditis?

A

an autoimmune disease associated with diabetes mellitus/addisons disease/pernicious anaemia

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27
Q

what is graves disease?

A

an autoimmune disease where your body attacks the thyroid gland causing overactivtaion

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28
Q

what will hormone levels look like in graves disease?

A

high free T4

low TSH

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29
Q

what will hormones levels look ike in primary hypothyroidism?

A

high TSH

low free T4

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30
Q

what antibodies are usually present in those with Graves disease?

A

TSH receptor antibodies

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31
Q

what antibodies are usually present in Hashimotos thyroiditis?

A

anti-TPO antibodies

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32
Q

outline the relative glucocorticoid and mineralocorticoid activity of fludrocortisone?

A

minimal gluco

very high mineralo

33
Q

outline the relative glucocorticoid and mineralocorticoid activity of hydrocortisone?

A

little gluco and high mineralo

34
Q

outline the relative glucocorticoid and mineralocorticoid activity of prednisolone?

A

mostly gluco

low mineralo

35
Q

outline the relative glucocorticoid and mineralocorticoid activity of dexamethasome?

A

very high gluco and minimal mineralo

36
Q

outline the relative glucocorticoid and mineralocorticoid activity of betmethasone?

A

very high gluco and minimal mineralo

37
Q

what are some adverse effects associated with excess glucocorticoids?

A 
thinning of skin, osteonecrosis and osteoporosis
immunosuppression
hyperglycemia
cushings syndrome
adrenal suppression
weight gain
38
Q

whats the main cause of acute primary adrenal insufficiency?

A

massive adrenal haemorrhage

39
Q

what are hormone levels lie in primary adrenal insufficiency?

A

low aldosterone and low cortisol

40
Q

what are hormone levels like in secondary adrenal insufficiency?

A 
cortisol low 
aldosterone normal (as not under ACTH control)
41
Q

what are hormones levels like in tertiary adrenal insufficiency?

A

low cortisol

normal aldosterone

42
Q

what are the common causes of tertiary adrenal insufficiency?

A

head trauma/intercranial tumours

sudden withdrawal of chronic glucocorticoid therapy and resolution of cushings syndrome

43
Q

what is adrenal crisis?

A

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
Q

how does acute adrenal insufficiency present?

A 
hypotension/shock
vomiting
abdominal pain
fever
mental state changes
45
Q

why can symptoms of chronic adrenal insufficiency often go unnoticed?

A

as the body can compensate for low cortisol and aldosterone

46
Q

what are the main symptoms of chronic adrenal insufficiency?

A

fatigue
anorexia
abdominal pain
muscle and joint pain

47
Q

what are the main symptoms of chronic adrenal insufficiency?

A

fatigue
anorexia
abdominal pain
muscle and joint pain

48
Q

what are some symptoms specific to primary adrenal insufficiency?

A

hyperpigmentation (of oral mucosa, creases on hands etc)
salt cravings
hypotension

49
Q

why do we see hyperpigmentation in primary adrenal insufficiency?

A

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
Q

why do we see salt craving in primary adrenal insufficiency?

A

because cortisol is too low to regulate Salt so not enough is retained and we crave it

51
Q

why do we see hypotension in primary adrenal insufficiency?

A

aldosterone levels being low means Na+ is not retained so we get Na+ loss and therefore volume loss

52
Q

what is aldosterone effect on K+?

A

increases excretion of potassium by the kidneys

53
Q

what are some symptoms specifically related to secondary and tertiary adrenal insufficiency?

A

headaches
visual abnormalities
features of hypopituitarism

54
Q

what symptoms will those with secondary and tertiary adrenal insufficiency not have that primary do?

A

hyperpigmentation
hyperkalaemia
(as aldosterone levels are normal and np ACTH excess)

55
Q

what is cosyntropin?

A

synthetic ACTH

56
Q

what does it mean if cortisol is low before and after cosyntropin administration?

A

primary adrenal insufficiency

57
Q

what does it mean if cortisol is low and then high once cosyntropin is given?

A

central adrenal insufficiency (secondary or tertiary)

58
Q

how is adrenal insufficiency treated?

A

with glucocorticoids e.g. hydrocortisone

and mineralocorticoids in cases of primary with decreased aldosterone (e.g. fludrocortisone)

59
Q

outline the steps of steroidogenesis that lead to aldosterone formation?

A

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
Q

outline the steps of steroidogenesis that lead to cortisol formation?

A

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
Q

outline the steps of steroidogenesis that lead to testosterone formation?

A

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
Q

what symptoms appear in carcinoid syndrome?

A

diarrhoea, shortness of breath and flushing

63
Q

whats the cause of carcinoid syndrome?

A

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
Q

what is MEN?

A

multiple endocrine neoplasias

a group of inherited diseases which cause tumours to grow in endocrine glands

65
Q

whats the cause of MEN type 1?

A

dominant mutations in MEN1 gene

66
Q

whats the cause of MEN type 2a and 2b?

A

mutations in the RET gene

67
Q

what are the 3 types of tumours in Men type 1?

A

pituitary
parathyroid
pancreatic

68
Q

what is Zollinger-Ellison syndrome?

A

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
Q

what do men2a and 2b cause?

A

medullary thyroid cancer and pheochromocytoma

70
Q

which drugs are CYP450s inducers?

A 
carbemazepines
rifampicin
alcohol
phenytoin
griseofulvin
phenobarbitone
sulphonylureas

(CRAP GPs)

71
Q

which drugs are CYP450 inhibitors?

A 
sodium valproate
isoniazid
crimetidine
ketoconazole
fluconazole
alcohol and grapefruit juice
chloramphenicol
erythromycin
sulfonamides
ciprofloxacin
omeprazole
metronidazole

(SICKFACES.COM)

72
Q

what is a pheochromocytoma?

A

an adrenal medulla tumour which causes excess catecholamines to be secreted

73
Q

what is Gilberts disease?

A

UGT gene variant results in decreased activity of bilirubin UGT enzyme so bilirubin is processed more slowly

74
Q

what is Wilsons disease?

A

rare genetic disorder characterized by excess copper stored in liver/brain/corneas. Can lead to liver disease, CNS dysfunction and even death

75
Q

what predisposes you to chronic pancreatitis?

A

heavy alcohol, autoimmune conditions, genetic mutations due to cystic fibrosis, blocked pancreatic or common bile duct, familial pancreatitis.

76
Q

what is acute cholangitis?

A

acute inflammation and infection of biliary tree due to bile stasis or bacterial growth in bile.

77
Q

what is primary biliary cirrhosis?

A

chronic disease affecting bile ducts which leads to blackage, causing a build up of bile within the liver, causing liver inflammation and scarring.

78
Q

what is primary sclerosing cholangitis?

A

a chronic liver disease in which the bile ducts inside and outside the liver become inflamed and scarred, and eventually narrowed or blocked.

REVISION EXTRAS (7 decks)

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