Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

phase 2a endocrinolgy > endocrinolgy > Flashcards

endocrinolgy Flashcards

1
Q

define hormone

A

to excite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

define endocrine

A

when glands pour secretions into the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

list the endocrine organs

A

thyroid, adrenal gland, endocrine pancreas (beta cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

define exocrine

A

pour secretions through a duct to site of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

give an example of an exocrine organ

A

exocrine pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

define endocrine action

A

blood born, acting at different sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

define paracrine action

A

acting on adjacent cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

define autocrine action

A

feedback on the same cell that secreted the hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe the transport in water-soluble and lipid-soluble hormones

A

water-soluble, unbound
lipid-soluble, protein bound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe cell interaction in water-soluble and lipid-soluble hormones

A

water-soluble, bind to receptor
lipid soluble, diffuse into cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe the half-life of water-soluble and lipid-soluble hormones

A

water-soluble, short
lipid-soluble, long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe the clearance of water-soluble and lipid-soluble hormones

A

water-soluble, fast
lipid-soluble, slow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

give 2 examples of water-soluble hormones

A
  1. peptides
  2. monoamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

give 2 examples of fat-soluble hormones

A

thyroid hormone and steroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how are peptides/monoamines stored?

A

in vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how are steroid hormones stored?

A

they’re synthesised on demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how are peptide hormones released?

A

in pulses or bursts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe how the insulin receptor works

A

1insulin binds to a receptor on the cell membrane
2. this causes phosphorylation of the receptor, and tyrosine kinase is now active
3. signal molecules are now activated, causing a cascade of effects and anabolic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe how the insulin receptor works

A

1insulin binds to a receptor on the cell membrane
2. this causes phosphorylation of the receptor, and tyrosine kinase is now active
3. signal molecules are now activated, causing a cascade of effects and anabolic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

there are 5 hormone stages in the formation of adrenaline, name them

A
  1. L-phenylalanine
  2. L-Tyrosie
  3. L-Dopa
  4. Dopamine
  5. Noradrenaline
  6. Adrenaline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

which hormone is essential for adrenaline synthesis?

A

cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what type of hormone is adrenaline?

A

amine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

when measuring adrenaline what do we measure instead?

A

it’s breakdown products so normetanephrine and metanephrines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what receptors does adrenaline act on?

A

alpha-adrenergic or beta-adrenergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

is thyroid hormone water soluble?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

describe T3 and T4 synthesis

A
  1. thyroglobulin is synthesized by RE and discharged into the follicle lumen
  2. Iodide is actively transported into the lumen
    3.iodide is oxidized into iodine
  3. in the colloid, iodine is attached to tyrosine, forming DIT or MIT
  4. iodinated tyrosine is linked together to form T3 or T4
  5. lysosomal enzymes cleave T3 and T4 from thyroglobulin, hormones diffuse into blood stream
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

which hormones act on the cell membrane receptors?

A

peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

which hormones act on cytoplasmic receptors?

A

steroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

which hormones act on nucleic receptors?

A

thyroid, oestrogen, vitmine D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what transports vitamin D?

A

vitamin D transporting protein?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

when are cortisol levels highest?

A

in the morning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what does synergism mean in regard to hormones?

A

2 effects of hormones amplified ie glucagon with epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

which sinus does the pituitary gland sit directly above?

A

sphenoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

which structure is directly above the pituitary?

A

the optic chiasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What synthesizes oxytocin and ADH?

A

hypothalamic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

where are oxytocin and ADH stored?

A

the posterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

how does hypotension affect ADH release?

A

it increases it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How do caffeine and alcohol affect ADH?

A

Causes it to decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what effect does ADH have on smooth muscle and the kidneys?

A

causes vasoconstriction in the muscle and causes more aquaporins to be present in the kidney leading to increased water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what does oxytocin initiate?

A

milk ejection and labour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

which hormones are secreted from the neurosecretory cells of the hypothalamus?

A

GHRH, GHIH (growth hormone inhibiting hormone, somatostatin), CRH, TRH, GnRH, Dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

which hormones are released from the anterior pituitary?

A

TSH, ACTH, FSH, LH, GH, prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

how may there be pituitary dysfunction?

A
  1. tumour mass effects
  2. hormone excess
  3. hormone deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what are the half lives of T3 and T4

A

T4- 5 to 7 days
T3 1 day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

give 3 functions of thyroid hormone

A
  1. accelerates food metabolism
  2. increases CO and HR
  3. accelerated growth rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

where is the adrenal gland located?

A

one on top of each kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How can the adrenal gland be subdivided?

A

into the medulla and the cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

which sections make up the adrenal cortex?

A

zona glomerulosa
zona fasciculata
zona reticularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what does the zona glomerulosa secrete?

A

mineralocorticoids- aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what does the zona fasciculata secrete?

A

glucocorticoids- cortisol androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what does the zona reticularis secrete?

A

androgens- androstenedione and DHEA- dihyrdroepiandrosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what does the adrenal medulla secrete?

A

adrenaline and noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

where is rnein released from?

A

juxtaglomerular cells in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what does renin do?

A

coverts angiotensinogen to angiotensin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what does renin do?

A

coverts angiotensinogen to angiotensin 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

how is angiotensin converted?

A

by angiotensin-converting enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

where is angiotensin 1 converted?

A

in the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what does angiotensin 2 do?

A
  1. causes NA+ reabsorption
  2. causes hypothalamus to secrete ADH
  3. causes noradrenaline secretion
  4. causes arterioles to vasoconstrict
  5. causes aldosterone secretion from zona glomerulosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what happens when angiotensin 2 causes increased NA+ reabsorption?

A

water absorption also increases, which also increases blood volume and blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what does aldosterone do?

A

increases renal K+ excretion and Na+ reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what has an inhibitory effect on aldosterone secretion?

A

atrial natruretic hormone, released by the heart when the blood pressure is too high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

which cells does LH affect in females

A

theca cells, the convert cholesterol to androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

which cells does FSH affect in females?

A

granulosa cells, converts androgens to oestrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

which cells does LH affect in men?

A

leydig cells, producing testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what cells does FSH affect in men?

A

Sertoli cells, they support the development of spermatogonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How are Sertoli cells involved in the negative feedback of FSH?

A

they produce inhibin B, which has an inhibitory effect on the anterior pituitary’s production of FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Describe prolactin secretion

A

dopamine inhibits prolactin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what hormone does the heart secrete?

A

atrial natriuretic peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

where is insulin-like growth factor 1secreted from?

A

the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

where is erythropoietin secreted from?

A

the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

name two hormones that the GI tract secretes.

A

gastrin and incretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

which 3 ways may someone with a pituitary dysfunction present?

A
  1. tumour mass effects
  2. hormone excess
  3. hormone deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what investigations would be done on a patient with suspected pituitary dysfunction?

A
  1. hormonal tests if abnormal then MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

define appetite

A

the desire to eat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

define hunger

A

the need to eat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

define anorexia

A

lack of desire to eat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

define satiety

A

the disappearance of appetite after eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what is the equation for BMI?

A

weight in KG / height^2(m^2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what BMI score would identify someone as being underweight?

A

less than 18.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what BMI score would identify someone as being normal weight?

A

between 18.5 and 24.9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what BMI would identify someone as being obese?

A

25 to 39.9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what BMI would identify someone as being morbidly obese

A

above 40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

describe the satiety cascade

A

internal physiological feelings prompting thoughts of food and eating
external psychological drive-
can be present even when not hungry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

how does the hypothalamus play a central role in appetite regulation?

A

lateral hypothalamus- hunger center
ventromedial- satiety center

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

how does the hypothalamus play a central role in appetite regulation?

A

lateral hypothalamus- hunger center
ventromedial- satiety center

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

which hormone switches off appetite?

A

leptin, also immunostimulatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what effect does peptide YY have on gastric motility and appetite?

A

reduces appetite and inhibits gastric motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

where are the receptors for cholecystokinin?

A

pyloric sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what does cholecystokinin do?

A
  1. delays gastric emptying
  2. gall bladder contraction
  3. insulin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

which cranial nerve does cholecystokinin stimulate?

A

the vagus nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what does ghrelin do?

A

stimulates growth hormone release and appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

in the fasting state, where does glucose come from?

A

majority liver, a bit from kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

how does the liver provide glucose in the fasting state?

A

gluconeogenesis using 3 carbon precursors such as alanine, lactate and glycerol
break down of glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

glucose is delivered to insulin-independent tissues during the fasting state, name these tissues

A

red blood cells and the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

describe insulin levels in the fasting state

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what supplies energy to muscles during the fasting state?

A

free fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what do low levels of insulin prevent?

A

unrestrained breakdown of fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

postprandial, where does the glucose go? (Non diabetic humans)

A

40% to liver, 60% to periphery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what causes lipolysis and non esterified free fatty acid levels to fall postprandial?

A

high glucose and insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

where are glucose and insulin secreted from?

A

islets of Langerhans in the endocrine pancreas, beta cells release insulin, alpha cells glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

describe the paracrine regulation between beta and alpha cells

A

local insulin release inhibits glucagon release and vice versa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

describe insulin secretion by beta cells

A
  1. glucose enters cells via glut2 transporter
  2. glucokinase causes glucose metabolism and ATP release
  3. potassium channel closes, causing cell membrane depolarization
  4. calcium channels open, stimulating insulin secretory granules to release insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

how does insulin cause the uptake of glucose in muscle and adipose cells?

A

mobilization of glut4 into the cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what does insulin supress?

A

the hepatic output of glucose via suppression of gluconeogenesis and glycogenolysis
lipolysis and break down of muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What does glucagon increase

A

the hepatic output of glucose via increasing gluconeogenesis and glycogenolysis

peripheral release of gluconeogenic precursors like glycerol and amino acids via stimulating lipolysis and muscle breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Define diabetes mellitus

A

a disorder of carbohydrate metabolism characterised by hyperglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

In which 3 ways does diabetes mellitus cause morbidity and mortality?

A

Acute hyperglycemia
chronic hyperglycaemia
hypoglycaemia caused by medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what serious complication occurs in 30% of people with diabetes?

A

diabetic retinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

what is the most common cause of death in people with diabetes?

A

cardiovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

what are the different types of type 2 diabetes?

A
  1. gestational and medication-induced
  2. monogenic diabetes
  3. pancreatic diabetes
  4. cushings/acromegaly
  5. malnutrition related
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

what value from random plasma glucose would indicate diabetes?

A

more than 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

what value from a fasting blood plasma glucose would indicate diabetes?

A

above 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

what value on a glucose tolerance test would indicate that someone is diabetic?

A

more than 11m/mol after 2 or 7 hour intervals, taken on 2 separate occasions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what HbA1c value would indicate diabetes?

A

48m/mol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

describe the pathogenesis of type 1 diabetes

A

an insulin deficiency caused by the loss of beta cells. Beta cells are destroyed in an chronic cell mediated autoimmune response after they display HLA antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

in type 1 diabetes what does failure to secrete insulin cause?

A
  1. hepatic breakdown of glycogen
  2. unrestrained lipolysis and breakdown of skeletal muscle
  3. inappropriate hepatic glucose output and impression of peripheral uptake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

what is the renal threshold for glucose?

A

10mM, exceeding causes urinary glucose loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Which 2 factors cause impaired glucose tolerance in type 2 diabetes?

A
  1. impaired insulin tolerance
  2. impaired insulin secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

what happens to the Beta cells as diabetes progresses?

A

they become more dysfunctional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

what does the impaired insulin action in type 2 diabetes cause?

A
  1. decreased suppression of lipolysis, leading to more circulating free fatty acids
  2. reduced uptake of glucose by muscle and fat after eating.
  3. abnormally high glucose output after a meal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

why are muscle catabolism and ketogenesis usually restrained in type 2 diabetes?

A

there is still a small amount of insulin, which prevents this from happening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

what symptom are you likely to see in type one diabetes that you are unlikely to see in type 2?

A

Ketonuria, there is insulin deficiency, meaning that ketogenesis isn’t prevented

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

which symptom are you likely to see in both type 1 and type 2 diabetes

A

glycosuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

what can reverse hyperglycemia in type 2 diabetes?

A

regular exercise and a healthy diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

what mechanism do sulphonylureas work by?

A

they bind to beta cells to stimulate insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

name 2 sulphonyl ureas

A

gliclazide and glibenclamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

what are the benefits of sulphonylureas?

A

they improve glycaemic control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

what are the side effects of sulphonylureas?

A
  1. cause significant weight gain
    2.don’t prevent gradual failure of insulin secretion
  2. can cause hypoglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

what action do thiazolidinediones do ?

A

they activate genes concerned with glucose uptake and utilization
and lipid metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

what benefit do thiazolidinediones have?

A

they increase insulin sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

where is glucagon-like peptide secreted from?

A

L cells in the intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

name 3 mechanisms of action that GLP-1 has

A
  1. stimulates insulin secretion
  2. reduces glucagon secretion
  3. reduces gastric emptying
  4. increase beta cell mass and maintains function
  5. improves insulin sensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

How is GLP-1 cleared?

A

enzymatically and renally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Name 2 drugs that reduce GLP-1 clearing

A

exenatide
liraglutide
dulaglutide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

How do SGLT-2 inhibitors work?

A

blocking sites of glucose reabsorption at the kidneys causing more to be excreted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

what are the 2 types of insulin given for T1DM AND T2DM?

A

fast acting prandial and basal insulin and you can get a mixed medicine of both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

when is basal insulin crucial for controlling blood sugar

A

in between meals and at night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

give 2 advantages of basal insulin in T2DM

A
  1. simple for the patient to adjust based on their fasting glucose measurements
    2.less risk of hypoglycemia at night
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

give 2 disadvantages of basal insulin in T2DM

A
  1. doesn’t cover meals
  2. best used with long-acting insulin analogs which are considered expensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Give 2 positives of pre-mixed insulin in diabetes

A
  1. basal and prandial insulin in a single mixture
  2. can cover insulin requirements for most of the day
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Give 2 disadvantages of premixed insulin

A
  1. not physiological
  2. requires regular exercise and diet routine
  3. can’t titrate individual components
  4. higher risk of nocturnal hypoglycemia
  5. higher risk of fasting hypoglycemia
  6. higher HBA1C target
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

what is the difference between severe and non-severe hypoglycemia

A

severe is when the patient is cognitively impaired and cannot treat themselves and requires external help, non severe is when they are slight;y cognitively impaired and can help themselves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

list symptoms of hypoglycemia

A
  1. trembling, palpitations, anxiety, hunger, sweating, difficulty concentrating, confusion, weakness, drowsiness, dizziness, vision changes, weakness, difficulty speaking, nausea, headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

what blood glucose level would be considered hypoglycemic?

A

less than 3.9mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

what would someone experiencing hypoglycemia respond to?

A

carbohydrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

what are some of the mechanisms that will protect a patient from hypoglycemia and how is this different in diabetes?

A
  1. inhibition of endogenous insulin secretion
  2. glucagon release
  3. adrenaline release

in diabetes insulin is gone in T1DM and glucagon is lost within 5 years, so the patient is reliant on adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

How does repeated hypoglycemia affect adrenaline response?

A

the brain becomes worse at responding to hypoglycemia so doesn’t stimulate adrenal to release adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

How do you treat hypoglycemia?

A
  1. recognize symptoms
  2. Confirm blood glucose is less than 3.9mmol/l
  3. treat with 15g fast acting carbohydrate
  4. retest in 15 mins to see if that had any effect
  5. eat a long acting carbohydrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

what effect does parathyroid hormone have on calcium reabsorption?

A

causes it to increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

what effect does parathyroid have on phosphate reabsorption?

A

it causes it to decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

what affect does parathyroid have on 1 alpha hydroxylation of 25-OH vitamin D?

A

it causes it to increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What effect does parathyroid have on bone remodeling?

A

it causes it to increase, bone resorption is quicker than bone formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

How does the parathyroid hormone act indirectly on calcium absorption?

A

Parathyroid hormone increase 1 alpha hydroxylation of 25-OH vitamin D, this causes calcium reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

what effect does parathyroid have on FGF-23?

A

it decreases it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is parathyroid hormone released in response to?

A

lowered serum calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

How does parathyroid hormone act to increase serum calcium?

A

it causes increased bone resorption, increases calcium reabsorption and increased 1-25 hydroxy vitamin D which causes increased Ca2+ absorption in the bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

what type of feedback is calcium homeostasis?

A

negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

what is the serum calcium set point?

A

1.1mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

what is the relationship between serum calcium and parathyroid hormone?

A

big changes in calcium cause big changes in parathyroid

159
Q

which interval of an ECG is affected by calcium levels and how?

A

the Q-T interval, low Ca2+ means long QT interval, high Ca2+ ,means short QT interval

160
Q

which 2 signs are associated with hypocalcemia?

A

chvostek’s sign- tapping facial nerve and looking for spasm
Trousseau’s sign, inflating blood pressure cuff to 20mmHG above systolic pressure and watching for hand cramping 5 minutes later

161
Q

Give 3 signs or symptoms of hypocalcemia

A
  1. abnormal ECG
  2. muscle spasms
  3. basal ganglia calcification
  4. cataracts
  5. seizures
162
Q

what are the causes of hypocalcemia?

A

hypoparathyroidism
vitamin D deficiency

163
Q

what are the causes of hypoparathyroidism?

A

surgery, radiation, syndromes such as di George syndrome, genetics, autoimmune problems, infiltration and magnesium deficiency

164
Q

what is pseudohypoparathyroidism?

A

resistance to parathyroid hormone,

165
Q

what would parathyroid levels look like in pseudoparathyroidism

A

High, as there is reduced calcium serum levels so loads of parathyroid hormone

166
Q

what may cause some results to look like hypercalcemia?

A

leaving a tourniquet on for too long, using old blood samples that have been heamolysed

167
Q

what are the symptoms of hypercalcemia?

A

polyuria, polydipsia, constipation, nausea, confusion that turns into a coma

168
Q

what are the signs of hypercalcemia?

A

short QT interval on ECG and renal stones

169
Q

what are the 2 main causes of hyperparathyroidism?

A

malignancy, primary hyperparathyroidism

170
Q

what are the effects of hypercalcemia on PTH and calcium absorption and reabsorption?

A

causes a decrease in PTH, a decrease in bone resorption, a decrease in calcium reabsorption and a decrease in calcium gut absorption

171
Q

what are the consequences of primary hyperparathyroidism?

A

Bones- osteoporosis
Stones- kindeys
Groans- confusion
Moans- constipation and acute pancreatitis

172
Q

How does primry hyperthyroidism affect calcium

A

causes hypercalcemia

173
Q

when is a corrected calcium appropriate to calculate?

A

when the patient has hypoalbuminemia, there serum calcium may look low however their ionised calcium will be normal

174
Q

what is the equation for corrected calcium?

A

total serum calcium + 0.02*( 40- serum albumin)

175
Q

where is the pituitary located?

A

sela turcica

176
Q

what sits above the pituitary?

A

optic chiasm

177
Q

what type of supply does the anterior pituitary have?

A

portal venous supply from hypothalamus

178
Q

describe the thyroid axis

A

the hypothalamus releases thyroid-releasing hormone which stimulates the anterior pituitary to release thyroid-stimulating hormone, which stimulates the thyroid to release T3 and T4, this has a negative feedback effect on the hypothalamus and pituitary

179
Q

what would the TSH levels look like in someone with an underactive thyroid?

A

they would be high

180
Q

what would the TSH levels in someone with thyrotoxic look like

A

they would be low

181
Q

In men what does LH stimulate?

A

the release of teststerone

182
Q

How does testosterone feedback to the hypothalamus and pituitary?

A

negatively, through conversion to oestrogen

183
Q

In men what role does FSH play in ?

A

fertility and sperm production

184
Q

In women what does LH stimulate?

A

release of oestradiol

185
Q

In women what is FSH important for?

A

egg production

185
Q

In women what is FSH important for?

A

egg production

186
Q

In women what is FSH important for?

A

egg production

187
Q

what happens to LH and FSH at menopause?

A

They go up, menopause is the failure of the ovary to secrete oestrogen

188
Q

Describe the hypothalamic-pituitary-adrenal axis.

A

Hypothalamus release corticotropin-releasing hormone, stimulating the pituitary to release ACTH ( adrenocorticotrophic hormone), causing the adrenal to release cortisol. negative feedback

189
Q

when does pulsatile growth hormone release occur?

A

at night

190
Q

Which hormone does the hypothalamus release to stimulate growth hormone release?

A

Growth hormone-releasing hormone

191
Q

Which hormone does the hypothalamus release to suppress the release of growth hormone?

A

somatostatin

192
Q

Where is growth hormone released from?

A

the anterior pituitary

193
Q

what has a negative feedback effect on the GH/IGF axis?

A

insulin like growth factor 1

194
Q

where is IGF-1 released from?

A

the liver

195
Q

what is the most common cause of disease of the pituitary?

A

benign pituitary adenoma

196
Q

what 3 things do tumours cause?

A
  1. pressure on surrounding structures
  2. pressure on the normal pituitary
  3. functioning tumor
197
Q

what is the normal presentation of a pituitary adenoma compressing the optic chiasm?

A

bitemporal hemianopia

198
Q

How does a benign pituitary adenoma present via causing pressure on the pituitary?

A

it causes hypopituitary

199
Q

what are the 3 functioning pituitary diseases?

A
  1. prolactinoma
  2. gigantism or acromegaly
  3. cushings
200
Q

what are the 3 functioning pituitary diseases?

A
  1. prolactinoma
  2. gigantism or acromegaly
  3. cushings
201
Q

what makes up testicular size?

A

germ size

202
Q

what is thelarche?

A

the start of breast development

203
Q

what induces thelarche?

A

oestrogen

204
Q

How long does thelarche take?

A

about 3 years

205
Q

which other hormones are involved in breast development?

A

prolactin, glucocorticoids, insulin

206
Q

How does a prepubertal and postpubertal uterus differ?

A

Prepubertal:
tubular shape, endometrium a single cuboidal layer, corpus-to-cervix ration 1:2
postpubertal:
pear shape, thick endometrium, corpus-to-cervix ratio 2:1

207
Q

How do the ovaries vary between prepubertal and postpubertal?

A

Prepubertal has no cysts, postpubertal is multicystic

208
Q

what grows under the influence of adrenal and ovarian androgens?

A

pubic and axillary hair

209
Q

what grows under the influence of oestrogens?

A

the labia majora and minora
hymen
clitoris

210
Q

what is adrenarche?

A

awakening of the adrenal gland (androgen producing zona reticularis)

211
Q

who is adrenarche more pronounced in?

A

obese children

212
Q

who does precocious puberty mainly occur in?

A

females

213
Q

why is a male going through precocious puberty something to be concerned about?

A

they may have a brain tumor

214
Q

what is pseudo-precocious puberty?

A

where they have androgens but the system isn’t activated

215
Q

is precocius puberty GNRH dependent or independent?

A

dependent

216
Q

what are the causes of true precocious puberty?

A

CNS tumors
CNS disorders

217
Q

what causes pseudo-precocious puberty?

A

increased androgen secretion
gonadotropin secreting tumors

218
Q

who is it most common to see with delayed puberty?

A

males

219
Q

Should you be concerned if a female presents with delayed puberty?

A

yes there is a high chance of pathology

220
Q

what test should you do on girls with short stature?

A

karyotyping, they may have turners syndrome

221
Q

If someone presents with delayed puberty, is it usually an endocrine problem?

A

no it’s usually something else

222
Q

Describe kallman syndrome.

A

hypogonadotropic hypogonadism, more common in males than females, caused by failure of pituitary neuron descension, small penis and testis

223
Q

How does turners syndrome present at birth?

A

oedema at dorsal of hands and feet, skin gathered at the knape of the neck

224
Q

what infection do girls with turners syndrome get?

A

otitis media

225
Q

what is the most common form of goitre?

A

iodine deficiency

226
Q

define hyperthyroidism

A

excess of thyroid hormone

227
Q

what are the 3 causes of hypothyroidism?

A
  1. overproduction of thyroid hormone
  2. leakage of premade thryoid hormone
  3. ingestion of excess thyroid hormone
228
Q

what is the most common cause of hyperthyroidism?

A

graves disease, autoimmune problem where TSH receptor antibodies are produced

229
Q

what are the 2 less common causes of hyperthyroidism?

A

multinodular goitre and toxic adenoma

230
Q

Name some clinical features of hyperthyroidism

A

anxiety
weight loss
tachycardia
hyperphagia
menstrual disturbance
diarrhea
sweating

231
Q

describe graves dermopathy

A

orange peel rash caused by protein deposition in subcutaneous tissues

232
Q

How may eyes affected by hyperthyroidism look?

A

bulging, swollen

233
Q

what results from a thyroid function test would you expect with primary hyperthyroidism?

A

increased T3/T4 and decreased TSH

234
Q

what would results from a thyroid function test would you expect in secondary hyperthyroidism?

A

High T3/T4 and high TSH

235
Q

would most patients be treated for destructive thyroiditis?

A

no most of the time the thyroid will recover after being hypothyroidism

236
Q

How is hyperthyroidism treated?

A
  1. antithyroid drugs
  2. radioiodine
  3. surgical
237
Q

which antithyroid drugs are usually prescribed?

A

carbimazole first line, propylthiouracil for young women who may be trying to get pregnant or are pregnant

238
Q

How do antithyroid drugs work?

A

block T3 to T4 conversion

239
Q

what is the most important side effect of antithyroid drugs?

A

reduction in white cells

240
Q

which isotope of iodine is used to treat hyperthyroidism and how does it work?

A

131 and by causes necrosis only to the thyroid

241
Q

How is hypothyroidism characterized?

A

abnormally low thyroid hormone

242
Q

what is the most common type of hypothyroidism?

A

hashimotos

243
Q

list some symptoms of hypothyroidism

A

fatigue
weight gain
cold intolerance
menstrual disturbance

244
Q

what thyroid function results would you expect from someone with primary hypothyroidism?

A

High TSH low T4/T3

245
Q

What thryoid function results would you expect from someone with hypothyroidism?

A

no TSH , reduced T3/T4

246
Q

what is the treatment of choice for hypothyroidism?

A

synthetic thyroxine, levothyroxine

247
Q

list some metabolic changes displayed in pregnancy

A

higher cardiac output
higher plasma volume
more erythropoietin
insulin resistance

248
Q

describe fetal thyroid development

A

from weeks 0-12 gestation the mothers T4 regulates fetal neurogenesis, migration and differentiation of the thyroid. after this fetal T4 takes over, fetal thyroid follicles and thyroxine synthesis occurs at 10 weeks, with the axis maturing at weeks 15-20

249
Q

why does a woman’s thyroxine level change during pregnancy?

A

hcg has a similar structure to TSH, meaning that it partially binds to TSH receptors, causing more thyroxine to be made, despite reduced levels of TSH. There is also an increased renal clearance of iodide

250
Q

How does hypothyroidism affect pregnancy if left untreated?

A

causes low birth weight
pre-eclampsia
fetal goiter
post partum heamorrage
placental abruption
preterm delivery
neonatal respiratory distress

251
Q

How does a woman with pre-existing hypothyroidism medication change during pregnancy?

A

increase by 30%

252
Q

who is included in targeted screening for hypothyroidism?

A

women over 30 with a BMI above 40, who have goiter and a history of miscarriages and T1DM

253
Q

list complications of hyperthyroidism during pregnancy

A

intrauterine growth restriction
still birth
miscarriage
low birth weight
preeclampsia

254
Q

which antithyroid medications would you use in pregnancy?

A

PTU (propylthiouracil) is the first choice however rarely causes hepatotoxicity, carbimazole can cause serious congenital abnormalities

255
Q

what causes fetal thyrotoxicosis?

A

transferal of TSH-receptors antibodies

256
Q

How is gestational thyrotoxicosis characterized?

A

lack of autoimmunity problems
limited to the first trimester

257
Q

where are oxytocin and vassopressin made?

A

paraventricular and supraoptic nucleus in the hypothalamus

258
Q

which part of the pituitary are oxytocin and vasopressin released from?

A

the posterior

259
Q

How does the structure of vasopressin and oxytocin affect their half life and releasal?

A

they’re both small molecules with a short half-life, they are released in acute bursts when needed

260
Q

what type of mid brain receptor signals to the paraventricular and supraoptic nuclei about water concentration?

A

an osmo receptor

261
Q

How does the brainstem input to the periventricular and supraoptic nuclei?

A

through the baroreceptors in the vagus nerve, they detect a decrease in pressure from the circulating blood volume and signal to the periventricular and supraoptic nuclei to put out more vasopressin and oxytocin

262
Q

what does arginine vasopressin, AVP and ADH all mean?

A

arginine vasopressin

263
Q

what type of receptors dooes vasopressin bind to ?

A

G-protein coupled

264
Q

list the receptors that vasopressin binds to?

A

V1a- vasculature
V1b- pituitary
V2- renal collecting tubules

265
Q

list the receptors that vasopressin binds to?

A

V1a- vasculature
V1b- pituitary
V2- renal collecting tubules

266
Q

How much water is their in the human body and how is this divided?

A

42L of water,
1/3 extracellular- 1/4 of this is intravascular and 3/4 of this is intersititial
2/3 intracellular

267
Q

which cation is most significant in extracellular fluid?

A

Cl-

268
Q

which is the most significant extracellular anion?

A

Na+

269
Q

which is the most significant intracellular cation?

A

K+

270
Q

describe what happens when you have a drink of water

A

plasma osmolality goes down, cellular hydration goes up, thirst decreases, vasopressin decreases, water intake stops and urine production increases

271
Q

describe what happens in water deficet

A

plasma osmolality goes up, cellular hydration goes down, thirst increases, vasopressin increases, water is drank and urine production decreases

272
Q

what is the average water excretion range?

A

1-1.5L

273
Q

How does vasopressin act?

A

when it binds to V2 receptors in the kidney aquaporin 2 channels are inserted into the loop on Henle, which causes more water to be reabsorbed

274
Q

what does osmolality measure and with what units?

A

concentration of plasma mOsml/kg

275
Q

How can osmolality be calculated?

A

doubling the sodium and adding the glucose, plus urea

276
Q

describe the relationship between vasopressin and osmolality

A

positive linear

277
Q

describe the relationship between vasopressin and urine concentration

A

positive sigmoidal.

277
Q

describe the relationship between vasopressin and urine concentration

A

positive sigmoidal.

278
Q

what are the symptoms of AVP deficiency and resistance

A

polyuria, polydipsia no glycosuria

279
Q

How is AVP deficiency and resistance diagnosed?

A

urine volume measured at more than 3L a day
renal function and serum calcium checked

280
Q

what can AVP resistance/ deficiency be confused with?

A

primary polydipsia

281
Q

How can you differentiate between primary polydipsia and AVP resistance or deficiency?

A

measuring copeptin, a precursor to vasopressin with a longer half-life, in people with primary polydipsia they produce more copeptin when given hypertonic saline drips, in people with AVP deficiency/resistance this doesn’t happen

282
Q

How do we treat AVP deficiency/resistance?

A

treat the underlying condition and then give desmopressin which has a high activity at V2 receptors

283
Q

define hyponatremia

A

less than 135 mmol/l Na+
biochemical severe is less than125mmol/l

284
Q

what is the normal range for Na+

A

135-144

285
Q

what happens the brain with the gradual onset of hyponatremia and what can happen if the patient is then not treated correctly?

A

it adapts, changing shape and size, it can become demyelinated

286
Q

which axons are affected by osmotic demyelination?

A

descending

287
Q

how long may osmotic demyelination take to present?

A

2 weeks

288
Q

what are some risk factors for developing osmotic demyelination and how can the risk be mitigated?

A

serum sodium of less than 105mmol/l
hypokalaemia
chronic excess alcohol
malnutrition
liver disease
give less sodium over 48 hours

289
Q

Outline the treatment for acute hyponatremia

A

give 150ml 3% saline infusion over 20 mins
check serum sodium
repeat 150ml 3% saline infusion twice until there is a 5mmol/l increase and confirm the diagnosis
give hypertonic saline once every six hours for 24 hours, limiting the total increase to 10mmol/l for the first day

290
Q

How does the pituitary develop?

A

The anterior pituitary ascends from the mouth in Rathke’s pouch, the posterior is from nerves that have descended from the floor of the 3rd ventricle

291
Q

at what ages are craniopharyngiomas common?

A

5-14 and 50-74

292
Q

what symptoms may someone with a craniopharyngioma present with?

A

increased intracranial pressure, visual disturbance, growth defect, weight gain, pituitary hormone deficiency

293
Q

describe Rathke’s cysts

A

mostly intracellular, single layer of mucoid or serous components in cyst fluid, patient may present with headache, amenorrhoea, hypopituitarism or hydrocephalus

294
Q

what usually causes meningiomas?

A

Radiotherapy when someone is young

295
Q

what symptoms are associated with meningiomas?

A

decrease in visual acuity, visual field defects

295
Q

what symptoms are associated with meningiomas?

A

decrease in visual acuity, visual field defects

296
Q

what is lymphocytic hypophysitis?

A

inflammation of the pituitary caused by an autoimmune response

296
Q

what is lymphocytic hypophysitis?

A

inflammation of the pituitary caused by an autoimmune response

296
Q

what is lymphocytic hypophysitis?

A

inflammation of the pituitary caused by an autoimmune response

297
Q

what is lymphocytic hypophysitis?

A

inflammation of the pituitary caused by an autoimmune response

298
Q

How may someone with lymphocytic hypophysitis present?

A

with hypopituitarism, possibly visual field defects if the pituitary has intruded on the optic chiasm

299
Q

What may trigger lymphocytic hypophysitis, and at what age does it usually present?

A

pregnancy and postpartum, women at 35 and men at 45

300
Q

What mass effects may indicate a nonfunctioning pituitary adenoma?

A

CSF rhinorrhea
headaches
visual field defects
cranial nerve palsy

301
Q

Which hormones may indicate a nonfunction pituitary adenoma?

A

any being secreted from the anterior pituitary

302
Q

Which 4 situations require immediate surgical intervention when dealing with a nonfunctioning pituitary adenoma?

A

acromegaly
Cushings disease
visual field defects
pituitary apoplexy (bleeding)

303
Q

when doing a pituitary test which results would indicate graves disease?

A

suppressed THS and high FT4
general hypothyroidism, thyroid making loads of T4 and having a negative feedback on the pituitary

304
Q

What results would indicate a TSHoma?

A

High FT4 with normal/high TSH

305
Q

What FT4 results would indicate hormone resistance?

A

High FT4 with normal/high TSH

306
Q

In men what results would indicate primary hypogonadism?

A

Low testosterone high LH/FSH

307
Q

In men what results would indicate hypopituitarism (gonadal)?

A

Low LH/FSH and low testosterone

308
Q

In men which results when testing the gonadal axis would indicate anabolic use?

A

Low testosterone, suppressed LH

309
Q

what conditions can gonadal hormones be measured in men?

A

fasted state at 9am

310
Q

what results would indicate primary ovarian failure?

A

when both LH and FSH are high, with FSH being higher than LH and estradiol being low

311
Q

which results would indicate hypopituitarism in women when testing their gonadal axis?

A

low estradiol and low/normal FSH/LH, along with amenorrhea and oligomenorrhea

312
Q

which axis is circadian-dependent?

A

HPA

313
Q

At which time should cortisol be measured and with what?

A

9 am and with synacthen

314
Q

which results would indicate primary adrenal insufficiency?

A

low cortisol, high ACTH and a poor response to synacthen

315
Q

what results may indicate hypopituitary HPA axis?

A

low cortisol low ACTH poor response to synacthen

316
Q

How is GH secreted?

A

Pulsatile, usually at night, decreases with age and are lower in obesity.

317
Q

what is measured when suspecting a growth hormone deficiency?

A

IGF-1 and GH stimulation test

318
Q

which hormone controls prolactin?

A

negative control of dopamine

319
Q

what may cause prolactin levels to be high?

A

stress
antipsychotic drugs
prolactinoma
stalk pressure

320
Q

How is adrenal insufficiency treated?

A

3x daily hydrocortisone

321
Q

How is thyroxine deficiency treated?

A

1.6 micrograms/kg/day of levothyroxine

322
Q

How is growth hormone replacement therapy done?

A

if the person is under 60 they have a daily injection of 0.2-0.4 mg/day
if they’re over 60, 0.1-0.2mg/day

323
Q

what does growth hormone replacement therapy improve for the patient?

A

bone density, lipid profile, bone mineral density

324
Q

when administering testosterone which things should be monitored and why>

A

Testosterone levels, full blood count and prostate antigen levels as testosterone can accelerate the progression of prostate cancer

325
Q

what does testosterone replacement improve for the patient?

A

bone mineral density, libido, energy levels, sense of wellbeing, muslce mass, fat reduction

326
Q

what can estrogen replacement therapy improve for patients?

A

night flushes, night sweats, reduces risk of CVS, mortality and osetoporosis

327
Q

is HRT for women aged 40-49 associated with an increased risk of breast cancer?

A

no

328
Q

What are the comorbidities of acromegaly?

A

increased risk of stroke, cardiovascular disease, sleep apnea, insulin resistance diabetes, cerebrovascular events and headaches, arthritis

329
Q

list some clinical features of acromegaly

A

acral enlargement, excessive sweating, maxillofacial changes, headaches, hypogonadal symptoms

330
Q

what is the growth hormone secretion like in people with acromegaly?

A

it pulses throughout the day and never returns to normal

331
Q

How can the results of a glucose tolerance test indicate acromegaly?

A

when 75mg of glucose is ingested by healthy people growth hormone is suppressed, however this doesn’t happen in acromegaly

332
Q

What are the options for the treatment of acromegaly, and which is the best?

A

best option is surgery, other options include medication and radiotherapy

333
Q

What is the disadvantage of using radiotherapy to treat acromegaly?

A

It causes hypopituitary with time.

334
Q

Which dopamine agonist is mainly used to treat acromegaly?

A

cabergoline

335
Q

Which 2 somatostatin analogues are used to treat acromegaly?

A

Octreotide, lanreotide

336
Q

How does pegvisomant work?

A

It’s a competitive antagonist for growth hormone, it blocks the receptors.

337
Q

Which gender has more chance of getting a prolactinoma?

A

women

338
Q

What are the clinical features of prolactinomas?

A

Headaches, visual field defects, CSF leaks, menstrual abnormalities, infertility, low libido, and low testosterone in men.

339
Q

What is galactorrhea?

A

milk production

340
Q

What is the main treatment for prolactinoma?

A

Dopamine antagonist, cabergoline.

341
Q

Describe primary, secondary and tertiary prevention of diabetes.

A

primary- preventing diabetes
secondary- diagnosing diabetes earlier
tertiary- better management and support of self management

342
Q

Describe the obesogenic environment.

A

Physical- Tv remote
socioeconomic- cheap to watch Tv, expensive to buy fruit
sociocultural- family eating patterns

343
Q

Which mechanisms maintain being overweight?

A

Physical/physiological- more weight makes it more difficult to exercise.
Psychological- stress and comfort eating
socioeconomic- reduced employment opportunities

344
Q

Define the random plasma glucose for diabetes.

A

More than 11.1 mmol/l.

345
Q

Define the fasting blood glucose of diabetes.

A

more than 7.0mmol/l

346
Q

Which HBA1C would indicate diabetes?

A

more than 48mmol/l

347
Q

List some symptoms of diabetes.

A

Hunger, poluria, polydipsia, the decline in vision, vaginal candidiasis

348
Q

Which features suggest T1DM?

A

Onset in adolescence, lean body type, partial to ketoacidosis, acute osmotic symptoms, autoimmune antibodies

349
Q

If unsure which type of diabetes, how should it be treated?

A

Insulin

350
Q

What effect does insulin deficiency have on fat?

A

Causes fat breakdown, the formation of glycerol and free fatty acids.

351
Q

What happens to free fatty acids?

A

They go to the liver for gluconeogenesis; they are oxidised to form ketones.

352
Q

Which ketones are made from free fatty acids?

A

beta-hydroxybutyrate, acetoacetate and acetone.

353
Q

What does a build of ketones cause?

A

It causes rising dehydration and hyperglycaemia, respiratory collapse and eventually death.

354
Q

Define ketoacidosis

A

Hyperglycemia- plasma glucose 50mmol/l
Raised plasma ketones- urine ketones of more than 2
metabolic acidosis- plasma bicarbinate more than 15mmol/l

355
Q

What are the clinical features of diabetic ketoacidosis?

A

Polyuria, polydipsia, nausea and vomiting, weight loss, abdominal pain, drowsiness

356
Q

What are the clinical signs of ketoacidosis?

A

hyperventilation, dehydration, hypotension tachycardia

357
Q

Describe the biochemical diagnosis of diabetic ketoacidosis.

A

urine ketones of more than 2
blood plasma of more than 3
urea and creatinine raised due to pre-renal failure
High potassium
low bicarbonate (less than 15)
Hyperglycemia more than 50mmol/l

358
Q

How is diabetic ketoacidosis treated?

A

3l of water in first 3 hours
Insulin
electrolyte replacement (potassium)
treating underlying cause

359
Q

What are the complications of diabetic ketoacidosis?

A

cerebral oedema
adult respiratory distress
death
thromboembolism
aspiration pneumonia

360
Q

What causes maturity-onset diabetes in the young?

A

A single autosomal dominant mutation.

361
Q

Do people with MODY diabetes need insulin?

A

No

362
Q

What is the pathophysiology of MODY?

A

the mutation causes beta cell dysfunction.

363
Q

What is used to treat MODY diabetes?

A

sulphonylureas

364
Q

What may indicate at birth that a child has MODY diabetes?

A

Birth weight higher than 4.4kg
hypoglycemia at birth

365
Q

What would indicate that a patient has MODY diabetes and not T1DM?

A

They have no autoimmune antibodies, they’re not insulin dependent, they have a parent who had diabetes and they’re reactive to sulphonylurea’s

366
Q

What is C-peptide a measurement for?

A

Insulin.

367
Q

What may indicate permanent neonatal diabetes?

A

small birth weight, muscle weakness, epilepsy

368
Q

How may someone with maternally inherited diabetes and deafness present?

A

similarly to someone with type 2 diabetes

369
Q

Where is the gene mutation for maternally inherited diabetes located?

A

Mitochondria

370
Q

What is the main cause of chronic pancreatitis, which may lead to diabetes?

A

Alcohol use

371
Q

Name 2 diseases which may cause diabetes.

A

Pancreatic neoplasm and cystic fibrosis.

372
Q

How does acromegaly cause diabetes?

A

Growth hormone causes increased insulin resistance, impairing glucose tolerance.

372
Q

How does acromegaly cause diabetes?

A

Growth hormone causes increased insulin resistance, impairing glucose tolerance.

373
Q

How does cushings syndrome cause diabetes?

A

Glucocorticoid excess reduced insulin and reduced glucose uptake into peripheral tissues.

374
Q

Which drugs commonly causes diabetes?

A

Glucocorticoids and thiazides.

375
Q

Which drugs commonly causes diabetes?

A

Glucocorticoids and thiazides.

376
Q

What is Addison’s disease?

A

Primary adrenal insufficiency caused by autoimmune destruction of the zona fasciculata.

377
Q

what is the most common secondary cause of adrenal insufficiency?

A

Hypopituitary caused by a tumour.

378
Q

What is the most common cause of adrenal insufficiency?

A

Taking steroids for a prolonged period of time.

379
Q

List some symptoms of a cortisol deficiency.

A

Fatigue, failure to recover from illness , weight loss, pigmentation of gums and palmar creases

380
Q

Which biochemical sign may indicate adrenal insufficiency?

A

Low sodium or low sodium with high potassium.

381
Q

When is cortisol measured?

A

in the morning

382
Q

Which stimulation test is carried out for adrenal insufficiency?

A

synacthen test, synthetic ACTH and then measuring cortisol

383
Q

What to do in an adrenal crisis?

A

Take a blood test to determine ACTH and cortisol levels and make diagnosis
Give 100mg hydrocortisone Iv OR IM
Fluid resuscitation, 1L in 1 hour
Hydrocortisone 50/100mg 6 hourly or 200mg in 24 hours
then wean down to physiological levels

384
Q

What are the sick day rules for adrenal insufficiency?

A

Carry 10x10mg hydrocortisone with you always
double the amount you take if you have the flu or fever
If vomiting or deteriorating take emergency 100mg IM
If unable to have injection take 20mg hydrocortisone hourly and repeat if vomiting
go to the emergency room or call an ambulance

385
Q

What is a side effect of sulphonylureas?

A

Weight increase, example is glibenclamide

386
Q

What effects does GLP-1 have on the body?

A

Promotes satiety
increases glucose-dependent insulin secretion
Helps to regulate gastric emptying
decreases post-prandial glucagon secretion in alpha cells

387
Q

What is GLP-1 an example of?

A

incretins

388
Q

How do DPP4 inhibitors work?

A

They’re competitive antagonists for the DPP-4 enzyme, which is what breaks down GLP-1 and GIP, this allows the incretins to be in the system longer, enhancing their effects.

389
Q

How can GLP-1 inhibitors be administered?

A

They can be administered by injections

390
Q

How do SGL-2 inhibitors work?

A

They block the action of the SGL-2 enzyme stopping glucose reabsorption at the kidneys.

phase 2a endocrinolgy (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions