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Phase 2 mine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the main components of the endocrine system?

A

the pituitary, thyroid, parathyroid, adrenal, pancreas, and ovaries/testes

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2
Q

What are the classes of hormones?

A

Peptides, amines, iodothyronines, cholesterol derivatives and steroids.

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3
Q

What are peptide hormoens like?

A

Linear or ring structures, vary in length, thwo chains can bind to a carbohydrate stored in granules released in pulses or bursts.

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4
Q

How do peptide hormones act?

A

They bind to receptors on cell membranes to cause an effect within the cell

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5
Q

What are some amine hormones?

A

Dopamine norepinephrin and epinephrin, melatonin

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6
Q

How is throxin formed?

A

Incorporation of iodine intotyrosine to make T3 and T4 iodothyrosines in the colloid

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7
Q

Where are receptors for thyroid hormones?

A

Int the nucleus

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8
Q

Where are receptors for steroid hormones?

A

In the cytolasm to bind to a receptor that then enters the nucleus to stimulate transcription

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9
Q

How does vitamin D act?

A

Enters cells directly to nucleus to stimulate mRNA production

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10
Q

What are the main ways hormones are secreted?

A

Continuously or pulsatile

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11
Q

What rhythms of secretion are there?

A

Monthly, day-night

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12
Q

What is the purpose of hormone metabolism?

A

reduces the function of the hormones

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13
Q

What is around the pituitary gland?

A

The cella tursica, the cavernous sinus around it

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14
Q

What are metanephrines?

A

Breakdown products of epinephrines

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15
Q

How much thyroid hormone is protein bound?

A

99%

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16
Q

What is a direct precursor to estradiol?

A

Testosterone

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17
Q

What are release inhibiting factors?

A

Dopamine inhibits prolactin. sometimes there are two types of releasing factors

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18
Q

What are the stimuli of hormone release?

A

Hmoral stimulus, Hormone stimulating release, neural stimulus

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19
Q

What is hormone receptor induction?

A

A hormone that stimulates the formation of of more receptors for a certain hormone

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20
Q

What is synergism?

A

Two hormones act together to the same effect

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21
Q

What is hormone receptor down regulation?

A

Some hormones reduce the receptors on the cells to reduce the effects of another hormone

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22
Q

What nuclei feed the posterior pituitary?

A

Paraventriclar nuclesu and supraoptic nucleus

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23
Q

Does the posterior pituitary produce hormones?

A

No the nuclei in the hypothalamus do

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24
Q

What are the actions of oxcytocin?

A

release of breastmilk and relaxation of the cervix

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25
Q

How are anterior hormonesreleased?

A

When the correct releasing hormone is released. or when dopamine is stopped in thae case of prolactin

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26
Q

What are the presentation of dysfuncton of the pituitary?

A

Tumour mass effects, hormone excess and hormone deficiency

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27
Q

When do you do MRI scan of pituitary?

A

Only after hormonal tests as lesions can occur in many normal people

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28
Q

Where does growth hormone act?

A

on the liver to produce insulin-like growth factors which act on the skeleton and extraskeletally, also on increasing fat breakdown and release and also increase carbohydrate metabolism increasing blood glucose leveles

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29
Q

What is the hypohtalamo-pituitary- thyroid axis?

A

The way the thyroid is controlled to release thyroid hormones

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30
Q

What does thyroid hormone do?

A

Accelerates food metabolism , heart rate and breathing rate, growth rate, increased fat metabolism

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31
Q

What is the half life of T3?

A

1 day

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32
Q

What is the half life of T4?

A

5-7 days

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33
Q

Which thyroid hormone is active?

A

T3

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34
Q

What is released from adrenal zona glomerulosa?

A

Mineralocorticoids aldosterone

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35
Q

What hormones are released in stress?

A

Cortisol, mineralocorticouds and glucoccortiocids

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36
Q

What does FSH do?

A

Releases oestrogen from granulosa cells, initates spermatogenesis in puberty

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37
Q

What does LH do?

A

It produces androgens in the theca cells of the ovaries and acts on leidig cells

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38
Q

How to treat high prolactin?

A

dopamine agonist

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39
Q

What contributes to the obesogenic environment?

A

Long shift working poor diet, culture that its ok, Less time to exercise

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40
Q

What is hunger?

A

Need to eat

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41
Q

What is appetiti?

A

Desire to eat food

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42
Q

What is satiety?

A

Feeling of fullness

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43
Q

What is the danger with obesity?

A

Type 2 diabetes hypertensif CHD stroke osteroartheritis obstructive s;ep apnoea and obesity

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44
Q

What is visceral obesity?

A

Fat around the organs rather than subcutaneous

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45
Q

Why can shift work cause obesity?

A

It can interrupt the circadian rhythms

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46
Q

What regulates weight?

A

Environment and genetics of homeostasis

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47
Q

What organs affect apetit?

A

GI tract, Adipose tissue and the brain

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48
Q

Why do we eat?

A

We are driven to eat by hormonal changes and thoughts of food and psycological drive to eat

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49
Q

What is the satiety cascade?

A

sensory, psycological, and physical want to eat including ghrelin. the stomach releases hormones to say you are full. after a meal the adipose releases leptin or insulin that tells the body it doesn’t need to eat yet

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50
Q

What plays a strong role in appetite?

A

Lateral hypothalamuls the hungercentre and ventromedial hypothalamus the satiety centre

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51
Q

What can increase appetite?

A

NPY MCH AgRP orexin endocannabinoid

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52
Q

What can decrease appetite?

A

alpha- MSH CART GLP-1 Serotonin

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53
Q

What does leptin do?

A

Inhibits NPY and AGRP and stimulates POMC/CART to stop ou wanting to eat

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54
Q

How does the GI tract affect the hypothalamus?

A

The vagus nerve and Cervical spine SNS afferents to the brain also release of CCK

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55
Q

What produces leptin?

A

White adipose cells

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56
Q

What does Peptide YY?

A

Binds to NPY inhibits gastric motility reduces apetite and secreed by neuroendocrine cells in ileum.

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57
Q

What does ghrelin do?

A

From the stomach, it stimulates growth hormone,

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58
Q

Wat is POMC?

A

proopiomelanocortin and melanocortin receptors, they are a group of hormones gamma MSH alpha MSH and beta MSH, involved in signalling of satiety

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59
Q

What does a POMC defficiency do?

A

Make you more overweight

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60
Q

What is agouti related peptide?

A

Can make you eat more

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61
Q

What is malonyl CoA?

A

if it is decreased in quantity it increases appetite

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62
Q

Why is diabetes a public health issue?

A

It is preventable (probably) Mortality, disability( renal failure and blindness, neuropathy and peripheral vascular disease), co-morbidity (physical and mental health conditions) and reduced quality of life

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63
Q

What percentage of diabetes cases are type 2?

A

90%

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64
Q

What needs to be done for changing prevalence of type 2 diabetes?

A

Primary prevention reduce incidence, secondary prevention prevalence would increase, tertiary prevention would increase prevalance as more would live longer

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65
Q

What affects getting type 2 diabetes?

A

exponential relation between BMI and relative risk of type 2 diabetes

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66
Q

Who is at risk of diabetes type 2?

A

High BMI, sedentary job and lifestyle, diet high in calorie dense food low in fruit vegetables and pulses

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67
Q

What are the aspects of the obesogenic environment?

A

Physical environment (TV remote controls car culture lifts), Economic environment cheap food is more callorific and fruit and veg is expensive, Sociocultural environment safety fears, family eating patterns

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68
Q

What are the mechanisms make it hard to lose weight?

A

Pysical more weight makes it harder to lose it, psycological low self-esteem and guilt and comfort eating, socioeconomic less time to work on losing it relationshis etc

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69
Q

What are clinical factors that increase risk of diabetes?

A

AGE more in men in minorities and with history, gestational diabetes, impared glucose tolerance

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70
Q

What are the screening for abnormal glucose metabolism?

A

HbA1c random capillary, random venous, fasting venous and oral glucose tolerance test

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71
Q

How do we diagnose diabetes earlier?

A

Raise awareness of diabetes and possible sy,ptoms in the community, raising awareness of diabetes and possible symptoms i health professionals and identify tose at risk

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72
Q

What includes a diabetes check?

A

NHS health check every 5 years from 40 - 74

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73
Q

What does nice say to pre-diabetes?

A

Cost-effective weight loss diet and physical interventions

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74
Q

Why is NHS England investing in type 2 diabetes prevention?

A

Trials show diet changes can reduce progression from impaired glucose tolerance and could help reverse it in identified patients

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75
Q

How can diabetes be self cared for?

A

Self monitoring diet exercise drugs education and peer support

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76
Q

Where is glucose from when in the fasting state?

A

the liver muscle and some from kidney

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77
Q

What is an insulin independent tissue?

A

the brain and RBC because only use glucose

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78
Q

How is insulin secreted?

A

Glucose enters the beta cells through GLUT2 transporter which leads to ATP production anc closes channels in membrane and voltage gated calcium does that and insulin is then secreted?

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79
Q

What is glucokinase?

A

Enzyme that turns leads ATP production without it insulin cannot be released

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80
Q

What is the effect of insulin in muscle and fat?

A

Bind to receptor causes intracelluar signalling to release GLUT4 transporter to allow glucose entry into the cell

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81
Q

What is the function of insulin?

A

Surpresses hepatic glucose output through glycogenolysis and gluconeogenesis. increases glucose uptake in tissue and supresses muscle breakdown and lipolysis

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82
Q

What does glucagon do?

A

Increases hepatic glucose output and reduce peripheral glucose uptake and stimulate the release of glucose from peripheraltissues

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83
Q

What counteracts insulin effect?

A

Glucagon, adrenaline and cortisol and frowth hormoens

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84
Q

What is diabetes mellitus?

A

disorder of carbohydrate metabolism characterised by hyperglycaemia

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85
Q

What causes morbidity and mortality in diabetes?

A

Acute hyperglycaemia which can lead to diabetic ketoacidosis o hyperosmolar coma, chronic hyperglycaemia can lead to tissue damage.

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86
Q

What are complications with diabetes?

A

Diabetic neuropathy peripheral usually, nephropathy, diabetic retinopathy, CHD and stroke

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87
Q

What are the types of diabetes mellitus?

A

Type1, type 2, maturity onset diabetes of youth monogenic, pancreatic, endocrine, malnutritional diabetes

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88
Q

What is diabetes diagnosis?

A

Symptoms(thirst, polyurea) plasma glucose>11. fasting plasma>7 no symptoms- GTT HbA1c

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89
Q

What is HBA1c?

A

measure of blood sugar over the last few weeks

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90
Q

What is the pathogenesis of type 1 diabetes?

A

insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction. Beta cells express HLA and can be attacked by the body

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91
Q

What happens without insulin in a diabetic?

A

continual breakdown of liver glycogen, unrestrained lipolysis and muscle breakdown. releases hepatic clucse output, as glucose conc goes high at 10mM/L then it is excreted but gives symtoms

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92
Q

What happens in long term with uncontrolled diabetes?

A

Increased stress hormones, catabolic state leading to ketoacidosis and loss of weight,

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93
Q

What causes type 2 diabetes?

A

Genetics and environment lead to impared insulin secretion and insulin resistance. Insulin requirements are increased and it causes resistance and eventually exhaustion of cells

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94
Q

Why does being obese cause problems for type 2 diabetes?

A

Increased production of insulin

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95
Q

What is main difference in type 2 and 1 onset?

A

The type 1 diabetes is quick onset type 2 is much slower

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96
Q

What happens in glucose metabolism in type 2?

A

Insulin is detectable, reduced muscles and fat uptake after eating, failure to surpress lipolysis and high circulating free fatty acids ad abnormally high glucose after a meal and low levels of inulin stop muscle breakdown and no ketone production to excess like in type 1

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97
Q

What is the key point fo type 1 diabetes?

A

One defect no insulin

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98
Q

What is the key point for type 2 diabetes?

A

Two defects impaired insulin secretion and hepatic and muscle/ fat insulin resistance

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99
Q

What are the principals of treatment for dibetes?

A

Control of symptoms, prevention of acute emergencies, ketoacidosis, hyperglycaemic hyperosmolar states, identification and prevention of long term complications, control CHD risk

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100
Q

What is treatement type 2 diabetes/

A

Lose weight, and exercise but doesn’t work very often in practice as people don’t want to change. Target hypertenion lipid and glucose levels

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101
Q

What are sulphonylureas?

A

Stimulate insulin release by binding to beta cell receptors, effectiv in reducing sugar levels, but can cause hypoglycaemia, it can increase weight. Use gliclazide normally be careful of real imparement

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102
Q

What are thiazolidinediones (pioglitazone)?

A

Bind to nuclear receptor to change genes surrounding glucose uptake improve insulin sensitivity. Need insulin for a theramutic rarely used because increase weight increase risk of heart failure and risk fractureseffect,

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103
Q

What does GLP1 do?

A

Stimulates insulin secretion, reduces glycogen increeases beta cell mass and enhances glucose disposal but it is broken down very fast

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104
Q

How are GLP1 extende in duration?

A

Inhibit DPP or modify the shape so it isnt broke down as fast

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105
Q

What are GLP analogues?

A

Exenatide, liraglutide, lixisematide, dulaglutide, semaglatide

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106
Q

What is SGLT2?

A

Produced in kidney to assist glucose reabsorption.

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107
Q

What do SGLT2 inhibitors do?

A

They make you wee more sugar out.

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108
Q

What do you chose in type 2 diabets?

A

Metformin, then DPP-IV, GLP1 analogues and SGLT2 inhibitors as second line

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109
Q

What are the types of insulin used?

A

long acting and short actin

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110
Q

How is T1DM managed with insulin?

A

Basal bolus of insulin to mimic physiology

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111
Q

What is the challenge?

A

pre-meal rapid acting boluses adjusted according to pre-meal glucose and carbohydrate content of food to cover meals. Basal insulin should control blood glucose in between meals and during the night basal insulin can be giben twice daily or sometimes once a day adjusted to maintain fasting blood glucose between 4-7 mmol/L

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112
Q

How many type 2 diabets need insulin?

A

about 50% will eventually need it

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113
Q

How are T2 diabetes treated with insulin?

A

Basal insulin to keep the levels lower and less hypoglycaemia at night,

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114
Q

What is the problem with premixed insulin?

A

Have both long acting and short acting. Doesn’t cover meals can’t change for over night

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115
Q

What is the low plasma glucose level 1?

A

less than 3.9

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116
Q

What is low plasma glucose level 2?

A

less than 3.0 mmol/L

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117
Q

What is non-sever hypoglycaemia?

A

patient has symptoms but can self-treat and cognotive function is mildly impared.

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118
Q

What is sever hypoglycaemia?

A

Patient has impared cognitive function to require external help to recover this is level 3

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119
Q

How common is hypoglycaemia?

A

in type 1 its very high 1 episode per patient per year. in type 2 diabetes 0.3 per person per year

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120
Q

What are the side effects of hypoglycaemia?

A

Brain cognitive dysfunction siesure, coma psychological effects, heart increased risk of ischaemia and arrhythmias also fall driving accidents inflammation blood coagulation abnormalities endothelial dysfunction

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121
Q

What is problem with insulin treatment?

A

Can gain lots from good control but can cause hospitalisation and damage when it goes wrong

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122
Q

What are the symptoms of hypoglycaemia?

A

Autonomic, tremblin plapations, sweating anxiety hunger from adrenaline release, neuroglyopenic hard to concentrate confused vision changes dificulty speaking, nausea and headach

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123
Q

why can diabetics get hypoglycaemia but non-diabetics can’t?

A

insulin stops being secreted after insulin lowers, and in diabetes lose glucagon response and adrenaline level activation is much lower

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124
Q

What is the defence against high insulin levels?

A

Glucagon, adrenaline,

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125
Q

What are the risk factors for hypoglycaemia in a diabetic?

A

Long duration of diabetes, age, alcohol, sleeping increased physical activity

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126
Q

How can patientsbe screened for hypoglycaemia?

A

Low HbA1c previous history, long duration of diabetes, impared awareness of hypoglycaemia big insulin dose, impared renal function and physical activity

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127
Q

What are prevention strategies of hypoglycaemia?

A

discuss hypoglycaemia risk factors educate families and report hypoevents

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128
Q

How to treat hypoglycaemia?

A

Recognise the symptoms, confirm it with blood glucose, treat with 15g fast acting carbohydrates, retest in 15 minutes to ensure blood glucose is back to normal then eat again

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129
Q

What is the action of parathyroid hormone?

A

Increased calcium reabsorption in the kidney, descreases phosphate reabsorption and increased hydroxylantion of Vit D, Bone remodelling increased, no direct effect on GI but vit D does

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130
Q

What is serum calcium?

A

1.1mmol/L

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131
Q

Why should calcium be controlled?

A

It is involved with contraction of muscle including the heart

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132
Q

What are the options when you see a change in PTH levels?

A

Could be part of the normal response to low calcium or it could cause a calcium imbalance

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133
Q

what can affect calcium levels in the blood?

A

The quantity of calcium or having varying levels of albumin in the blood

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134
Q

How is the total calcium calculated?

A

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

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135
Q

What can hypocalcaemia cause?

A

tingling Paresthesia, muscle spasm, seizures basal ganglia calcification cateracts and ECG abnormalities long QT intervals

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136
Q

What is Trousseau’s sign ?

A

inflate the blood pressure cuff above systolic and leave for 5 minutes and muscles tense up

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137
Q

What is Chvostek’s sign?

A

Tapping on facial nerve causes spazm

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138
Q

What can cause hypocalcaemia?

A

Osteomalacia, surgical, radiation often for cancer treatments, Genetic syndromes, genetic problems, autoimmune disorders, infiltration of metal (haemochromatosis and wilsosns too much iron and copper) also Mg deficiency

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139
Q

What are stages of vitamin D production?

A

Formation in skin to 7-dehydroxycholesterol and then in the liver it is 25 hydroxylates then 1,25 hydroxylated in the kidney

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140
Q

What are Di George?

A

Devevelopmental abnormality of third and 4th branchial pouches hypoparathyroidsism thympic aplasis, immunodeficiency cardiac defects cleft palate and abnormal facies

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141
Q

What is pseudohypoparathyroidism?

A

resistance to parathyroid hormone type 1 albright hereditary osteodystrophy. 4th finger sign

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142
Q

What can can cause artificially high Calcium levels?

A

Leaving touniquet on for too long or old haemolysed blood sample, also albumin levels

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143
Q

What are the sumptoms of hypercalcaemia?

A

Thirst, polyuria, nausea, constipation, confusion coma and kidney stones, Short QT interval

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144
Q

What are the causes of hypercalcaemia?

A

Malignancy bone metasticies, primary hyperparathyroidism very common. Thiazides, thyrotoxoxosis, sarcoidosis, familial hypocalciuric/benign hypercalcaemia, immobilisation, Milk-Alkali, adrenal insufficiency, Phaechromocytoma

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145
Q

What are are consequences of primary hyperparathyroidism?

A

Bones osteitis fibrosa cystica osteoporosis, kidney stones, psychic groans confusion and abdominal moans constipation acute pancreatitis

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146
Q

What causes most primary hyperparathyroidism?

A

80% from single benign adenoma15-20 four gland hyperplasia. MEN I or II rarely malignant

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147
Q

How can surgical damage cause hypocalcaemia?

A

Removal of parathyroid by accidnet

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148
Q

Why can autoimmune disorders cause hypoparathyroidism?

A

Polyglandular type 1 attacks the cells of parathyroid

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149
Q

How can infiltration cause hypoparathyroidism?

A

Build up of copper and iron in the parathyroid

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150
Q

What is the need for magnesium in the parathyroid?

A

Helps with vesicular transport of PTH hormone out of Parathyroid cells

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151
Q

What is pseudohypoparathyroidism?

A

End organ ressistance to PTH

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152
Q

How do malignancies cause hypercalcaemia?

A

cancer damages bone that releases calcium, secreted parathyroid related protein, lymphoma from macrophages overprodicuing vitamin D

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153
Q

How do thyrotoxicosis cause hypercalcaemis?

A

Bone is turned over too fast

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154
Q

What is problem with hypocalciuric/benign hypercalcaemia?

A

It can’t be fixed by removing parathyroids

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155
Q

What is the blood supply to the anterior pituitary?

A

From the hypothalamus it recieves a venous portal system

156
Q

What is invoves in thryroid stimulation?

A

Hypothalamus releases thyroid releaseing hormone then pituitary trelaese thyroid stimulating hormone then thryroid releases thyroxin as T3 or T4 which can inhibit pituitary and hypothalamus

157
Q

Where does growth hormone act?

A

on the liver to produce insulin like growth factor 1

158
Q

What are the presentations of Pituitary tumours?

A

visual disturbances bitermporal hemianopia, pressure on normal pituitary hypopituitarism or in functioning tumour prolactinoma, acromegaly and cushing’s disease

159
Q

What are symptoms of prolactinomas?

A

Galactorrhoea infertiliy amenorrhoea loss of libido and visual field defect treat with dopamine agonist

160
Q

What are growth hormone disorders?

A

very tall or short statures, and acromegaly in older age

161
Q

What are the causes of cushings syndrome?

A

Pituitary tumours can be ectopic, synthetic ACTH adrenal tumours, steroids

162
Q

What is cushings disease?

A

A pituitary tumour causing cushings syndrome

163
Q

What are the clinical features of cushings syndrome?

A

Carbohydrate metabolism, diabetes and impared glucose tolerance, immune suppression, susceptibility to infection, electrolyte disturbance sodium retention hypertension, potassium losss hypokalaemia, central effects malais depression psychoiss, suppressed gonadal function. Oligo/amenorrhoea and loss of libido

164
Q

How do you diagnose cushings?

A

recognise symptomes then investigate the cause. need to do urinar free cortisol low dose dexamethasoone supression tests late night/ midnight serum or salivart cortisol

165
Q

How to find cause of cushings?

A

Look at ACTH evels if low it is independant so look for Adrenal issues with CT otherwise pituitary MRI /CT

166
Q

How likely is MRI to pick up pituitary tumour?

A

40% have normal MRI

167
Q

What causes acromegaly?

A

too much growth hormone leading to too much IGF-1

168
Q

What is mean duration of symptoms of acromegaly?

A

8 years

169
Q

What are comorbities of acromegaly?

A

Hypertension heart disease, sleep apnea, insulin resistant diabetes arthritis cerebrovascular events and headache

170
Q

What are the key elements of diagnosing acromegaly?

A

clinical features, GH and IGF-1 levels

171
Q

What are clinical features of acromegaly?

A

acral enlargement arthralgias, maxillofacial changes, excessive sweating headach hypogonadal symptoms

172
Q

When is growth hormone normally secreated?

A

after waking at lunch an evenings

173
Q

What does GH levels look like in acromegally?

A

Randome and always present

174
Q

If sugar levesl increase what should happen to growth hormone?

A

Should reduce

175
Q

What are the objectives of acromegaly treatments?

A

Restoration of GH and IGF levels, relief of symptoms, reversal of viaual and soft tissue changes, prevention of skeletal deformity and normalization of pituitary function

176
Q

What is primary treatment of acromegaly?

A

transphenoidaly surgery to remove it, radiotherapy, dopaning agonist SMS and SH receptor antagonists

177
Q

What does a dopamine agonist do in acromegaly?

A

Controls GH and IGF-1, no hypopituitarism oral administration and rapid onset but has side effects and relatively ineffective

178
Q

What do somatostatin analogues do?

A

They inhibit GH so IGF bu inhibiting anterior pituitary, quite affective depends on GH levels and tumour size but is injectable and side effects

179
Q

What is the symptoms of prolactinaemia?

A

Headache visual, menstural irregularity, Infertility, galactorrhoea low libido and low testosterone in men

180
Q

What is main treatment of prolactinoma?

A

Medical not surgical as can shrink

181
Q

What are tests on hormones we can do?

A

There are tests for pituitary hormones but not from hypothalamus

182
Q

Which cranial nerve palsy can happen with pituitary tumour?

A

3rd nerve

183
Q

When is cortisol the lowest?

A

During the night

184
Q

How can IGF lead to diabetes?

A

It counteracts action of insulin and can cause resistance

185
Q

When is cortisol usually high?

A

just aftr waking around 9 or 10

186
Q

What sets the circadian system?

A

Light levels relayed to suprachiasmatic nuclei

187
Q

What is primary adrenal insufficiency?

A

Addison’s disease, autoimmune adrenalitis sometiems, APS adreoleukodystrophy

188
Q

How is growth hormone released?

A

Pulsatile, usually low with spikes GH measurements might not be useful unless its very low

189
Q

What can cause secondaryadrenal insufficincy?

A

Pituitary macroadenoma, apophysitis mets, infiltration infection radiotherapy or congenital

190
Q

In acromegally what happens in Glucose tolerance test?

A

GH remains elevated with glucose

191
Q

What are the diagnosis test for acromegally?

A

GH random is less than 0.4 and IGF normal its excluded, GTT shows increase or no decrease

192
Q

What can cause tertiary adrenal insufficiency?

A

Steroids oral inhaler or creams supress the HPA axis

193
Q

What determines surgery success rate of pituitary?

A

the size of the tumour, and the surgeon

194
Q

How long does it take for radiotherapy to reduce growth hormone?

A

5 years or so

195
Q

What are sumptoms of addisons disease?

A

pigmentation on creases from increases ACTH

196
Q

What do you need for diagnosis of adrenal insufficieny?

A

signs and smptoms and low sodium high potassium eosinophillia and elevated TSH high suspicion. need low cortisol at 9am and ACTH low if secondary high if primary

197
Q

What is the management of an adrenal crisis?

A

take cortisol and ACTH hydrocortisone 100mg IV or IM Fluid give hydrocortisone then reduce afterwards and also fludrocortisone 100-200ug replace,emt for aldosterone

198
Q

What should you do with Addison’s disease acute presentation?

A

Give steroids as no harm in short term.

199
Q

What is the treatment of adrenal insufficiency?

A

hydrocortisone that tries to mimmic circadian rhythm

200
Q

What is most common endocrine problem?

A

Thryroid problems

201
Q

Who is most affected by thyroid issues?

A

Women 5-10 fold different

202
Q

What are ytpes of thryoid autoimmunity?

A

Focal thyroiditis and or positive TPO

203
Q

What is postpartum thyroiditis?

A

hyper after birth then hypo usually returns back to normal

204
Q

What are the autoimmune thyroid diseases?

A

Hashimoto’s thyroiditis and atrophic thyroiditis

205
Q

What is goitre?

A

Palpable and visible thyroid enlargement, can have a variety of causes,

206
Q

What mechanisms can cause hyperthyroidism?

A

Ingestion of excess thyroid hormone. leackage as it is produces and also too much TSH

207
Q

What are the common causes of hyperthyroidism?

A

Graves disease, nodules

208
Q

What can cause hyperthyroidism all acuses?

A

Congenital hyperthyroidism, non autimmune hereditary hyperthryroidism, subacute thyroiditis iodine induced excess hyperthryroidism, hyperemesis gravidarum, thyrotoxicosis, thyrotoxicosis factitia (not caused by body), metastatic differentiated thyroid Ca, Strum ovarii, pituitary resistance to thryroid hormone pituitary adenoma

209
Q

What drugs can cause hyperthyroidism?

A

iodine amiodarone, lithium and radiocontrast agents

210
Q

What are clinical features for hyperthyroidism?

A

Weight loss, tachycardia, hyperphagia, anxiety, tremor, heat intolerance diarrhoea, diarrhoea lid+lag +stare, mestrural disturbances

211
Q

What are disease specific clinical signs of hyperthyroidism?

A

Diffuse goitre, thyroid eye disease puffy eyes retibial mycoedema, acropachy for Graves disease. MNG multinodular goitre, Adenoma, solitary nodule

212
Q

How can hyperthyroidism be diagnosed?

A

High levels of thyroid hormone increased T3 T4 low TSH for primary, clinical history also look for antibodies and thryoid uptake scan

213
Q

What are treatement options for hyperthyroidism?

A

Sntithyroid drugs, radioiodine, surgery to remove it

214
Q

What are antithyroids?

A

Thionamides, carbimazole, propylthiouracil. they decrease synthesis of new thryroid hormone PTU inhibits T4-T3 conversion. doesnt treat underlying cause

215
Q

How are antithyroids used?

A

Titration over 12-18 months, block and replace regimen for graves’ disease or a short thryroid before distructive treatment or surgery long term for those not wanting surgery

216
Q

What are remission rates in graves disease?

A

30-50%

217
Q

What are side effects of thionamides?

A

rash, sometimes arthralgia, hepatitis serious is agranulocytosis, has sore throat fever mouth ulcers, must check full blood count if have these

218
Q

What is problem with radioactive iodine?

A

can produce gamma radiation so must stay away from others for a while

219
Q

What are the early effects of radioactive iodine?

A

Necrosis of follicular cesls vascular occlusion occir over weeks of months, Long eterm short cell survival hashimoto thyroiditis

220
Q

When to use iodine radioactive treatment?

A

Graves disease Toxig nodular goiter, adenoma

221
Q

When is surgery used?

A

sometimes graves

222
Q

What are types of hyothyroidism?

A

primary absense of sysfunction hashimotos, secondary pituitary disease hypothalamic disease

223
Q

What can cause primary hypothyroidism?

A

Hashimoos, thyroidectomy post partum, durgs thyroidited

224
Q

What are clincial features of hypothyroidism?

A

Fatigue weight gain, cold intollerance, constipation, menstrural disturbance, muscle cramps slow thinking, periorbital oedema, delayed muscle reflexes, low in mood

225
Q

What are the investigations for hypothyroidism?

A

lowered T3 and T4,TSHincreased is the most sensitive marker only for primary

226
Q

What are the treatments of hypothyroidsim?

A

syntheticT4 or T3 treatment used to be from animals

227
Q

What to be careful of with giving thyroid hormone?

A

IHD need to give slowly

228
Q

how is treatment monitoringin thyroid disease?

A

Monitor the levels after weeks or so

229
Q

How can thyroid cells be destroyed in autoimmune?

A

CD8+ cell mediated and thyroglobulin and TPO antibodies may cause secondry damage but no effect on own can have TSH receptor blocking can take place

230
Q

What causes graves disease?

A

Theyroid stimulating antibodies

231
Q

What are TSH receptor antibodies?

A

They can bind to TSH receptors to activate or block activation of the thyroid

232
Q

What can presdisposition you to theyroid autoimmunity?

A

HLA target organ T cell response immunoglobulin, cytokine, sex hormones, glucocorticoids prolactin, birthweight pregnancy, diet infection drugs toxins stress

233
Q

What is thyroid associated ophthalmopathy?

A

swelling in extra occular musclesMost likely due to an autoantigen in the extraocular muscles

234
Q

When does the foetus get thyroid?

A

10 weeks and matures up to 20 weeks maternal T4 regulates 0-12 then foetal takes over

235
Q

What happens to women’s hormone changes during pregnancy?

A

increased thyroid stimulation from HCG and TBG increase and reduces TSH from raised thyroxine levels.

236
Q

What are the glycoprotein hormones?

A

TSH, LH FSH and hCG

237
Q

What are changes in foetus for thryoid hormones?

A

increase from week 10. thyroid can com from mother but not TSH by anti immunoglobulins can

238
Q

Is hypothyroidism common in pregnancy?

A

2-3% but usually predates the pregnancy

239
Q

What can be a problem with hypothyroidism in pregnancy?

A

gestational hypertension and pre-eclampsia placental abruption and post partum haemorrhage. Low birth rate preterm delivery neonatal goitre and neanatal respiratory disress

240
Q

What to do in hypothyroidism?

A

Screening for function and also increase dose if needed and start if not before

241
Q

When are targeted screening for hypothyroidsm?

A

older than 30, Bim>40 miscarrage, goitre, anti TPO type 1DM and other factors

242
Q

What is first line treatment for thyrotoxiosis?

A

Start metical treatmetn PTU high level

243
Q

What happens to graves disease during pregnancey?

A

Worse innitially then improves befoe worsening after birth

244
Q

What is the treatment of graves disease?

A

Beta blockers for symptoms, aitthyroid medications PTU or carbimazole cant do radiotheray during pregnancy thyroidectamy can be used later use pTU in pregnancy as carbimazol can cause congenital abnormalities.

245
Q

What is the problem with TSH-R antibodies?

A

Can pass to placenta and to baby to give the baby hyperthyroidism

246
Q

How can foetal thyrotoxicosis be treated?

A

anti thyroid medications

247
Q

What is gestational thyrotoxicosis?

A

it is oly during pregnancy and dont have antibodies and usualy doesnt need treating.

248
Q

What is post partum thyroiditis?

A

Initially have hyper thyroid then underactive in response usually normal within 3 months. 7% high rish if graves in remission or T 1 DM

249
Q

what can cause thyroid problems from outisde sources?

A

amiodarone lithium interferon immune theraies and a lot more

250
Q

Why does amiodarone have an effect on the thyroid?

A

Stored in adipose and has iodine levels that are high and can induce hypo or hyper

251
Q

What happens with AIH?

A

Hypo succeptibility, inhibits thyroid hormone synthesis, inability of gland to escape from wolf-chaikoff effect from inhibiting iodine ionisation can accelerate hashimotos trend

252
Q

What is AIT?

A

Amiodarone induced thyrotoxicosis type 1 latent pre-existing low iodine areas cant regulate iodine too much iodinethemselves Jode-basedow phenomenon type 2 caused by direct affect on thyrocytes

253
Q

How to avoid Amiodarone?

A

use another one like Dronedarone

254
Q

which class of drugs is having a large effect on the thyroid?

A

monoclonal antibodies

255
Q

Where are oxytocin and vasipression produced?

A

In the supraoptic and paraventricular nucleus

256
Q

How long is half life of oxytocin and agenine vasopresin?

A

5-10 minutes

257
Q

what controls ADH release day to day and other?

A

osmoreceptors in hypothalamis day to day and in emergencygreat vein receptors

258
Q

What are main anions intracellular?

A

Posphates and protein

259
Q

What are main extracellular anions?

A

Chloride and HCO3

260
Q

what changes osmolality?

A

Number of particles not size

261
Q

What is normal osmolality of cells?

A

282 to 295 mosmol/kg

262
Q

What are diseases associated with posterior pituitary?

A

lack of vasopressin, cranial diabetes insipidus, resistance to action of vasopressin, nephrogenic diabetes insipidus, too much vasopressin SIADH

263
Q

What are the symptoms of Diabetes insipidus?

A

plyuria polydipsia and no glycosurea measure urine volume, renal function and serum sodium look as plasma and greater than 3L urine

264
Q

How does vasopressin work?

A

binds to G couples receptos that can be foumd in V1 a in vascuarter V2 n renal and V1b in ituitary

265
Q

What causes a plateau in urine osmolarity even with maximal arginine vasopressin?

A

The concentration gradient of the kidney

266
Q

How is vasopressing released?

A

linear relationship with osmolarity

267
Q

What is cranial diabetes insupitus?

A

Not cmmon but lifethreating

268
Q

What is nephrogenic diabetes insipidus?

A

Not common but life threatening

269
Q

What is SIADH?

A

too much ADH for something can be producing tumour or stimulation of excess ADH production it is common

270
Q

What is primary plydipisa?

A

Over drinking

271
Q

What is seen in AVP response in cranial diabetes insipidus?

A

Lower levels of AVP when plasma concentration is high

272
Q

What can cause aquired nephrogenic diabetes insipidus?

A

Anything that changes the concentration gradient of the kidney, renal imparement some drugs, osmotic diuresis

273
Q

What does water deprivation test?

A

If stop drinking can they concentrate urine

274
Q

What does desmopressin do?

A

stimulates the kidney artificially but won’t work in the nephrogenic version

275
Q

What is copeptin?

A

it is prodces with AVP and neurpophysin it is a surrogate masure of AVP production

276
Q

How is cranial DI treated?

A

desmopressin tablets injection or nasal spray careful with water intake if not thirst

277
Q

How is nephrogenic DI treated?

A

very hard to treat. lots of desmopressin

278
Q

What is hyponatraemia?

A

Definition sodiu serum less than 135mmol/l or severe is less than 125

279
Q

Signs and symptoms of hyponatraemia?

A

not often symptoms, if acute can have symptoms, can be stupor coma conculsions resp arrest, confusion headache irritability confusion mental slowing

280
Q

What affects whether symptoms of hyponatraemia are displayed?

A

How fast the onset is

281
Q

Why are gradual onset hyponatraemia not as bad symptoms?

A

Brain can adapt over time to the change but in acute it cannot compensate for it.

282
Q

How can hyponatraemia be classified?

A

Biochemical on levels, on symptoms, aetiology and acuity of onset

283
Q

How to treat hyponatraemia?

A

Stop hypotonic fluids, review drugs, plasma unine osmolarity, urinary sodium glucose TFTs assessment of cortisol

284
Q

How to tread low sodium dehydrated?

A

give saline replacement solutions

285
Q

How to treat fluid overload or normovolaemic with low sodium?

A

fluid restriction

286
Q

What is SIADH?

A

Common 25% of hyponatraemia too much AVP when shouldnt be produced. can have many causes often drugs

287
Q

How can SIADH be treated?

A

AVP receptor blockers, Vasopresin andtagonists

288
Q

Why not rapidly increase sodium?

A

It leads to osmotid demyelination as draws water

289
Q

What is osmotic demyelination syndrome?

A

White areasin middle of pons can take 2 weeks to show

290
Q

Emergency management of sever symptomatic hyponatraemia?

A

sever symptoms. bolus doses of IV saline, check serum sodium only to increase 5 mmol/l per day to avoid problems

291
Q

What type of tissue is the anterior pituitary?

A

Glandular tisue

292
Q

What type of tissue is the posterior pituitary?

A

neural tissue

293
Q

What are the typesof pituitary mass lesions?

A

Non-fuctioning pituitary adenoma, functioning, rare malignant ones, metastasies from other cancers, pituitary cysts, cranial pharengealoma, priparytumour of CNA cascualr tumous systemic cancers, granulatomatus disease vascular aneurisms

294
Q

What is craniopharyngioma?

A

from squamous epithelial from remenants of rathke’s pouch, can be cystic or solid with calcification, it is benign but can infiltrate, causes normal pituitary symptoms

295
Q

What is rathke’s cyst?

A

From the pouch single layer of epithelial cells. mostly intrasellar componend but can extend often symptomatic and smallhave to advise of hypopituitarism

296
Q

What is meningioma?

A

Commenest tumour of region after pituitary adenoma usually after radiotherapy, usually lose visual aquity

297
Q

what is lymphocytic hypophsitis?

A

autoimmune reaction very low levels. more commen in women. can be infindibiloneurohypophsitis panhypophysitis, adenohypophysits

298
Q

How to diagnose non-functioning pituitary adenoma?

A

Exclude the fact it could be secreting hormones with hormone function tests

299
Q

When to operate on non functioning pituitary adenoma?

A

If causing headache severely and eyesight ris and progressive increase in size

300
Q

What are testing of pituitary function?

A

Testing all axes can be in one or all of them and often borderline cases and sircadian rhythms to takke into account

301
Q

How to tell if pituitary is working weell?

A

If hormones are being produced by target organs properly

302
Q

What do you do to test pituitary-thyroid axis and interpret results?

A 
free tT4 and TSH testing
\+TSH -Ft4 primary hypothyroid
Low Ft4 normal or low TSH hypopituitary
low tsh ight Ft4 graves disease
TSHoma high FT4 hight TSH
Hormone resistance High Ft4 with normal or hight TSH
303
Q

How to test gonadal axis men?

A

Primary low T high LH/FSH
hypopituitary Low T low LH/FSH
Anabolic use wil lower T and Low LH
do at 9 am fasting

304
Q

What is gonadal function like prepuberty in women?

A

Oestradiol very low Low LH and FSH FSH higher than LH.

305
Q

When should you take ACTH levels to see low levels?

A

9am as should be high now

306
Q

Hoe is GH tested?

A

IGF-1 and GH stimulation test reduce blood glucose or glucagon

307
Q

What is dynamic testing?

A

useful in select cases for pituitary hyperfunction.

308
Q

CRH TRH dynamic tests are used for what?

A

CRH for cushings would expect it to go down normally

309
Q

What gives best view of pituitary?

A

MRI T1 for high signal intensity for fat T2 for cystic lesions

310
Q

What are presenting features of type one diabetes?

A

Thirst, polyuria from osmotic diuresis, weight loss and fatigue, (lipid and muscle loss, hungry, pruitis valvae and balanitis, chest infections from increased sugar, blurred vision

311
Q

What are suggestive features of type 1 diabetes?

A

often childhood onset, lean body habitus, acute onset of osmotic symptoms, prone to ketoacidosis, high levels of islet autoantibodies

312
Q

What are suggestie type 2 diabetes symptoms?

A

Usually presents in over 30s, onset is gradual. FH is often positive, can have family history,diet and exercise can work but eventually can need insulin

313
Q

Why is it getting harder to diagnose type 2 or type 1?

A

youger presentation of type 2, uncontrolled type 2 can present with ketones if long

314
Q

Where is type 1 more common?

A

Finland sweden kuwait norway

315
Q

What is genetic component of type 1?

A

mother to child less than father to child, sibling is higher, polygenic.

316
Q

what is the use of diabetes antibodies?

A

antibodies doesnt mean you will get it

317
Q

What causes ketoacidosis in diabetes?

A

free fatty acids released from lipolysis due to lack of insulin and ketones are produced and casuses acidosis

318
Q

What are the problems with ketoacidosis?

A

associated with high glucose and ketones going to urine and lead to osmotic diuresis which leads to dehydration and ketones cause metabolic acidosis, causes anorexia and vomiting

319
Q

How is diabetic ketoacidosis diagnosed?

A

Hyperglycaemia, raised plasma ketones, metabolic acidosis- plasma bicarbonate less than 15

320
Q

What can cause diabetic ketoacidosis happen?

A

Unknown, infection, MI, treatment errors stop or reduce insulin or unknown diabetes

321
Q

What are clinical features of diabetic ketoacidosis?

A

develop over days, polyuria and polydipsia, nausia vomiting, wight oss, weakness, abdo pain, dowdiness, hyperventilation, dehydration, tachycardia coma

322
Q

What happens to potassium levels in diabetic ketoacidosis?

A

The potassium rises with acidosis but total potassium is low so potassium will fall as correct for acidosis. cardia arrhymias possible

323
Q

How to manage diabetic ketoacidosis?

A

Fluid 3L in first 3 hours, iv insulin to reverse acidosis, replace electrolytes like potassium, treat underlying cause of not diabetes. Follow DKA protocol

324
Q

What are complications of diabetic ketoacidosis?

A

cerebral oedema( children more at risk), ARDS, thromboembolism increased, aspiration pneumonia if drowsy and comatose

325
Q

What are the aims of treatmentin type 1 diabetes?

A

Relieve symptoms and prevent ketoacidosis, micro and macrovascular complications,

326
Q

What complication usually causes shortening of life in type 1 diabetics?

A

CHD

327
Q

What are the problems with neuropathies?

A

Cant feel damage to feet and then get infections

328
Q

What is basal bolus?

A

take bolus with food then basal long acting over night

329
Q

What are the symptoms of hypoglycaemia?

A

sweating dizziness confusion brain disfunction,

330
Q

What causes effects of hypoglycaemia?

A

When glucose lowers usually et less insulin as lower get glucagon and adrenaline this continues as it drops lower

331
Q

what is DAFNE?

A

Dose adjustment for normal eating for how to calculate insulin

332
Q

What percentage of diabetes are not type 1 or 2?

A

5%

333
Q

What are other types of causes of diabetes other than type 1 and type 2?

A

Monognic causes, diseases of the exocrine pancreas, endocrine causes, drug-induced diabetes

334
Q

What is MODY?

A

Maturity-onset diabetes of the young? under 25 commonest monogenetic dominant, non-insulin dependent, alters way beta cells function and are none obese can be several types

335
Q

What are types of MODY?

A

Sulphonylurea treatment MODY3 MODY1 often neonatal hypoglycaemia, macrosomia young onset MODY 2 Glucokinase mutation so insulin not released normally causes higher tight control.

336
Q

What is MODY similar to?

A

Type 1 as young not usually obese non can have family history

337
Q

What suggests MODY vs type 1?

A

Strong family history, abesnce of autoantibodies, evidence of non-insulin dependance, o ketoacidosis and have measurable C peptide.

338
Q

What can cause neonatal diabetes?

A

mutation in potassium channel in beta cells

339
Q

What is MIDD?

A

Mutation in mDNA loss of beta cell mass similar presentation to type 2 wide phenotype

340
Q

How can diabetes be cuased by inflammation?

A

Acute from increased glucagon secretion, chronic pancreatitis from alcohol which blocks the ducts to stop insulin getting to the blood

341
Q

What can haemochromotiosis?

A

Triad of cirrhosis, diabetes bronzed hyperpigmentation, excess iron deposited in liver pancreas pituitary heart and parathyroids

342
Q

Which cancer can cause diabetes?

A

Pancreatic neoplasia, removal of pancreas, and enzyme replacements,

343
Q

How does cystic fibrosis cause diabetes?

A

the secretions can block the ducts to block insulin release and fibrosis, ketoacidosis is rare though

344
Q

which cause of diabetes can be potentially reversed?

A

endocrine causes

345
Q

How does acromegaly cause diabetes?

A

Excess GH causes raised glucose in the blood then high insulin and beta cells fail but can be reversed by treating GH excess

346
Q

How can cushings syndrome cause diabets?

A

Reduces glucose uptake gluconeogenesis is upregulated. causing insulin resistanceq

347
Q

What is pheochromocytma?

A

Excessive epinephrin increased gluconeogenesis and decreased glucose uptake

348
Q

What drugs can cause diabetes?

A

Glucocorticoids increase insulin resistance, thiazides protease inhibitors antipsychotics, not always sure why

349
Q

What are the major complications of diabetes?

A

Neuropathy, nephropathy, retinopathy, amputation

350
Q

What are symptoms of neuropathy?

A

pain burning allodinya, autonomic hypotension cardiac AN gastroparesis, diarrhoes, constipation, insesitivity, infection foot ulceration charcot foot

351
Q

Where does diabetic peripheral neuropathy happen?

A

from feet then maybe hands, not usually motor deficit.

352
Q

What can increase risk of neuropathy?

A

Hypertension, smoking

353
Q

What can be used in diabetic painful neuropathy?

A

Medications, antidepressants, lidocaine. very hard to control

354
Q

What is the problem with diabetic foot ulceration?

A

ulcers can end up with need for amputations

355
Q

how does the neuropathy in diabetes lead to foot shapes?

A

motor damage stops the support from the shape

356
Q

What are typical symptoms of peripheral vascular disease?

A

intermittent claudication, rest pain

357
Q

How can peripheral vascular disease be evaluated?

A

Doppler pressure studies duplex arterial studies

358
Q

What are treatments for peripheral vascular disease?

A

Quit smoking, walk through the pain, surgical intervention

359
Q

What leads to diabetic amputation?

A

vascular issues, trauma, ulcers, failure to heal, infection amputation

360
Q

What is the treatment for retinopathy?

A

Laser treatment doesnt improves sight but aims to stabilize the changes

361
Q

What is the hallmark of diabetic nephroathy?

A

proteinuria and decline in renal function

362
Q

What causes diabetic nephropathy symptoms?

A

Basement membrane has issues.

363
Q

What is macroalbuinuria?

A

large amounts of albumin in the urine

364
Q

What can also cause albuminuria?

A

exercise infection fever heart failure hyperglycaemia marked hypertension pregnancy urinaryinfection haematuria menstruration.

365
Q

hOW CAN kidneys be protected in diabetes?

A

ARBs or ACE inhibitors blood pressure and glycaemic control

366
Q

What are the 4 mechanisms of drug intervention in type 2 diabetes?

A

replace, sensitise, secrete and excrete

367
Q

What is primary treatment for type 2 diabetes?

A

metformin

368
Q

What does metformin do?

A

neutral/loss of weight, inhibition of liver releasing glucose, sensitieses body to insulin

369
Q

Which drugs of diabetes increase weight?

A

Insulin, sylphoilureas,

370
Q

What are GLP-1 anaogues?

A

It has glucose lowering properties tells brain to stop eating, decreases hepatic glucose output increased glucagon, stimulates beta cells, slows gastric emptying.

371
Q

What is the problem with GLP-1 ?

A

IT is broken down fast y DPP-4

372
Q

What are DPP-4 inhibitors?

A

They stop GLP-1 being broken down either natural or unnatural, weight neutral

373
Q

What are GLP-1 analogues?

A

injectable large increase in GLP-1 delayed gastric emptying induces weight loss

374
Q

What do TZDs do?

A

Lower blood sugar levels by increasing glucose uptake receptors in cells and can cause weight gain. pioglitazone

375
Q

What are SGLT-2inhibitors?

A

They stop reasorption of glucose in the kidneys to excrete more into the blood

376
Q

What do sulphonyl ureas do?

A

They cause insulin to be released by acting on receptors on beta cells

377
Q

Where are SGLT-2 transporters?

A

In PCT 1 is in descending and can take up this role

378
Q

What are the tanner stages?

A

The stages of pubertal development in boys, looking at testicular size and pubic hair

379
Q

What does oestrogen do to the breasts?

A

ductal proliferation, site specific adipose deposition, enlargement of the areola and nipple

380
Q

How does the shape of the uterus change?

A

tubular shape to pear shape

381
Q

What is adrenarche?

A

maturation of process of the adrenal gland, only developmental progess of zona reticuaris cells produced increased DHEA

382
Q

What is precocious puberty?

A

Early puberty

383
Q

What is true precocious puberty?

A

When the pituitary causes puberty to happen early rather than something lower down mostly female male idopathic much less likely

384
Q

What can cause pseudo puberty?

A

secreting tumours of gonads bran liver retroperitoneaum of adrenal hyperplasia

385
Q

how can you see true precocious puberty?

A

can stimulate LH and FSH with GnRH

386
Q

is delayed puberty more normal in males or female?

A

in males so worry about late in females

387
Q

When to investigate girls for puberty problems?

A

lack of breast deelopment by 13 years, more than five years between breasts and period, lack of pubic hairby 15 absent menarche by 15-16

Phase 2 mine (13 decks)

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