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endo Flashcards

1
Q

define endocrinology

A

study of hormones (and their gland of origin), their receptors, the intracellular signalling pathways, and their associated disease

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2
Q

what do hormones do?

A

excite

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3
Q

what’s the diff btwn endocrine and exocrine?

A

endocrine (within glands - pour secretion into blood stream)

exocrine (outside glands - pour secretions through a duct to site of action)

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4
Q

name some examples of endocrine glands (2)

A

thyroid

adrenal

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5
Q

where are peptides/monoamines stored?

A

in vesicles

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6
Q

how are steroids synthesised?

A

on demand

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7
Q

list the hormone classes

A

peptides
amines
iodothyronines
cholesterol derivatives and steroids

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8
Q

what are the 3 stages of hormone production

A

preprohormone
prohormone
hormone

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9
Q

what response do amines stimulate?

A

sympathetic NS - fight or flight

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10
Q

where are peptide hormones stored

A

in secretory granules

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11
Q

what % of T3 in the circulation is secreted directly by the thyroid?

A

20%

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12
Q

what are T4/T3 cleaved from

A

thryoglobulin

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13
Q

are thyroid hormones water soluble?

A

no, 99% protein-bound

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14
Q

what does vitD stimulate the production of?

A

mRNA

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15
Q

what type of basal secretion involves hormones?

A

continuously or pulsatile

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16
Q

define synergism

A

combined effects of 2 hormones amplified (eg glucagon with epinephrine)

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17
Q

define antagonism

A

when 1 hormone opposes another (eg glucagon antagonises insulin)

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18
Q

what is hormone receptor down regulation?

A

hormone secreted in large quantities cause down regulation of its targets receptors

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19
Q

what do hypothalamic neurone synthesise?

A

oxytocin

ADH

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20
Q

where’s oxytocin/ADH transported to from the hypothalamus?

A

the posterior pituitary

via the hypothalamic-hypophyseal tract

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21
Q

what is somatostatin aka

A

(GHIH) growth hormone inhibiting hormone

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22
Q

what are the direct actions of GH?

A

metabolic
anti-insulin
(fat/carb metabolism)

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23
Q

what are the indirect actions of GH?

A

growth-promoting (skeletal and extraskeletal)

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24
Q

what kinda effect does thyroid hormone overall have?

A

increases!

food metabolism
protein synthesis
carbohydrate metabolism
fat metabolism
ventilation rate
CO and HR
growth rate
brain development
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25
where are mineralocorticoids produced?
zona glomerulosa
26
where are glucocorticoids produced?
zona fasciculata
27
where are androgens produced?
zona reticularis
28
name a mineralocorticoid
aldosterone
29
name a glucocorticoid
cortisol androgens
30
which cell is FSH produced in?
granulosa cell
31
which cell is LH produced in?
theca cell
32
which hormone is produced in the heart?
ANP (atrial natriuretic peptide)
33
which hormone is produced in the liver?
IGF-I (insulin-like growth factor I)
34
which hormone is produced in the kidney?
erythropoetin
35
which hormones are produced in the GI tract? (2)
gastrin | incretin
36
which hormones are produced in blood vessels?
prostanoids NO endothelin
37
how do alcohol and caffeine impact ADH release?
inhibits
38
how does a lack of ADH influence urine
u urinate more
39
what are the 3 diff presentations of pituitary dysfunctions?
tumour mass effects hormone excess hormone deficiency
40
what are the investigations for hormone abnormalities? (2)
hormonal tests | if hormonal tests abnormal or tumour mass effects, perform MRI pituitary!
41
define appetite
desire to eat food
42
define hunger
need to eat
43
define anorexia
lack/loss of appetite
44
define satiety
feeling of fullness (disappearance of appetite after a meal)
45
define BMI
weight (kg) _________ height (metre squared)
46
what is a bmi of under 18.5?
underweight
47
what is a bmi btwn 18.5 - 24.9
normal weight
48
what is a bmi btwn 25.0 - 29.9?
overweight
49
what is a bmi of 30.0 - 39.9?
obese
50
what is a bmi of >40?
morbidly obese
51
list 7 risks of obesity
``` t2 diabetes hypertension coronary artery disease stroke osteoarthritis obstructive sleep apnoea carcinoma (breast, endometrium, prostate, colon) ```
52
what type of fat is obesity?
abdominal (visceral) rather than subcutaneous
53
how does sleeping out of phase contribute to obesity?
sleeping out of phase - -> lower leptin levels - -> eat more - -> cortisol levels higher than they should be - -> high cortisol levels at night - -> metabolic issues
54
what are the opposing forces in appetite regulation?
energy expenditure vs energy intake
55
why do we eat? (3)
internal physiological drive feelings that prompt thoughts of food external psychological drive
56
what does highly refined sugar lead to?
quick and short satiety
57
what kinda foods are better?
low glycemic index food | also high protein - prolonged satiety
58
where is the hunger centre?
lateral hypothalamus
59
where is the satiety centre?
ventromedial hypothalamic nucleus
60
which part of the brain plays a central role in appetite regulation?
hypothalamus
61
what are the main players in appetite regulation?
``` peripheral factors (leptin, insulin) gut peptides (ghrelin, GLP1, CKK) centra areas, hypothalamus (NPY, POMC, serotonin) ```
62
where is leptin expressed?
white fat
63
what does leptin do?
switches off appetite | immunostimulatory
64
after a meal, how do leptin levels change?
increase
65
where are CCK (cholecystokinin) receptors?
pyloric sphincter
66
what does CCK do? (4ish)
delays gastric emptying initiates gall bladder contraction stim insulin release via vagus - satiety
67
where is ghrelin expressed?
stomach
68
how do blood levels of ghrelin change after meal?
high
69
what are the net effects of leptin and insulin?
increased satiety and decreased appetite
70
what is the net effect of ghrelin?
increased appetite
71
what do stretch receptors in the stomach do?
increase satiety
72
define obesity (WHO definition)
abnormal or excessive fat accumulation that may impair health
73
what are the 4 tiers of obesity care pathway at an individual level?
tier 1 - universal prevention tier 2 - lifestyle intervention tier 3 - specialist services tier 4 - surgery
74
why is diabetes a PH issue? (4)
mortality disability co-morbidity reduces QOL
75
what does the obesogenic environment involve?
``` physical env (car culture) economic env (expensive fruit n veg) sociocultural env (family eating patterns) ```
76
what is a physical mechanism that maintains being overweight?
more weight = more difficult to exercise (arthritis, stress incontinence) and dieting --> metabolic response
77
what is a psychological mechanism that maintains being overweight?
low self-esteem and guilt, comfort eating
78
what is a socioeconomic mechanism that maintains being overweight?
reduced opportunities, employment, relationships, social mobility
79
what are risk factors for obesity?
age, sex, ethnicity, FH, weight, BMI, waist circumference, hypertension, vascular disease, impaired glucose tolerance (IGT) or impaired fasting glucose
80
what is IGT
impaired glucose tolerance
81
what is IFG
impaired fasting glucose
82
list 5 screening tests for obesity
``` HbA1c random capillary blood glucose random venous blood glucose fasting venous blood glucose oral glucose tolerance test (OGTT) ```
83
what does OGTT involve
venous blood glucose 2 hrs after oral glucose load
84
what is the diagnostic range for IGT?
7.8 - 11.0 mmol/l
85
what is the diagnostic range for IFG?
6.1 - 6.9 mmol/l
86
how can society reduce the impact of t2 diabetes? (4)
identifying ppl at risk early prevention in those at risk diagnosing diabetes earlier effective management and supporting self-management
87
what does the pituitary gland regulate?
growth and development fertility metabolism body composition
88
does the anterior pituitary gland have a blood supply?
no but receives blood through a portal venous circulation from the hypothalamus
89
where is prolactin released from?
the anterior pituitary gland
90
what is prolactin under neg control by?
dopamine
91
if anything damages the pituitary stalk and thus delivery of dopamine, WHAT levels increase?
prolactin
92
what hormone can tumours secrete?
prolactin!
93
what is the most common disease of the pituitary gland?
benign pituitary adenoma
94
which disease of the pituitary tends to be in younger ppl?
craniopharyngioma
95
what do a lot of endocrine organs get?
adenomas
96
what are most adenomas like?
benign
97
define adenoma
benign tumour formed from glandular structures in epithelial tissue
98
what are the 3 VITAL points of tumour presentation?
can cause: pressure on local structures (eg optic nerves) pressure on normal pituitary (hypopituitarism) functioning tumour
99
what is prolactinoma?
too much prolactin
100
what is acromegaly?
too much GH
101
what is Cushing's disease?
too much ACTH
102
what can pituitary adenoma pressure cause?
headaches
103
which vision do u lose first?
colour!
104
what is the field defect u get with a pituitary tumour?
bitemporal hemianopia starting upper quadrantic
105
pituitary tumours can go through the bottom of the pituitary fossa and drain the nose .... what is a clue to an important diagnosis to make?
CSF has sugar | snot doesn't
106
what is the most common prolactinoma?
prolactin microadenoma
107
prolactin causes suppression of what?
gonadotrophins
108
as prolactin causes suppression of gonadotrophin, what tends to happen to females? (2)
lose periods | get milk into breasts
109
how do prolactin levels change during pregnancy?
increase
110
if somebody checks with period loss/infertility issues... check what?
prolactin (ngl this always seems to be the answer, but maybe bc I've only covered this lecture LOL @ future me, come back to this)
111
how difficult is it to treat hyperprolactin?
87% ppl respond to dopamine agonist! | 80% women got pregnant within 3m of starting this
112
prolactinomas are more common in who?
women
113
what can be a symptom of prolactinoma?
libido loss, infertility, amenorrhoea
114
how can a tumour result in gigantism?
tumour presses on pituitary gland, increases GH - don't go through puberty as bones don't fuse
115
what are signs of acromegaly?
thick skin greasy sweating frontal bossing
116
too much steroid/cortisol can result in which syndrome?
cushing's
117
what is the commonest cause of too much steroid?
anti inflammatory drugs
118
if u have a patient with a pituitary tumour, what are the 3 questions to ask?
is it pressing on the optic chasm? are they hypopituitary? do they have a functioning tumour?
119
cortisol deficiency can result in death - why?
due to an adrenal crisis
120
what is the HPA axis a classic example of?
negative feedback loop
121
what does HPA (axis) stand for
hypothalamic-pituitary-adrenal
122
if deficient with cortisol, what to replace it with?
hydrocortisone
123
what is hydrocortisone?
the pharmacological name for cortisol
124
what is the distinct circadian rhythm of cortisol?
rises in the early hours of morning (3am, peaks shortly after waking, declines during the day)
125
what do cortisol levels parallel?
energy levels
126
what is the primary zeitgeber?
light
127
what is a primary disease of adrenal insufficiency?
addison's disease
128
what is a secondary disease of adrenal insufficiency?
hypopituitarism
129
if u ever see low Na and high K - think of what?
addison's
130
what is cortisol important for retaining/getting rid of?
retaining Na | getting rid of K
131
when looking at circadian rhythm & deficiency - look when it's at its...... ?
highest
132
when looking at circadian rhythm & excess - look when it's at its...... ?
lowest
133
how to treat cortisol deficiency?
2/3x daily hydrocortisone 15-25mg
134
in primary adrenal insufficiency, replace aldosterone with what?
fludrocortisone
135
what is a common presentation of adrenal insufficiency?
adrenal crisis
136
what does an adrenal crisis involve?
``` hypotension and CV collapse fatigue fever hypoglycaemia hyponatraemia and hyperkalaemia ```
137
how would u manage an adrenal crisis?
take bloods (for cortisol and ACTH) immediate hydrocortisone 100mg IV, IM fluid resuscitation (1L saline 1 hr) hydrocortisone 50-100mg IV/IM 6 hourly
138
what does TDS stand for in pharmacology
3x a day
139
for adrenal insufficiency, always consider what?
recent steroid use | check cortisol and ACTH
140
describe the regulation of HPA axis
circadian rhythm controlled by central clock
141
describe causes of adrenal insufficiency
primary (Addison's and CAH) | secondary (pituitary)
142
what is the diff btwn gigantism and acromegaly?
gigantism = before puberty
143
what are the commonest endocrine disorders?
thyroid diseases
144
FHx of t1 diabetes is a strong association w what?
thyroid disease ;/
145
what is found in almost all patients with autoimmune hypothyroidism
thyroglobulin and thyroid peroxidase (TPO) antibodies
146
what is the mechanism of thyroid cell destruction?
cytotoxic (CD8+) T cell mediated | thryglobulin and TPO antibodies may cause 2ndary damage, but alone have no effect
147
what are some symptoms of Graves' disease?
retracted eyelids bulging eyes redness
148
what does Graves' disease cause
hyperthyroidism | often an enlarged thyroid
149
what is the cause of Graves' disease?
thyroid stimulating antibodies
150
what is Graves' disease aka
hyperthyroidism
151
what is myxoedema aka
hypothyroidism
152
what is the biggest risk factor to thyroid disease?
being female
153
what are some autoimmune diseases associated w thyroid autoimmunity?
t1 DM addison's disease pernicious anaemia vitiligo
154
what is swelling in extra ocular muscles?
thyroid associated opthalmopathy
155
how can graves disease occur in pregnancy
caused by thyroid stimulating antibodies that may cross the placenta
156
what is goitre?
palpable and visible thyroid enlargement | endemic in iodine deficient areas
157
what is sporadic non-toxic goitre?
commonest endocrine disorder
158
define hyperthyroidism
excess of thyroid hormones in blood
159
what are 3 mechanisms for increased levels of thyroid hormone?
overproduction of thyroid hormone leakage of preformed hormone from thyroid ingestion of excess thyroid hormone
160
what is pituitary adenoma aka
TSHoma
161
list some clinical features of hyperthyroidism
``` weight loss tachycardia hyperphagia anxiety heat intolerance sweating diarrhoea menstrual disturbance ```
162
what are thionamides?
anti thyroid drugs
163
what is essential for thyroid hormone production?
iodine
164
how is iodine actively transported into thyroid follicular cells?
via Na/I symporter
165
what are some causes of hypothyroidism
``` Hashimoto's thyroiditis thyroidectomy iodine deficiency thyroid hormone deficiency pituitary/hypothalamic disease ```
166
list some clinical features of hypothyroidism
``` fatigue weight gain cold intolerance constipation dry, rough skin delayed muscle reflexes ```
167
what can u see in the investigation of primary hypothyroidism
``` increased TSH (most sensitive marker) usually decreased free T4/T3 ```
168
what is the most sensitive marker of hypothyroidism
TSH
169
amiodarone (iodine rich) often used to treat what?
atrial fibrillation
170
many drugs can affect the thyroid, particularly what?
amiodarone
171
what are the 2 most important hormones in calcium homeostasis?
PTH and calcitriol
172
what is calcitriol aka
1,25 dihydroxy vit D
173
what is 1,25 dihydroxy vitD aka?
calcitriol
174
PTH release is increased in response to what?
low serum ionised calcium
175
what are the 3 ways in which PTH works to increase serum calcium?
-CONFUSED- decreasing renal calcium excretion increasing bone resorption enhancing dietary calcium absorption (by stimulating prod of calcitriol in kidney) ``` ? increased calcium absorption increased one resorption increased calcium reabsorption ? ```
176
what can abnormal circulating calcium levels result in?
impaired muscle and nerve function | cardiac dysrhymias
177
abnormalities of which hormone levels can be an appropriate response to calcium imbalance OR can be the primary cause of calcium imbalance?
PTH
178
In secondary hyperparathyroidism, how do PTH levels change?
increase
179
In secondary hyperparathyroidism, how do calcium levels change?
decrease
180
In secondary hyperparathyroidism, how do phosphate levels change?
decrease
181
is PTH appropriate or inappropriate in secondary hyperparathyroidism?
appropriate
182
In hypoparathyroidism, how do PTH levels change?
decrease
183
In hypoparathyroidism, how do calcium levels change?
decrease
184
In hypoparathyroidism, how do phosphate levels change?
increase
185
what is pseudohypoparathyroidism aka?
PTH resistance
186
what is another way to say a disorder of PTH resistance?
pseudohypoparathyroidism
187
in pseudohypoparathyroidism, how do PTH levels change?
increase
188
in pseudohypoparathyroidism, how do calcium levels change?
decrease
189
in pseudohypoparathyroidism, how do phosphate levels change?
increase
190
what kind of feedback is calcium homeostasis?
negative
191
what is the set point of serum ionised calcium?
1.1 mol/l ish
192
If Ca decreased by 10%, how much does PTH increase by?
200%
193
if Ca increases by 10%, how much does PTH decrease by?
70%
194
what is the equation for corrected calcium?
total serum calcium + 0.02(40 - serum albumin)
195
if serum calcium = 2.08 mmol/L and serum album = 30 g/L what is the corrected calcium? (mmol/L)
2.28
196
list 6 consequences of hypocalcaemia
``` parasthesia (burning/prickling sensation in limbs) muscle spasm seizures basal ganglia calcification cataracts ECG abnormalities (long QT interval) ```
197
what is a fairly common cause of hypocalcaemia?
osteomalacia
198
how to test chvostek's sign?
tap over facial nerve | look for spasm of facial nerves
199
how to test trousseau's sign?
inflate BP cuff to 20mmHg above systolic for 5 mins - clawing dinosaury thing
200
name some syndromes of hypoparathyroidism
di george HDR kenney-caffey
201
list 4 consequences of hypoparathyroidism
decreased renal Ca reasborption incresed renal phosphate reabsorption decreased bone resorption decreased formation of calcitriol
202
what are some symptoms of pseudohypoparathyroidism?
short stature obesity mild learning difficulties normal calcium metabolism!
203
list 6 symptoms of hypercalcaemia
``` thirst, polyuria nausea constipation confusion (--> coma) renal stones ECG abnormalties (short QT) ```
204
define parasthesia
burning/prickling sensation in limbs, consequence of hypocalcaemia
205
define polyuria
excessive urine prod/passage | above 2.5/3L in 24hrs
206
what are 2 main causes of hypercalcaemia?
malignancy (bone mets, myeloma, lymphoma etc) | primary hyperparathyroidism
207
primary hyperparathyroidism can cause what?
hypercalcaemia
208
what are consequences of primary hyperparathyroidism?
bones, stones, grones, and moans lol osteoporosis kidney stones confusion constipation/acute pancreatitis
209
what's the main cause of primary hyperparathyroidism?
80% due to single benign adenoma :/
210
what happens in tertiary hyperparathyroidism?
renal failure cant activate vit D§ hypercalcaemia
211
define puberty !
physiological, morphological, and behavioural changes as the gonads switch from infantile to adult forms
212
what is the definitive sign of puberty in boys?
1st ejaculation, often nocturnal
213
what is the definitive sign of puberty in girls?
menarch - 1st menstrual bleeding
214
when do secondary sexual characteristics occur
at puberty
215
how does ovarian oestrogen contribute to secondary sexual characteristics?
regulate growth of breast and female genitalia
216
how do ovarian and adrenal androgens impact secondary sexual characteristics?
pubic and axillary hair
217
how do testicular androgens contribute to secondary sexual characteristics?
external genitalia and pubic hair growth | enlargement of larynx/laryngeal muscles (voice deepening)
218
what is a good marker of puberty in boys
testicular growth
219
how do tanner stages differ?
1 - no pubic hear, testicular vol less than 3ml/elevation of papilla only 5 - adult-type hair spread to medial surface of thighs - genitalia adult size n shape / classic inverse triangle hair type in females, adult contour breast
220
what is significant about testicular volume in klinefelters?!
they hardly ever get testicular vol above 5ml
221
what is testicular size mainly dependant on?
number of germ cells
222
what is the diff btwn s1 and s2 of tanner stages in girls
s1 - breast bud | s2 - no breast bud
223
what is a good marker of puberty in girls?
presence of breast bud - can't grow without oestrogen
224
define thelarche
breast development
225
what is thelarche (breast development) induced by?
oestrogen
226
how long does it take for breasts to develop?
3 years ish
227
what are the effects of oestrogen on the breast? (3)
ductal proliferation site specific adipose deposition enlargement of areola and nipple
228
other than oestrogen, what other hormones are involved in breast development?
prolactin glucocorticoids insulin
229
can both breasts be in diff stages of tanners?
yuh
230
what is the (basic) diff btwn prepubertal and postpubertal uterus?
pre - tubular shaped, 2-3cm length | post - pear shaped, 5-8cm length
231
what are 3 questiosn to ask during a pelvic ultrasound in girls?
1. are mullerian structures present? 2. is there morphology of the uterus? is there morphology of ovaries?
232
what are the 5 ways in which the external genitalia in females changes under the effect of oestrogens?
labia majora/minora increase in size n thickness rogation/?rotation and change in colour of labia majora hymen thickens clitoris slightly enlarges vestibular glands begin secretion
233
define adrenarche
the onset of androgen-dependent body changes eg axillary/pubic hair, body odour and acne!
234
define pubarche
1st appearance of pubic hair at puberty
235
what is the most pronounced clinical result of adrenarche
pubic hair
236
what is the hpg axis?
hypothalamus (tertiary) pituitary (secondary) gonads (primary)
237
where is GnRH released
hypothalamus
238
what does GnRH result in the formation of
LH, FSH from pit gland
239
for males with early puberty, what is it important to rule out?
brain tumour
240
"true" precocious puberty - 90% of patients are what?
female
241
in true precocious puberty, what is the rise in LH:FSH?
above 1
242
which type of puberty is GnRH dependent?
true precocious puberty
243
which type of puberty is GnRH independent?
precocious pseudo-puberty
244
CNS tumours/disorders can result in what?
true precocious puberty
245
increased andorgen secretion and gonadotropin secreting tumours can reuslt in what?
precocious pseudopuberty
246
congenital adrenal hyperplasia can result in what?
increased androgen secretion
247
3 resaons why puberty may be delayed? (they loooong)
idiopathic (constitutional) delay in growth and puberty hypogonadotropic hypogonadism hypergonadotropic hypogonadism
248
what is idiopathic (constitutional) delay in growth and puberty?
delayed activation of the hypothalamic pulse generator
249
what is hypogonadotropic hypogonadism
sexual infantilsm related to gonadotropin deficiency
250
lwhat is sexual infantilism?
lack of sexual development after expected puberty or delayed puberty
251
is delayed puberty more common in boys or girls?
boys
252
how does delayed puberty impact bone mass?
reduces it
253
what are some indications of investigation for delayed puberty in girls?
lack of breast development by 13 5+ yrs btwn breast development n period lack of pubic hair by 14 no period by 15-16
254
what are some indications of investigation for delayed puberty in boys?
lack of testicular enlargement by 14 lack of pubic hair by 15 5+ yrs for complete genital enlargement
255
what does CDGP stand for
constitutional delay of growth and puberty
256
what are some signs of constitutional delay of growth n puberty (cdgp)
shorter for age delay in bone maturation, adrenarche FH of late menarche
257
what are lab investigations for puberty? (low conc of any of these)
complete RBC count U&E, renal, LFT, coeliac ab LH,FSH testosterone, oestradiol thyroid function, prolactin DHEA-S, ACTH, cortisol
258
in ALL girls w short stature and delayed puberty: rule out whAT?
turner's (X0)
259
is skeletal or chronological age more closely correlated with pubertal development?
skeletal
260
what are some functional causes of delayed puberty?
``` chronic renal disease sickle cell anorexia psychological/stress extreme exercise drugs cushing's hypothyroidism ```
261
which type of hypogonadism is it if ovary/testis fails?
primary
262
what happens in primary hypogonadism
ovary/testis fails: oestrogen/tesotsterone decrease slack of feedback LH n FSH increase
263
which type of gonadism is it if hypothalamus/pituitary gland fails?
secondary
264
what happens in secondary hypogonadism
hypothalamus/pituitary fails: LH n FSH low no response to feedback so oestrogen/testosterone decreases
265
define hyposmia/microsmia
reduced ability to smell and detect odours
266
define anosmia
when no odours can be detected
267
what is kallman syndrome
hypogonadotrophic hypogonadism
268
what is the key symptom of kallman syndrome (hypogonadotrophic hypogonadism)
inability to detect odours
269
what is hypergonadotropihc gonaidsm?
ripmary gonadal failure (males - klinefelters, females - turners)
270
list some signs of klinefelter
primary hypogonadism reduced 2ndary sexual hair osteoprosis tallstature
271
define azoospermia
medical cond of a man whose semen contains no sperm
272
define gynaecomastia
enlargement of a man's breast
273
what are 3 diff presentations of klinefelters
dont go into puberty go into puberty but stopped, don't develop fully infertile (germ cell failure)
274
list some signs of turners, bitch
at birth - oedema of dorsa of hands/feet webbing of neck CV malformations short stature
275
what is a horseshoe kidney
fusion of kidney at upper poles | can happen in turner's
276
what does female replacement therapy involve?
``` ethinyl estadirol (Tablet) or oestrogen (tablets, transdermal) ```
277
what does male replacement therapy involve?
testosteronen enthane (IM injection)
278
what is the diff btwn precocious and delayed puberty?
precocious - onset of 2ndary sexual characteristics before 8/9yrs delayed - absence of 2ndary sexual characteristics by 14/16 yrs
279
what is the hypothalamic regulation of GnRH secretion
increased stim factors (mostly glutamate and kisspeptin)
280
what % of the human body is fluid?
60%
281
what is the distribution of ECF vs ICF?
ECF - 1/3 total body water (14L) | ICF - 2/3 total body water (28L)
282
what can ECF be split into?
intravascular fluid - 1/4 ECF (3.5L) | interstitial fluid - 3/4 ECF (10.5L)
283
how does osmotic pressure of fluid compartments differ?
it doesnt, its approx equal
284
what kinda ions does ECF contain
Na, Cl and bicarb
285
what kinda ions does ICF contain?
K, Mg and phosphate
286
ECF/plasma osmolarity and what conc should be considered together n why?
Na conc - bc Na+ comprise majority of solute in ECF
287
how does the body respond to changes in ECF osmolarity, BP or blood vol?
by altering water reabsorbed by kidneys and fluid ingested
288
what happens in conditions of water excess?
there's a fall in plasma osmolality and an influx of water into the cells, increasing the intracellular water content. this reduces thirst, suppresses ADH release thus decreasing water intake and increasing water excretion
289
what does ADH bind to?
g-protein coupled 7 transmembrane domain receptors
290
what are the diff g-protein coupled 7 transmembrane domain receptors adh binds to?
V1a (vasculature) V2 (renal collecting tubules) V1b (pituitary gland)
291
what 2 things is ADH release controlled by?
osmoreceptors in thalamus (day to day) | baroreceptors in brainstem/great vessels (emergency)
292
in a day to day situation, what controls ADH release?
osmoreceptors in the thalamus
293
in an emergency situation, what controls ADH release?
baroreceptors in the brainstem/great vessels
294
which receptor does ADH bind to in the renal collecting duct principle cells?
V2 receptors
295
which receptor does ADH bind to in vasculature?
V1a
296
which receptor does ADP bind to in the pituitary gland?
V1b
297
what is the main driver for fluid intake?
thirst
298
what are 2 main drivers of variable water excretion by urine output?
GFR | ADH
299
what is omolality
concentration per kilo
300
list some exogenous solutes that may affect osmolality
alcohol, methanol or mannitol etc
301
urine osmolality should be _______ serum osmolality
double
302
what is a normol osmolality?
282-295 mOsmol/kg
303
how do u approx calculate plasma osmolality?
2xNa+ + glucose + urea
304
where does rine conc by kidney occur
along theneprhon
305
vasopressin activates V2 receptors in renal collecting ducts, leading to what?
increased reabsorption of water via the kidneys (aquaporin2 proteins synthesised and inserted into apical membrane, increasing permeability of renal collecting duct - water is reabsorbed and returned to blood)
306
when the stimulus for water reabsorption ends, how is aquaporin 2 removed from apical membrane?
endocytosis
307
what is the cause of cranial diabetes insipidus
lack of ADH acquired (idiopathic - tumours, infections, inflammatory. primary - genetics, developmental)
308
how do u manage cranial DI?
treat any underlying cond desmopressin (tablets 100-1200 mg/day, nasal spray 10-40mg/day, injection 1-2mg/day)
309
what is desmopressin used to treat?
cranial DI (or in v high dose, nephrogenic CI)
310
what is nephrogenic DI?
resistance to ADH action
311
what are some causes of nephrogenic DI?
acquired (osmotic diuresis / DM), drugs eg lithium, chronic renal failure) familiar (x linked - v2 receptor defect, autosomal recessive(AQP2 defect)
312
how can u manage nephrogenic DI?
try and avoid precipitating drugs
313
define hyponatraemia
serum sodium < 135 mmol/l
314
what is severe hyponatraemia
serum sodium < 125 mmol/l
315
what is normal serum sodium range?
137-144 mmol/l
316
what are some causes of hyponatraemia? (4)
SIADH drip arm sodium deficiency renal failure
317
what do the signs/symptoms of hyponatraemia depend on?
speed of onset! quicker onset = greater symptoms
318
what are some signs of hyponatraemia (less to more severe)
``` asymptomatic headache lethargy weakness confusion decreased concious level coma ```
319
what happens in ECF hypo-osmolality?
water moves into the brain brain oedema brain expels electrolytes and osmolytes water loss accompanies loss of solutes, reducing swelling
320
what is the diff btwn acute n chronic hyponatraemia?
acute - 48H (rapid correction safer n may be necessary) | chronic - CNS adapts (correction must be slow)
321
what are the tests to do when hyponatrameia presents? (this is important )
``` plasma osmolality urine osmolality plasma glucose urine sodium urine diptestfor protein TSH cortisol ```
322
what are 3 causes of hyponatraemia
flui doverloaded normovolaemic dehydrated
323
what is SIADH
syndrome of inappropriate ADH secretion
324
what happens in SIADH
``` too much ADH when it should not be being secreted low osmolality plasma sodium low urine inappropriately concentrated water retention normal thyroid and adrenal function ```
325
what are some causes of SIADH?
CNS disorders (head injury, meningitis, brain tumour) tumours (carcinoma, lymphoma, leukaemia) resp causes (pneumonia, tuberculosis, severe asthma) drugs (carbamazipine, thiazides, MAO inhibitors, vasopressin, desmopressin, SSRIs)
326
what is the treatment of SIADH? (acute and chronic)
fluid restriction! acute - daily U+E in hosp chronic - weekly-monthly U+E
327
what should be the fluid restriction if SIADH?
<1L/24hr
328
what is hypertonic saline for?
symptomatic hyponatraemia
329
what are vaptans?
selective v2 receptor oral antagonist | competitive to ADH
330
so what can cause DI?
lack of ADH | resistance to ADH
331
what kind of tissue is the anterior lobe of the pituitary gland?
glandular tissue (75% of total weight)
332
what kind of tissue is the posterior lobe of the pituitary gland?
nerve tissue (contains axons that originate in the hypothalamus)
333
what kind of tumours are there in the pituitary gland?
``` non-functioning pituitary adenomas endocrine active pituitary adenomas malignant pituitary tumours metastases in the pituitary pituitary cysts ```
334
where do craniopharyngiomas arise from?
squamous epithelial remnants of Rathke's pouch
335
what happens w craniopharyngioma?
``` remnants of rathe's pouchraised ICP visual disturbances growth failure PH deficiency weight increase ```
336
what do rathke's cysts derive from?
derived from remnants of rathke's pouch
337
what does rathke's cyst present with?
headache and amenorrhoea, hypopituitarism and hydrocephalus
338
after a pituitary adenoma, what is the commonest tumour there?
meningioma
339
what is a meningioma associated with
visual disturbance and endocrine dysfunction
340
what is lymphocytic hypophysitis
inflammation of the pituitary gland due to an autoimmune reaction
341
what are 3 types of pituitary dysfunction?
tumour mass effects hormone excess hormone deficiency
342
what are investigations for pituitary dysfunction?
hormone tests | if hormone tests abnormal or tumour mass effects, perform MRI pituitary
343
what are local mass effects of the pituitary? (4)
cranial nerve palsy and temporal lobe epilepsy visual field defects headaches CSH rhinorrhoea (nasal cavity filled w mucus fluid)
344
a chiasmal compression from the pituitary tumour results in what?
bitemporal hemianopia
345
what are the 6 hormones the pituitary gland secretes?
``` gonadotrophins growth hormone prolactin adrenocorticotropin hormone (ACTH) melanocyte-stimulating hormone (MSH) thyroid stimulating hormone (TSH) ```
346
what should u measure in pituitary disease
ft4
347
what does Ft4 stand for?
free thyroxine
348
what does Ft3 stand for?
free tri-iodothyronine
349
in primary hypothyroidism, what are the hormone levels?
raised TSH | low ft4
350
in hypopituitary, what are hormone levels?
normal/low TSH | low ft4
351
in graves disease, what are hormone levels?
suppressed TSH | high ft4
352
in TSHoma, what are hormone levels?
normal/high TSH | high ft4
353
how can u test primary hypogonadism in men
low/raised LH/FSH
354
how can u test gonadal diseases in women?
before puberty - estradiol low with low LH/FSH | puberty - pulsatile LH and oestradiol ncreases
355
what happens in primary ovarian failure
high FSH (with high but slightly lower) LH and low oestradiol
356
how is GH secreted
in pulses with greatest at night | GH levels fall w age ad low in obesity
357
why might prolactin be raised?
stress drugs - antipsychotics stalk pressure prolactinoma
358
oral glucose GH suppression test can be used for what?
acromegaly
359
glucagon test can measure what?
GH deficiency
360
GnRH stimulation test measures what?
gonadotrophindeficiency
361
what is the preferred imaging for the pituitary?
MRI
362
what are symptoms of low GH?
short stature abnormal body composition reduced muscle mass
363
what do u prescribe someone w low GH?
GH
364
what are the symptoms of low LH/FSH?
hypogonadism reduced sperm count infertility menstruation issues
365
what do u prescribe someone w low LH/FSH?
tester one in males | oestradiol +/- progesterone in females
366
what is the symptom of low TSH ?
hypothyroidsim
367
what is the prescription for someone w low TSH (hypothyroidism)?
levothyroxine
368
what are the symptoms of low ACTH?
adrenal failure | decreased pigment
369
what is the treatment for low ACTH?
hydrocortisone
370
what are the symptoms of low ADH?
DI (ADH deficiency - polyuria)
371
oestrogen replacement can reduce the risk of what?
cardiovascular disease and osteoporosis
372
what is the definition of diabetes (measurementS)?
fasting plasma glucose ≥7mmol/l OGTT fasting ≥7 HbA1c >48mmol/mol
373
HbA1c measurement >? indicates diabetes?
48 mmol/mol
374
what are suggestive features of T1 diabetes?
big 3 symptoms: constant thirst frequent urination rapid weight loss
375
what are T1 diabetics prone to?
ketoacidosis
376
what are suggestive features of t2 diabetes?
gradual onset | FH positive
377
T1 or T2?
can be difficult T1 in younger patients T2 can be obese if in doubt: treat w insulin
378
what happens if t1 diabetes diagnosis is missed?
formation of ketone bodies | reduced insulin leads to fat breakdowna nd formation of glycerol and FFA
379
what do FFAs do
impair glucose uptake transported to liver, providing energy for gluconeogenesis oxidised to form ketone bodies
380
define ketoacidosis
absence of insulin and rising counter-regulatory hormones which leads to increasing hyperglycaemia and rising ketones
381
what can ketones cause
anorexia and vomiting- vicious circle of increased dehydration
382
define hyperglycaemia
plasma glucose above 50 mmol/l
383
define raised plasma ketones
urine ketones >2+
384
define metabolic acidosis
plasma bicarb <15mmol/l
385
what are the causes of DKA?
unknown in half | intercurrent illness
386
what is DKA a triad of?
hyperglycaemia ketones acidosis
387
what are symptoms of DKA
``` develops over days polyuria/polydipsia nausea n vomiting weiht loss weakness abdominal pain drowsiness confusion ```
388
define polydipsia
excessive thirst
389
what are some signs of DKA
``` hyperventilation dehydration hypotension tachycardia coma ```
390
what is the biochemical diagnosis of DKA?
hyperglycaemia (<50mmol/l) K+ high on press despite total K+ deficit urea and creatinine raised due to pre-rena failure urinary ketones dipstick >2+ ketones blood ketones >3
391
what do u do to manage DKA?
rehydration (3L in first 3hrs) insulin electrolyte (K+) replacement treat underlying cause
392
what are some complications of DKA?
cerebral oedema adult resp distress syndrome thromboembolism death:/
393
what are the aims of treatment in t1 diabetes
relieve symptoms prevent ketoacidosis prevent vascular complications
394
what are some microvascular complications of t1 diabetes
diabetic nephropathy (tend to develop retinopathy)
395
what does the treatment of t1 diabetes aim to achieve
restoration of beta cell physiology
396
inappropriately high insulin levels confer a high risk of what?
hypoglycaemia
397
what are some physiological defences of hypoglycaemia
symptoms of sweating, tremor, palpitations | loss of conc, hunger
398
what is the dilemma for t1 diabetics?
setting higher glucose targets reduces risk of hypoglycaemia but increases risk of diabetic complications n vice versa
399
what is HbA1c?
avg blood glucose levels for the last 2-3m
400
what is the commonest type of monogenic diabetes
MODY (maturity onset disease of the young) | it's non insulin dependant
401
what are some endocrine causes of diabetes?
acromegaly | cushing's syndrome
402
how is acromegaly an endocrine cause of diabetes
excessive GH secretion similar to T2 insulin resistance rises, impairing insulin action in liver n peripheral tissues
403
how is Cushing's syndrome an endocrine cause of diabetes
increased insulin resistance, reduced glucose uptake into peripheral tissues hepatic glucose prod incr through stimulating of gluconeogenesis via increased substrates
404
do glucocorticoids increase or decrease insulin resistance
increase
405
what are the 3 main microvascular diabetes complications
neuropathy retinopathy nephropathy
406
how can DM cause mortality
acute hyperglycaemia - if untreated leads to a cute met emergencies, DKA chronic hyperglycaemia - leads to tissue complications
407
what are some clinical consequences of diabetic neuropathy
pain (burning, paraesthesia) autonomic (cardiac AN, diarrhoea) insensitivity (foot ulceration, amputation)
408
what are some risk factors for diabetic neuropathy
``` hypertension smoking hba1c change diabetes duration BMI total cholesterol ```
409
what involves the treatment of diabetic neuropathy
good glycaemic control TCAs/SSRIs anticonvulsants opioids
410
what are some consequences of peripheral neuropathy in diabetes
diabetic foot ulceration | peripheral vascular disease
411
what are some symptoms of PVD
intermittent claudication | rest pain
412
what is claudication
limping lol
413
what are some signs of PVD?
diminished/absent pedal pulses coolness of feet n toes poor skin n nails
414
what is the treatment of PVD?
quit smoking walk through the pain surgical intervention
415
what is the journey to diabetic amputation?
``` neuropathy or vascular trauma ulcer failure to heal infection amputation ```
416
what is the hallmark for diabetic nephropathy
development of proteinuria followed by progressive decline in renal function major risk factor for CVD
417
what is the pathophysiology journey of diabetic nephropathy
glomerulus changes increase of glomerular injury filtration of proteins diabetic nephropathy
418
what does treatment for diabetic nephropathy involve
BP control glycemic control ARB/ACEi proteinuria and cholesterol control
419
what is the most common cause of kidney failure/end stage renal disease?
diabetic nephropathy
420
in the fasting state, where does most glucose come from?
liver (a bit from the kidney)
421
in the fasting state, where does glucose come from?
gluconeogenesis (utilises 3 C precursors to synthesise glucose inc lactate, alanine n glycerol)
422
in the fasting state, where is glucose delivered to?
insulin independent tissues, brain and RBC
423
what are insulin levels like in the fasting state?
low
424
what do the muscles use for fuel in the fasting state?
FFA
425
post prandial is aka?
?post prandial
426
what happens after feeding?
physiological need to dispose of nutrient load
427
what stimulates insulin secretion and suppresses glucagon after eating, and when?
rising glucose levels | 5-10min after eating
428
after feeding, where does glucose ingested go?
40% - liver | 60% - periphery, mostly muscle
429
what suppresses lipolysis after feeding
high insulin and glucose levels | levels of FFA fall
430
ingested glucose helps to replenish what?
glycogen stores both in liver n in muscle
431
what is the site of insulin and glucagon secretion in the endocrine pancreas?
islet of langerhans
432
which cells in the islet of langerhans secrete insulin?
beta cells
433
which cells in the islet of langerhans secrete glucagon?
alpha cells
434
which effect (paracrine 'crosstalk') is lost in diabetes?
paracrine 'crosstalk' btwn alpha n beta cells is physiological ie local insulin release inhibits glucagon. an effect lost in diabetes
435
what is the transporter for glucose to enter beta cell?
GLUT2 glucose transporter
436
???how does glucose go to insulin in muscle n fat cells
??confused?glucose enters cell via GLUT4 (glucose transporter 4) GLUT4 vesicle mobilisation to plasma membrane intracellular GLUT4 vesicles intracellular signalling cascades insulin receptor insulin
437
how does insulin impact hepatic glucose output
suppresses | decreases glycogenolysis and gluconeogenesis
438
how does glucagon impact hepatic glucose output
increases glucogeolysis n gluconeogenesis
439
how do insulin n glucagon differ in peripheral glucose uptake
insulin - increases into insulin sensitive tissues eg muscle, fat glucagon reduces
440
does insulin suppress or stimulate lipolysis n muscle breakdown?
suppresses
441
does glucagon suppress or stimulate lipolysis n muscle breakdown?
stimulates
442
counterregulatory hormones such as adrenaline, cortisol and GH have similar effects to what???
glucagon | they become relevant inc certain disease states inc diabetes
443
what does insipid mean?
dilute n odourless | hence in DI, kidneys pass abnormally large amt of insipid urine
444
what is the diff btwn diabetes insipid n mellitus
insipidus - normal blood glucose levels; kidneys cannot balance fluid in the body mellitus - high blood glucose
445
how would u describe t1 diabetes?
an insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction
446
what does failure of insulin secretion lead to?
continued breakdown of liver glycogen unrestrained lipolysis n skeletal muscle breakdown providing gluconeogeneic precursors inappropriate increase in hepatic glucose output n suppression of peripheral glucose uptake
447
rising glucose conc results in increased urinary glucose _____?
losses ...as renal threshold (10mM) is exceeded
448
failure to treat with insulin leads to WHAT?(3)
increase in circulating glucagon, further increasing glucose perceived 'stress' leads to increased cortisol and adrenaline progressive catabolic state and increasing levels of ketones
449
how does ketoacidosis happen?
absence of insulin and rising counter regulatory hormones leads to increasing hyperglycaemia and rising ketones
450
what do ketones cause?
anorexia n vomiting
451
what is IGT?
impaired glucose tolerance | pre-diabetic state of hyperglycaemia (associated with insulin resistance an increased risk of CV pathology)
452
impaired insulin action leads to what?
reduced muscle/fat uptake after eating failure to suppress lipolysis n high circulating FFAs abnormally high glucose output after a meal
453
what's the diff btwn t1/t2 diabetes????
t1 - severe insulin deficiency due to autoimmune destruction of beta cell, initiated by genetic susceptibility n env triggers t2 - insulin resistance n impaired insulin secretion due to a combo of genetic predisposition and env factors
454
why doesn't DKA happening t2 diabetes?
low insulin levels r sufficient to suppress catabolism and prevent ketogenesis can happen if hormones such as adrenaline rise to high levels
455
why does obesity cause t2 diabetes?
obesity impairs insulin action. in those already insulin resistant/predisposed, this brings out diabetes at an early stage
456
in t1d, what should basal insulin control?
blood glucose in btwn meals n particularly during night
457
basal insulin is adjusted to maintain fasting glucose btwn what?
5-7 mmol/L
458
how does insulin differ in t1dm vs t2dm?
t1 - insulin deficiency | t2 - insulin resistance
459
what's the diff btwn basal n prandial insulin?
basal - long-acting | prandial - rapid-acting/meal time
460
prandial insulins mimic meal-time insulin secretion and their faster action allows for what?
greater flexibility at meal times
461
what are the adv of basal insulin in t2 diabetes?
simple for patient, adjust insulin themselves, based on fasting glucose measurements carries on w oral therapy less risk of hypoglycaemia at night
462
what are the disadvantages of basal insulin in t2 diabetes?
doesn't cover meals | best used with long-acting insulin analogues which are considered exp
463
what are the adv of pre-mixed insulin?
both basal n prandial components in a single insulin prep | can cover insulin requirements through most of the day
464
what are the disadvantages of pre-mixed insulin today?
not physiological requires consistent meal n exercise pattern increased risk for nocturnal hypoglycaemia
465
what is the definition of hypoglycaemia
low plasma glucose causing impaired brain function neuroglycopenia 3mmol/l
466
what is mild hypoglycaemia vs severe
mild - self-treated (many epodes asymptomatic) | severe - requiring help for recovery (excepting children)
467
what are the 3 types of hypoglycaemia symptoms n some examples of each?
autonomic: trembling, palpitations, sweating, anxiety, hunger neuroglycopenic: difficult concentration, confusion, weakness, dizziness, vision changes, difficulty speaking non-specific: nausea, headache
468
what is neuroglycopenia?
shortage of glucose (glycopenia) in the brain, usually due to hypoglycemia. glycopenia affects the function of neurons, and alters brain function and behaviour
469
in most patients, what prevents severe hypoglycaemia/
counter regulatory n symptomatic defences
470
in t1dm, what are some risk factors for severe hypoglycaemia
``` history of severe episodes HbA1c < 6.5% (48mmol/mol) long duration of diabetes renal impairment extremities of age ```
471
in t2dm, what are some risk factors for severe hypoglycaemia
``` advancing age cog impairment depression aggressive glycaemia treatment duration of MDI insulin therapy renal impairment n other comorbidities ```
472
what are some consequences of hypoglycaemia?
``` accidents fear QOL prevents desirable glucose targets CV risk seizures coma cog dysfunction ```
473
what are glucose targets like in t1dm/t2dm?
aim for lowest hba1c not associated w freq hypoglycaemia it may sometimes be appropriate to relax targets in patients w advanced disease, complications or limited life expectancy
474
a target of hba1c < 7.5% (58 mmol/mol) is good 4 what?
few comorbidities good physical function preserved cog function
475
a target of hba1c < 8% (64 mmol/mol) is good 4 what?
multiple chronic illnesses mild cog impairment risk of falls n hypoglycaemia
476
a target of hba1c < 8.5% (69 mmol/mol) is good 4 what?
end-stage chronic illness moderate-to-severe cog impairment in long-term care
477
what are some strategies to prevent hypoglycaemia?
discuss risk factors w patients on insulin educate patients n caregivers on how to recognise n treat it instruct patients to report episodes to doctor
478
what are the 5 steps to treating hypoglycaemia?
1. recognise symptoms so they can be treated asap 2. confirm need for treatment (blood glucose <3.9mmol/mol is the alert value) 3. treat w 15g fast-acting carb to relieve symptoms 4. retest in 15mins to ensure blood glucose >4.0 mmol/mol n retreat if needed 5. eat long-acting carb to prevent recurrence
479
what is the alert value for hypoglycaemia in treatment?
<3.9mmol/mol
480
what is an inevitable side effect of diabetes treatment
hypolycaemia
481
why does hypoglycaemia occur?
due to inability of insulin therapy to mimic physiology of beta cell
482
what does metformin help?
liver | inhibition of glucose prod and increase in hepatic insulin sensitivity
483
nocturia
excessive nighttime urination
484
what does NAD stand for? (2)
no abnormality detected OR no apparent distress
485
what are incretins
hormones secreted by intestinal endocrine cells in response to nutrient uptake
486
how do incretins influence glucose homeostasis
``` via multiple actions including: glucose-dependant insulin secretion postprandial glucagon suppression slowing of gastric emptying ```
487
when are incretins secreted
by the gut, into circulation in response to food
488
name 3 antihyperglycaemics
metformin SUs (sulfonylureas) TZDs (thiazolidinediones)
489
what are SUs
sulfonylureas, antihyperglycaemics
490
what are TZDs
thiazolidinediones, antihyperglycaemics
491
what are the benefits of using metformin as an anti hyperglycaemic?
low risk of hypoglycaemia BP reduction cardioprotective benefits
492
what are the drawbacks of using metformin as an anti hyperglycaemic?
``` lactic acidosis (rare) caution indicated in older patients w CHF ```
493
how does metformin affect weight?
weight neutral or slight weight loss
494
what are the benefits of using SUs (sulfonylureas) as an anti hyperglycaemic?
newer class entrants may have reduced CV risk
495
what are the drawbacks of using SUs (sulfonylureas) as an anti hyperglycaemic?
may increase risk of CV events | hypoglycaemia
496
how do SUs affect weight?
weight gain
497
what are the benefits of using TZDs (thiazolodinediones) as an anti hyperglycaemic?
low risk of hypoglycaemia | positive effects on biomarkers
498
what are the drawbacks of TZDs as an antihyperglycaemic?
increased CV risk | lipid abnormalities
499
how do TZDs affect weight?
weight gain

(SG) Phase 2A lectures (14 decks)

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