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Endo Flashcards

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1
Q

System through which hypothalamic factors travel to ant. pituitray?

A

hypothalamus-pituitary portal system

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2
Q

What hormone level changes will there be in primary hypothyroidism?

A

low T3 and T4

high TSH

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3
Q

Explain secondary hypopituitarism?

A

Eg. pituitary tumour damages cells (corticotrophs, gonadotrophs, thyrotrophs) → no ACTH/TSH/LH + FSH
→ no cortisol/t3/4/oestroge/testpsterone

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4
Q

What happens to aldosterone levels in secondary hypoadrenalism and why?

A

Remain the same
Because aldosterone is not regulated by ACTH
Controlled by renin-angiotensin system

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5
Q

Describe congenital hypopituitarism

A

eg PROP1 mutation → abnormal ant. pit. development

→ GH deficiency and at least one more hormone

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6
Q

Clinical findings of congenital hypopituitarism?

A

Short stature

Hypoplastic ant. pit. on MRI

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7
Q

Name 5 causes of acquired hypopituitarism

A 
tumours
radiation
infection
TBI
pituitary surgery
Hypophysitis
Pit. apoplexy
Sheehan's syndrome
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8
Q

common cause of post. pit. dysfunction?

A

Hypophysitis

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9
Q

What do you call total loss of ant. and post. pit. function?

A

Panhypopituitarism

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10
Q

Why does prolactin increase after radiotherapy?

A

Due to loss of hypothalamic dopamine which usually inhibits prolactin release

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11
Q

Which pituitary hormones are most sensitive to radiotherapy?

A

GH and gonadotrophin (LH and FSH)

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12
Q

Why do you need annual assessment after radiotherapy and for how long?

A

Risk of hypopituitarism remains up to 10 years after radiotherapy

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13
Q

Presentations of hypopituitarism related to each hormone?

A

FSH/LH - reduced libido, 2* amenhorrea, ED, ↓ pubic hair
TSH & ACTH - fatigue
GH - ↓QoL, short stature in kids
PRL - unable to breastfeed

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14
Q

Pathophysiology of Sheehan’s syndrome?

A

postpartum haemorrhage leads to hypotension → less/no blood supply to pituitary → pituitary infarction → hypopituitaruism

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15
Q

Why does the ant pit enlarge in pregnancy? What is it called?

A

Lactotroph hyperplasia as more prolactin production is required for lactation

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16
Q

How can Sheehan’s syndrome present?

A

tiredness, anorexia/weight loss, inability to lactate, no postpartum menses

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17
Q

What are the causes of pituitary apoplexy?

A

intra-pituitary haemorrhage/infarction

pituitary adenomas

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18
Q

What drug can be a risk factor pit. apoplexy?

A

Anti-coagulants

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19
Q

How can pit. apoplexy present?

A

severe sudden onset headache
bitemporal hemianopia due to compressed optic chasm
diplopia + ptosis

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20
Q

What is the half life of t4?

A

6 days

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21
Q

when are cortisol levels highest?

A

in the morning around 9am

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22
Q

How can you test for ACTH and GH levels?

A

Insulin induced hypoglycaemia → stress on body → GH and ACTH should be released

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23
Q

What can you use to radiologically diagnose hypopituitarism? What would you see?

A

MRI

empty sella

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24
Q

What is the biochemical test used for hypopituitarism?

A

Dynamic pituitary function test

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25
When and how is GH deficiency treated?
If QoL is low | Daily GH injections
26
How is GH injection response measured?
QoL improvement? | plasma IGF-1 levels?
27
How is TSH deficiency treated? And how is dose adjusted?
Levothyroxine daily tablet Dose adjusted to fT4 levels Should be above mid reference range
28
What are 2 treatment options for ACTH deficiency?
Prednisolone - 3mg once daily | Hydrocortisone - 3x/day - 10/5/2mg
29
How can adrenal crisis present? What can trigger it?
dizziness, hypotension, vomitting, weakness, collapse | Intercurrent illness
30
What are the sick day rules for ACTH deficient patients?
Double steroid dose when feverish/intercurrent illness Wear steroid alert bracelet Vomitting → inject steroids IM or go to a&e
31
What are the treatment options for fsh/lh deficiency in men?
topical/IM testosterone | gonadotropin injections if fertility is needed → spermatogenesis (takes 6-12 months)
32
What are the treatment options for fsh/lh deficiency in women?
Oestrogen - oral/topical progesterone (sometimes) gonadotropin injections if fertility is needed (IVF) → ovulation
33
When is progesterone needed to treat fsh/lh deficiency and why?
If uterus is intact | Prevents endometrial hyperplasia
34
Which neurone contain AVP and oxytocin?
Magnocellular neuons
35
Where do magnocellular neurones originate?
Paraventricular and supraoptic hypothalamic nuclei
36
What are the actions of vasopressin?
Stimulate water reabsorption in the renal CD (concentrates urine) Vasocontrictor Stimulates ACTH release
37
which receptors does vasopressin act on>
V2 in CD | V1 in vasoconstriction
38
how does vasopressin lead to increase reabsorption in the CD?
acts on v2 receptors → cAMP → protein kinase A → vesicles containing aquaporins move to apical membrane more aquaporins = more water reabsorption
39
Describe the two stimuli for vasopressin release
osmotic - osmorecptors detect high plama osmolality | non-osmotic - atrial stretch receptors detect low atrial pressure
40
where are the osmoreceptors found?
Subfornical organ | Organum vasculosum
41
How are the SO and OV suited to their function?
Around 3rd ventricle → no BBB → can respond to changes in systemic circulation Highly vascularised Project to supraoptic nuclei with vasopressinergic neurons
42
how do osmoreceptors regulate vasopressin release`se?
high plasma osmolality → water leaves osmoreceptor → shrinks→ increased firing rate to hypothalamic neurone→ ↑ avp released
43
what is the function of atrial stretch receptors?
detect pressure in RA | normal pressure → stretch → inhibition of avp release via vagal afferents to hypothalamus
44
mechanism of vasopressin after a haemorrhage?
haemorrhage → less stretch → less inhibition of avp release → ↑ circulating volume → ↑ BP vasoconstriction via V1r
45
mechanism of vasopressin in water deprivation?
↑ plamsa osmolality → osmoreceptors stimulated → ↑ avp release → ↑ water reabsorption in CD → ↓ urine and ↑ urine osmolality → ↓ plasma osmolality
46
3 symptoms associated with diabetes insipidus?
polyuria nocturia polydipsia
47
most common cause of polyuria nocturia polydipsia?
diabetes mellitus
48
explain the two types of diabetes insipidus
Cranial - hypothalamus/post pit cannot make avp - insufficiency Nephrogenic - kidney CD unable to respond to avp - resistance
49
causes of cranial diabetes insipidus? (7)
``` TBI pit surgery pit tumours metastasis to pit granulomous infiltration autoimmune congenital ```
50
causes of nephrogenic diabetes insipidus?
congenital - mutation in gene coding for v2 receptor/aquaporin drugs - lithium
51
what drug can cause nephrogenic DI?
lithium
52
how do patients with DI present?
very dilute, large volumes of urine high plasma osmolality hypernatraemia normal glucose
53
why do DI patients have polydipsia?
avp problem → no water reabsorption in CD → ↑ dilute urine → ↑ plasma osmolality + Na → osmoreceptors stimulated → thirst → water intake → maintains circulating volume
54
when can DI lead to death?
if patient has no access to water
55
what are two differentials for DI?
DM | Psychogenic polydipsia
56
what happens in psychogenic polydipsia?
↑ water intake → ↓ plasma osmolality → less avp by post pit → ↓ water reabsorption in CD → ↑ volume of hypotonic urine → plasma osmolality normalises
57
what test is used to distinguish between DI and PP? what 4 things are measured?
water deprivation test no access to fluids measure urine volume, urine osmolality, plasma osmolatiy, weight
58
why should you weigh patients regularly in the water deprivation test?
>3% body weight indicates significant dehydration which can happen in DI
59
how does DI differ to PP in the water deprivation test?
urine osmolality increase in PP but remains the same in DI
60
how do you distinguish cranial DI and neprhogenic DI?
give ddAVP CDI - urine will concentrate NDI - urine remains concentrated as kidneys do not respond
61
what is approx normal plasma osmolality range? what do above and below mean?
270-290 mOsm/kg H20 ``` above = DI below = PP ```
62
How do you treat cranial DI?
give desmopressin as tablets or intranasal
63
What receptor is desmopressin selective for and why?
the v2 receptor | v1 receptor activation would lead to unhelpful vasoconstriction
64
Treatment for nephrogenic DI?
Thiazide diuretics - eg bendrofluazide
65
What is SIADH?
Syndrome of inappropriate adh | Too much vasopressin released
66
Presentations of SIADH? and mechnaism?
↑ ADH → ↓ urine output and ↑ water retention → ↑ urine osmolality and ↓ plasma osmolality Dilutional hyponatraemia
67
Causes of SIADH? (6)
``` CNS - head injury, stroke, tumour Pulmonary - pneumonia, bronchiestatis Malignancy - lung cancer Drugs - carbamazepine, serotonin reuptake inhibitors Idiopathic Hypothyroidism/pituitarism ```
68
How can lung cancer lead to SIADH?
Ectopic production of ADH
69
SIADH management?
Fluid restrictions | Vaptan (vasopressin antagonist on v2 receptor)
70
What is the purpose of fluid restriction in SIADH?
to raise plasma sodium levels whilst looking for underlying cause
71
most common functioning pituitary tumour?
prolactinoma
72
three ways to classify pituitary tumours
MRI - size (micro or macro, sellar or suprasellar) functioning (excess hormone secretion) or non-functioning benign or malignant (v rare)
73
how does hyperprolactinaemia lead to hypoginadism?
excess prolactin → binds to kisspeptin neurons in hypothalamus → inhibits kisspeptin release → decreased downstream release of GnRH, LH, FSH, testosterone, oestrogen → hypogonadism
74
what serum prolactin is normally indicative of a prolactinoma?
>5000 mU/L
75
how does a prolactinoma present?
``` menstrual disturbance erectile dysfunciton reduced libido glactorhhea subfertility ```
76
what else can cause an elevated prolactin aside from prolactinoma? (physiological, pathological, iatrogenic)
pregnancy/brerstfeeding stress eg. exercise, seizure, venepuncture nipple, chest wall stimulation primary hypothyroidism (↑TRH → ↑ PRL) PCOS chronic renal failure ``` antipsychotics SSRIs anti-emetics high does oestrogen opiates ```
77
what can cause a false serum prolactin elevation? | when would you suspect this?
macroprolactin venepuncture consider when patient has mild elevation and no clinical symptoms
78
what is macroprolactin?
polymeric form of prolactin → antigen-antibody complex of monomeric prolactin with IgG on assay it's recored as elevated prolactin levels
79
how can you measure prolactin if you suspect stress of venipuncture is causing elevated levels?
a cannulated prolactin series | measure serum prolactin 20 mins apart with an indwelling catheter to reduce stress
80
if serum prolactin is truly high what would you do next?
arrange pituitary MRI
81
what is the first line treatment for a prolcatinoma? how does it work?
cabergoline | dopamine agonist → binds to D2 receptors on tumour → inhibit prolactin release → prolcatinima shrinks
82
acromegaly has an insidious presentation, what does this mean?
a long time from onset of symptoms to diagnosis, ~10yrs
83
symptoms of acromegaly?
sweating headaches macroglossia, prominent nose, prognathism big hands and feet snoring, OSA hypertension imparted glucose tolerance/dibetes mellitus
84
which two places does somatotrophin act? what are its effects?
body tissue → metabolic actions → growth & development | liver → IGF-1 → body tissue
85
how is GH secreted?
pulsatile
86
what two ways can you diagnose acromegaly?
elevated serum IGF-1 OR oral glucose tolerance test with a paradoxical rise in growth hormone
87
what other hormone can be raised in acromgealy?
prolactin (cosecreted with GH)
88
what is a complication untreated acromegaly?
increased CVD risk
89
what is the first line treatment in acromegaly?
trans-sphenoidal pituitary surgery
90
what can be done before surgery to shrink acromegaly tumours? (or if resection is incomplete)
somatostatin analogues eg. octretotide dopamine agonists eg. cabergoline radiotherapy (slow)
91
symptoms of Cushing's syndrome?
``` proximal myopathy buffalo hump (inter scapular fat) red/purple striae moon face red cheeks thin skin pendulous abdomen - centripetal obesity depression easy bruising hypertension ```
92
4 causes of cushing syndrome?
ACTH independent excess corticosteroids adrenal adenoma/carcinoma ACTH dependent pituitary corticotroph adenoma lung cancer - ectopic ACTH
93
what causes cushings disease?
pituitary adenoma securing excess ACTH
94
what 3 investigations would indicate cushings syndrome?
24h urine free cortisol → increased cortisol late night cortisol (blood or salivary) → increased give oral dexamethasone → failure to suppress cortisol levels (cortisol should fall to zero)
95
what is dexamethasone? how does it work?
exogenous glucocorticoid → body should recognise cortisol levels are increased → ACTH levels decrease → cortisol levels should fall to zero
96
how can non-functioning pituitary tumours present?
bitemporal hemianopia → compression of optic chiasm hypopituitarism and hyperprolactinoma → releasing hormones and dopamine cannot travel from hypothalmus down pituitary stalk to ant pit
97
how can you treat non-functioning pituitary tumours?
trans-sphenoidal pituitary surgery
98
explain graves disease?
graves disease - autoimmune | antibodies bind to and stimulated the TSH receptors in the thyroid
99
symptoms of graves disease?
``` smooth goitre sweating weight loss with increased appetite tachycardia, breathlessness oligo/amenhorrea exopthalmus pretibial myxoedema tremor myopathy insomnia, restlessness, excitability heat intolerance ```
100
how does exophthalmus arise in graves disease?
antibodies bind to muscles behind the eyes
101
how does pretibial myxoedema arise in graves? what will you observe?
antibodies stimulate the uncontrolled growth of soft tissue (hypertrophy) non-pitting swelling on the patient's shins
102
what scan can be used to visualise a goitre? what will be seen in graves disease?
radioiodine uptake scan | diffuse enlargement and engorgement of thyroid,uniform radio iodine uptake
103
two main causes of hyperthyroidism?
graves disease | toxic multinodular goitre
104
how does a toxic nodular goitre form?
iodine definciency → ↑ no of follicular cells in attempt to make more thyroid hormones mutation → permanently stimulated TSH receptor → follicular cells contstanly dividing (adenomatous) → nodules
105
what two symptom will you not see in toxic nodular patients when compared to graves disease patients?
no pretibial myoxoedam nor exophthalmus (no antibodies)
106
what will you see in a radioiodine uptake scan if there us a toxic nodular goitre?
only 'hot nodules' show up as rest of thyroid atrophies
107
what is the effect off thyroxine on the SNS? what symptoms does this lead to if its in excess?
sensitises beta adrenoreceptors to ambient levels of adrenaline and NA → excess → apparent sympathetic activation → tachycardia, palpitations, tremor, lid lag
108
what is a medical emergency in hyperthyroidism patents? what are the features?
``` thyroid storm heat intolerance → hyperpyrexia tachycardia → arrhythmia cardiac failure delirium/frank psychosis jaundice ```
109
what are the three main treatment options for hyperthryodism?
thyroidectomy surgery radioiodine drugs
110
why would you give beta blockers to hyperthyroidism patients? give an example of one
to help symptoms whilst waiting for thyroid hormones to decrease, eg reduce tachycardia, tremors propanalol - non-selective
111
what re the two thionamides that can be used in hyperthyroidism?
propylthiouracil PTU | carbimazole CBZ
112
how does potassium iodide work in hyperthryoidism? what is the effect called?
↑ iodine → ↓ thyroid hormone synthesis hyperthyroid symptom reduce in 1-2 days gland sizes reduces in 10-14 days Wolff-Chaikoff effect
113
what is the mechanism of thionamides?
inhibit thyroid peroxidase → less t3/4 synthesis and secretion
114
why does it take time to see clinical effects of thionamides?
takes a few weeks for the body to use up the excess t3/4
115
two unwanted actions of thionamides?
agranulocytosis (↓ neutrophils) (rare and reversible) | rashes
116
when would you give potassium ioidine in hyperthyroidism?
in preparation for surgery | thyroid storm
117
4 risks of a thyroidectomy?
voice change losing parathyroid glands scar anaesthetic
118
what are the symptoms of viral thyroiditis?
painful dysphagia fever hyperthyroidism symptoms thyroid inflammation, tender and palpable
119
explain viral thyroiditis
virus attacks thyroid → pain and tenderness → thyroid stops making thyroxine → makes viruses→ no radioiodine uptake → all stored thyroxine released → hyperthyroid symptoms → after 4 weeks all the thyroxine is exhausted → hypothyroidism → resolution of virus after another 4 weeks → euthyroid
120
what can have similar features to viral thyroiditis without the pain?
postpartum thyroditis
121
what steroids do the three layers of the adrenal cortex secrete?
zona glomerulosa - aldosterone zona fasiculata - cortisol zona reticularis -androgens
122
what enzymes does angiotensin II activate in the adrenals?
side chain cleavge 3 hydrozysteroid dehydrogenase 21, 11, 18 hydroxylase
123
what is the action of aldosterone?
increases blood pressure by increasing sodium levels and decreasing potassium levels
124
what enzymes does ACTH activate in the adrenals?
side chain cleavage 3 hydrozysteroid dehydrogenase 17, 21, 11 hydroxylase
125
what enzyme do the cortisol and androgen production pathways share?
17 hydroxylase
126
what are two commonest causes of Addison's disease?
autoimmune - uk | TB - worldwide
127
signs and symptoms of Addisons disease?
``` vitiligo weight loss low BP nausea, vomitting, diarrhoea, constipation muscular weakness hyperkalaemia loss of salt in urine low glucose due to glucocorticoid deficiency ```
128
explain the increased pigmentation seen in patients with Addisons
high levels of ACTH precursor of which is pro-opio melanocortin which is also the precursor to MSH therefore ↑ ACTH → ↑ MSH
129
name another cause of adrenocortical failure
congenital adrenal hyperplasia
130
what three tests can you do if you suspect Addison's disease?
9am cortisol → low ACTH → high synACTHen test → 250 ug IM → measure cortisol → still low = Addisons
131
why is fludrocortisone used instead of aldosterone in treating Addisons?
half life of aldosterone is too short for once daily injection the fluorine in fludrocortisone makes it non-biodegradable as fluorine is not naturally found in the body so its effects last for much longer
132
in what pattern is cortisol secreted?
diurnally , high in the morning, low at night
133
why is prednisolone given instead of hydrocortisone in treating Addisons?
oral hydrocortisone has too short half life for once daily administration → give 3x per day → multiple cortisol peaks harmful → each subsequent dose is lower 10mg, 5mg, 2.5mg prednisolone has a longer half life and is more potent → only needs to be taken once daily , 2-4mg
134
what are the two main drugs used in treating Addisons disease?
fludrocortisone 50-100 mcg/day (adjust for potassium levels and hypertension) prednisolone 3mg/day
135
what is the commonest cause of congenital adrenal hyperplasia?
21 hydroxylase deficiency (complete or partial)
136
what effects does the absence of 21 hydroxylase have on the adrenal steroids pathways?
no aldosterone and cortisol | ↑ androgens and oestrogen
137
if you have complete 21 hydroxylase deficiency at birth how long can you survive? how does the baby survive in utero? what should be given straight away?
24 hours give IV saline for salt losing addisonian crisis in utero foetus gets steroids from mother across placenta
138
how might babies with complete 21 hydroxylase deficiency present?
with ambiguous genitalia (could be variety of causes but treat immediately as CAH just in case)
139
what is the age of presentation in partial 21 hydroxylase deficiency? how will they present?
any age as they survive hirsutism and virilisation in girls precocious puberty in boys
140
what is the second most common cause of CAH?
11 hydroxylase deficiency
141
what effects does the deficiency of 11 hydroxylase have on the adrenal steroids pathways?
deficient cortisol and aldosterone ALSO increase 11-deoxycorticosterone excess sex steroids
142
how can 11 hyrdroxylase deficiency present? (relate to excess steroids)
virilisation from excess sex steroids | hypokalaemia and hypertension as 11-deoxycorticosterone behaves like aldosterone
143
what effects does the deficiency of 17 hydroxylase have on the adrenal steroids pathways?
deficient cortisol and sex steroids | excess aldosterone
144
what are the problems seen in 17 hydroxylase deficiency?
hypertension hypokalaemia low glucose from glucocorticoid deficiency sex steroid deficiency
145
what happens in the low does dexamethasone test?
give 0.5mg 6 hourly for 48 hours → cortisol should be supressed to zero
146
what 2 drugs can be used to treat cushings? what is their action?
metyrapone ketoconazole (no longer used) inhibit steroid biosynthesis
147
what is the mechanism of action for metyrapone?
inhibits 11b-hydroxylase → no cortisol → ↑ deoxycortiol (no negative feedback on HPA) → ACTH ↑
148
how should metyrapone be adjusted?
according to cortisol levels , aim for 150-300 nmol/L
149
why is metyrapone given in cuhsings patients prior to surgical intervention/after radiotherapy?
improves patients symptoms and leads to better post op outcomes
150
what are 2 unwanted actions of metyrapone? explain
hypertension and hypokalaemia - inhibition of 11b-hydroxylase leads to excess 11-deoxycorticosterone → aldosterone-like effects hirsutism in women → ↑ androgens
151
what enzyme does ketoconazole inhibit?
17a-hydroxylase → ↓ cortisol
152
why is ketoconazole no longer used?
hepatotoxicity , possibly fatal
153
treatment options for cushings syndrome?
``` transphenoidal pituitary surgery for pituitary adenoma bilateral adrenalectomy unilateral adrenalectomy for mass metyrapone (ketoconazole) ```
154
what is Conns syndrome? what causes it?
excess aldosterone | benign adrenal adenoma in zona glomerulosa (primary hyperaldosteronism)
155
what are two signs of conns syndrome?
hypertension and hypokalaemia
156
How can you confirm primary hyperaldosteronism? (as opposed to secondary)
suppression of renin-angiotensin system
157
what 2 drugs can be used to treat conns syndrome? what is their action?
spironolactone epleronone mineralcorticoid receptor antagonists
158
what is the mechanism of action of spironolactone?
converted to canrenone → competitive antagonist of mineralocorticoid receptor → inhibits na resorption and k excretion in kidney tubules
159
how is spironolactone administered and where is it metabolised?
orally | in liver
160
2 unwanted actions of spironolactone?
menstrual irregularities | gynaecomastia
161
mechanism of action of epleronone?
mineralocorticoid antagonist similar to spironolactone
162
why is epleronone better tolerated compared to spironolactone?
less binding to androgen and progesterone receptors → less menstrual irregularities and gynacomastia
163
what is a phaeochromocytoma?
adrenal medulla tumours that secrete catecholamines (adrenaline and NA)
164
what are the clinical features of phaeochromocytoma?
episodic severe hypertension (especially in young people) palpatations sweating headache
165
why is hypertension intermittent in phaeochromocytoma?
cells degranulate all at once and release a load of adrenaline → hypertension
166
what are some complications of phaeochromocytoma?
MI stroke ventricular fibrillation
167
why does a patient with a phaeochromocytoma need careful management prior to surgery?
anaesthetic can precipitate a hypertensive crisis
168
what are the steps in managing a phaeochromocytoma?
alpha blockade IV fluids beta blockade to prevent tachycardia
169
what hormones increase serum calcium?
vitamin D | parathyroid hormone
170
what hormone decreases calcium?
calcitonin from parathyroid follicular cells
171
what are the 2 forms of vitamin d and their sources?
D2 from the diet | D3 - UVB → 7-dehydrocholestrol → pre vitamin D3 → vitamin D3
172
how does vitamin D3 get converted to calcitriol?
vitamin D3 → liver → 25-hydroxylase converts it to 25(OH)cholecalciferol → kidney → 1-alpha hydroxylase converts it to 1,25(OH)2cholcalciferol (calcitriol)
173
what is the active form of vitamin D?
calcitriol
174
how does calcitriol regulate its own synthesis?
negative feedback on 1-alpha-hydroxylase
175
what are the effects of calcitriol on the body?
↑ osteoblast activity → ↑ca2+ ↑ ca2+ and PO43- absorption in gut ↑ ca2+ and PO43- reabsorption in kidney
176
what are the effects of PTH on the body?
↑ca2+ resorption from bone ↑ca2+ reabsorption and ↑PO43- excretion in kidney ↑1-alpha-hydroxylase activity in kidney → ↑calctirol → ↑CA2+ and PO43- absorption in gut
177
how is serum phosphate regulated bye FGF-23?
it inhibits the sodium phosphate co-tranporter in the kidney proximal tubule so less is reabsorbed and more is excreted (it also inhibits calcitriol → ↓ phosphate resabsorptiion in gut)
178
what two hormones inhibit the sodium phosphate cotransporter in the PCT?
FGF-23 | PTH
179
What are the signs and symptoms of hypocalcaemia?
``` paraesthesisa convulsions arrhythmias tetany (involuntary muscle contraction) muscle cramps chvosteks and trousseau's signs ```
180
what are chvostek's and trousseau's signs? when are they seen?
chvosteks - facial muscles twitch when zygoma is tapped trousseaus - carpopedal spasm (compress arm with blood pressure cuff → involuntary contraction of hand and wrist muscles) seen in hypocalcaemia
181
what are 5 causes of hypocalcaemia?
``` ↓ PTH -surgery -autoimmune -magnesium deficiency -congenital ↓ vit D levels -diet, malabsorption, low UVB, retail failure ```
182
how can renal failure lead to hypocalcaemia?
→ no 1-alpha-hydroxylase → impaired production of calcitriol
183
what are the signs and symptoms of hypercalcaemia?
stones, GI moans and psychic groans - nephrocalcinosis → kidney stones & renal colic - anorexia, nausea, dyspepsia, constipation, pancreatitis - fatigue, depression, impaired concentration, coma (≥3mmmol/L)
184
what are 4 causes of hypercalcaemia?
- primary hyperparathyroidism due to parathyroid gland adenoma → autonomous secretion → ↑PTH → ↑ calcium - bony metastases → activate osteoclasts - cancers like scc secrete PTH related peptides - vitamin d excess
185
why is phosphate low in primary hyperparathyroidism?
↑ PTH inhibits sodium phosphate transporter in kidney PCT → ↑ phosphate secretion
186
what is another complication of hyperparathyroidism aside from those seen with the hypercalcaemia?
osteoporosis
187
what is the first line treatment for primary hyperparathyroidsim?
parathyroidectomy
188
why does secondary hyperparathyroidism occur?
as a normal physiological response to hypocalcaemia | PTH is high secondary to low calcium
189
what is the commonest cause of secondary hyperparathyroidism?
vitamin d deficiency (diet, ↓ sunlight, renal fialure)
190
what are the treatment options for secondary hyperparathyroidism?
normal renal function: give 25 hydorxyvitamin D (ergo or cholecalciferol) ``` renal failure: give alfacalcidol (1a-hydroxycholecalciferol) ```
191
what drug would you give to a patient in renal failure who has high levels of PTH and low calcium?
alfacalcidol (secondary hyperparathyroidism)
192
when does tertiary hyperparathyroidism occur?
in chronic renal failure/vit D deficiency
193
what happens in tertiary hyperparathyroidism?
chronic renal failure → ↓ calcitriol → ↓ calcium → chronic ↑ PTH → parathyroid glands enlarge (hyperplasia) → become autonomous → ↑↑ calcium
194
treatment for tertiary hyperparathyroidism?
parathyroidectomy
195
how is vitamin d measured?
as 25(OH)vitamin D because calcitriol is very difficult to measure
196
How is infertility defined?
failure to achieve clinical pregnancy after more than 12 months of regular unprotected sexual intercourse
197
primary vs secondary infertility?
``` primary = not had a live birth previousoly secondary = had a live birth more than 12 months ago ```
198
what is cryptorchidism?
when testis do not descend through the inguinal canal
199
what is endometriosis?
presence of functioning endometrial tissue outside of the uterus that resounds to oestrogen
200
what are the symptoms of endometriosis?
irregular menstruation ↑ menstrual pain deep dyspareunia (painful intercourse) infertility
201
what are the 4 treatment options for endometriosis?
hormones eg. continuous OCP/progesteorone laparascopic ablation hysterectomy bilateral salpingo-oophorectomy
202
what are fibroids?
benign tumours of the myometrium that respond to oestrogen
203
symptoms of fibroids?
``` usually asymptomatic irregular menstruation ↑ menstrual pain deep dyspareunia (painful intercourse) infertility ```
204
fibroid treatments?
hormones eg.. ocp, prog, GnRH agonists | hysterectomy
205
what are 4 pretesticular causes of male infertility? | what will be low in all 4?
congenital hypogonadotrophic hypogonadism (Kallman syndrome) acquired hypogonadotrophic hypogonadism (stress, exercise, low bmi) hyperprolactinaemia hypopituitarism (tumour, apoplexy, radiation, surgery) ↓ LH, FSH, T
206
what are 2 causes of testicular infertility?
congenital primary hypogonadism - kleinfelters syndrome 47XXY acquired primary hypogonadism - trauma, radiation, cryptorchidism, chemo
207
how does kallmann syndrome arise?
congenital | failure of migration of GnRH neurones to migrate with olfactory fibres from olfactory placed to hypothalamus
208
what are the signs & symptoms of kallmann syndrome?
``` ↓Lh, FSH, T cryptorchidism failure of puberty - micropenis, lack of testiuclar development primary amenorrhea infertility ```
209
what does 47XXY indicate?
kleinfelters syndrome
210
how does kleinfelters syndrome present?
``` tall stature ↓ facial and chest hair gynacomastia small penis & testes narrow shoulders and wide hips mildly impaired iq infertility ```
211
how will HPA hormones present in Klinefelters?
↑ FH and LSH | ↓ T
212
what are the 4 main investigations carried out for male infertility?
semen analysis blood tests microbiology (urine test and chlamydia swab) Imaging (scrotal US and MRI pituitary)
213
what levels are looked at in blood tests for male infertility?
``` LH, FSH, PRL morning fasting testosterone SHBG albumin iron pituitary/thyroid profile karyotyping ```
214
what are the treatment options for male infertility?
lifestyle - reduce bmi, smoking cessation, alcohol redution dopamine agonist for hyperPRL gonadotrophin for fertility testosterone hrt if no fertility required surgery
215
what is primary ovarian insufficniency? how is it diagnosed?
early menopause high FSH≥25iU/L (2 measurements at least 4 weeks apart) (low E2)
216
what are 3 causes of premature ovarian insufficiency?
autoimmune Turners syndrome cancer treatment - radio/chemotherapy
217
what are causes of hypergonadotrophic hypogonadism in women?
↑ FSH & LH, ↓ E2 | POI, turners syndrome, surgery, chemo, radiation, trauma
218
what are the Rotterdam PCOS diagnostic criteria? how many re required for a diagnosis?
oligomenorrhoea or anovulation clinical and/or biochemical hyperandrogegism (acne, hiruitism, alopecia OR raised androgens) polycystic ovaries on US (≥20 follicles) need 2 out 3 for diagnosis
219
what is the worst metabolic risk combination of the Rotterdam criteria?
hyperandrogegism and oligomenorrhoea
220
what is the first line treatment for PCOS in someone who wants children? other treatments?
metformin | letrozole, clomiphene, IVF
221
what can be used to treat the amenhorrea in PCOS?
metformin | OCP
222
why is it imortamt to give lifestyle advice to PCOS patients?
they are at a higher risk of developing t2dm and gestational diabetes due to an increased insulin resistance
223
what are treatment options for hirsutism?
creams, waxing, laser, spironolactone (anti-andorgen)
224
which cancer is PCOS associated with a risk of developing? what can be given to reduce this risk?
endometrial cancer | give progesterone
225
what does 45X0 indicate?
turners syndrome
226
what are the symptoms of turners syndrome?
``` short stature low hairline shield chest, wide spaced nipples, poor breast development short 4th metacarpal and small fingernails brown nevi webbed neck, elbow deformity coarctation of the aorta underdeveloped repro tract amenorrhea ```
227
what type of hypogonadism is turners syndrome? what are HPA hormone levels?
hypergonadotrophic | ↑ FSh & LH, ↓ E2
228
what are the tubal causes of female infertility?
infection trauma endometriosis
229
what are the uterine causes of female infertility?
chronic endometriosis fibroids adhesions congenital malformation
230
what disease can cause chronic endometriosis?
TB
231
what are the cervical causes of female infertility?
chronic cervicitis antisperm antibodies (lead to ineffective sperm penetration)
232
what are the ovarian causes of female infertility?
anovulation due to endocrine problems | corpus lute insufficiency
233
when would you give testosterone replacement?
in a man who has hypogonadism but doesn't desire fertility | used to treat symptoms
234
what are the symptoms of male hypogonadism?
decreased shaving less energy loss of early morning erections decreased libido
235
how are testosterone levels measured?
2 serum T measurements before 11 am (should be highest in the morning)
236
what are the options for testosterone replacement?
daly gel (risk if contamination) 3 weekly/ 3 monthly IM injections implants/oral preparations
237
what needs to be regularly monitored and why in testosterone HRT?
Haematocrit → ↑ RBCs → hyperviscosity → stroke (T increases EPO production) PSA levels for prostate cancer
238
how do you treat secondary hypogonadism in terms of fertiltiy? in males
give gonadotrophins to induce spermatogenesis 1. give hCG injections (act on LH receptors) 2. if no response after 6 months then add FSH injections
239
what cells does LH stimulate in males? what increases?
leydig cells | intratesticular testosterone
240
what does FSH stimulate in men?
seminiferous tubule development and spermatogenesis
241
why is testosterone not given to men wanting fertility?
testosterone would lower LH and FSH levels and further reduce spermatogenesis
242
what are the 4 options for retiring ovulation in pcos patients?
1. lifestyle and metformin 2. letrozole 3. clomiphene 4. IVF
243
how does letrozole work?
aromatase inhibitor so inhibits conversion of androgens to oestradiol ↓ E2 → less negative feedback on HPA→ ↑ GnRH → ↑ FSH & LH → stimualtion of follicle growth
244
how does clomiphene work?
oestradiol receptor antagonist in hypothalamus → reduced negative feedback → ↑ FSH & LH → stimulation of follicle growth
245
what are the steps in IVF?
1. induce superovulation by giving FSH 2. prevent premature ovulation by giving GnRH antagonist (short protocol) or GnRH agonist (long protocol) to prevent LH surge 3. give hCG → LH exposure to allow oocytes to go from diploid to haploid 4. oocyte retrieval 5. fertilise via IVF or ICSI 6. embryo transfer to endometrium
246
what is ICSI and when is it done?
intra-cytoplasmic sperm injection done in male factor infertility
247
what are the positives and negatives of condoms?
+ves : protect against STIs, easy to obtain, no contraindications -ves : can internet sex, reduce sensation, interfere w erections
248
how does the oral contraceptive pill work? 3 ways
1. ↑ oestrogen and prog. → negative feedback → ↓ FSH & LH → anovulation 2. thickens cervical mucus 3. thins endometrial lining to reduce implantation
249
what are the positives and negatives of OCP?
+ves : easy to take , effective, doesn't interrupt sex, reduce endometrial and ovarian cancer -ves : can be difficult to remember , no protection against STIs, not great if breastfeeding , can be less effective with p450 enzyme inducers
250
what are some side effects of the OCP?
``` spotting nausea sore breasts changes in mood/libido more hungry blood clot (v rare) ```
251
what are non-contraceptive uses of the OCP?
helps make periods less painful and lighter (eg. in endometriosis) helps make periods more regular i.e. regular withdrawal bleeds helps reduce LH and hyperandrogenisms in PCOS
252
what are two differences with the POP compared to the OCP?
can be used when breastfeeding | shorter acting so needs to be taken at same time each day
253
what are the long-acting reversible contraceptives?
IUD - eg copper coil, mechanically prevent implantation, lasts 5-10yrs IUS - secrete progesterone eg. mirena coil, thins endometrium and thickens mucus progesterone injections or subdermal implants
254
what are the emergency contraception options?
IUD , fitted up to 5 days after unprotected sex (most effective) emergency contraceptive pill : ulipristal acetate , within 5 days levonorgestrel, within 3 days (least effective)
255
3 side effects of emergency contraceptives?
headache, nausea, abdominal pain
256
what can make emergency contraception less effective?
liver P450 enzyme inducer medications
257
when should the OCP be avoided and why?
patients with: migraine w aura , smoking + age ≥35 yrs, stroke or cvd hx, breast cancer , liver cirrhosis, diabetes w complications increased risks of venous thromboembolism, cvd and stroke
258
what 4 things should be considering when choosing contraception?
- risk of VTE, stroke and cvd - other conditions that may benefit eg. endometriosis from OCP - need for STI prevention? - concurrent medication eg. tartogenic drugs, p450 liver enzyme inducing drugs
259
why do oral oestrogens have a higher risk of VTE compared to transdermal oestrogens?
they undergo first pass metabolism in the liver which leads to an increase in SHBG, triglycerides and CRP because of this first pass metabolism oral also has to be given in larger doses to achieve the same effect
260
when should transdermal oestrogens be given as opposed to oral?
BMI ≥ 30
261
what cancers are associated with HRT?
breast, ovarian , endometrial
262
when should progestogens be given in HRT and why?
if the woman has an endometrium otherwise endometrial hyperplasia can occur and lead to cancer
263
when should HRT safety and efficacy be assessed?
at 3 months and then annually
264
what can indicate endometrial cancer?
postmenopausal bleeding
265
Is there cvd risk with hrt?
only if started more than 10 yrs after menopause | no increased risk if started before 60
266
which HRT forms have a higher risk of stroke?
oral as opposed to transdermal | combined as opposed to oestrogen only
267
what are 2 main benefits of hrt?
relief of menopausal symptoms eg. flushing, disturbed sleep, reduced libido less osteoporosis related fractures
268
what hormones can be given to transgender prepubertal young people?
GnRH agonists to suppress puberty and then sex steroids
269
what hormones can be given to transgender men?
testosterone | progesterone to suppress menstrual bleeding
270
what changes will occur in trasngender men after commencing hormone treatments?
``` balding deeper voice, acne, more hair changes in body fat distrubution clitoris enlargement menstruation stops increased muscle mass and strenght (1-6 months) ```
271
what hormones can be given to transgender women?
estrogen 4-5mg/day to increase oestradiol to about 734pmol/L | GnRH agonists and anti-androgen medication to reduce testosterone
272
give an example of an anti-androgen medication? (what else can it be used for?)
spironolactone (also used for conns)
273
what changes will occur in trasngender women after commencing hormone treatments?
``` decrease in sexual desire baldness slows or reverses softer skin changes in fat distribution decrease in testicle size ands breast development softer finer hair ```
274
in what ways can T2DM be similar to T1DM?
can present in childhood | DKA can occur
275
what is T1DM that presents in adults called?
LADA - latent autoimmune diabetes in adults
276
what are the 2 triggers for T1DM?
environmental and genetics (polygenic)
277
how is insulin measured in the blood?
via c-peptide | pro-insulin → insulin + c-peptide
278
online the immune response in T1DM
beta cells auto-antigen is presented to auto-reactive CD4+ cells → these activate CD8+ cells → these travel to islets and lyse B cells w auto-antigen → damage increases by release of pro-inflammatory cytokines defects in Treg cells also leads in failure to suppress autoimmunity
279
what are 4 auto-antibodies associated with T1DM?
insulin antibodies - IAA glutamic acid decarboxylase antibodies - GAD65 insulinoma-assoictaed-2-autoantibodies - IA-2A zinc transporter 8 - ZnT8
280
signs and symptoms of t1dm?
polyuria, nocturia, polydipsia, blurred vision, recurrent infections, weight loss, fatigue dehydration, cachexia, hyperventialtion, smell of ketones, glycosuria, ketonuria
281
what are 3 metabolic effects of reduced insulin?
↑ proteinolysis, HGO and lipolysis → ↑ amino acids, glucose and NEFA
282
why and how do ketone bodies form in t1dm?
no insulin to inhibit the conversions of fatty acyl coA → acetyl coA, → acetoacetate → acetone and 3-OH beta → ketone bodies
283
what are the 4 aims of t1dm treatment?
maintain glucose levels restore close to physiological insulin profile prevent acute metabolic decompensation prevent vascular complications
284
what are the complications of t1DM?
acute - dka chronic - retino, neuro and nephropathy | ischaemic hd , cerbrovascular disease , peripheral vascular disease treatment - hypoglycaemia
285
4 management options for t1dm?
insulin structured education programme and diet support technology transplant
286
what are the types of insulin?
short-acting taken with meals - human insulin - insulin analogue long-acting basal insulin - bound to zinc/protamine - insulin analogue
287
what is the typical basal bolus regime?
short-acting insulin 3xday | once/twice daily long-acting
288
how does insulin pump therapy work?
continuous delivery of short-acting insulin analogue in subcutaneous space programme device to deliver fixed amount per hour for basal actively bolus for meals
289
how does an artificial pancreas work?
real-time continuous glucose sensor to monitor glucose levels insulin pump delivers insulin based on glucose levels
290
what are the transplant options for t1dm?
islet cell transplants - taken from deceased donor and transplanted into hepatic portal vein simultaneous pancreas and kidney transplant - better survival with both both require life long immunosuppression
291
what guides insulin doses?
self-monitoring of glucose levels (capillary or continuous) and HbA1c levels every 3 months
292
when can DKA occur?
new onset t1dm acute illness missed/inadequate insulin doses
293
how is dka diagnosed?
ph<7.3 increased plasma/urine ketones HCO3- <15mmol/L glucose ≥11mmol/L
294
how is hypoglycaemia defined in terms of glucose levels?
~<3.6mmol/L
295
how is severe hypoglycaemia defined?
when 3rd party assistance is required
296
what are the symptoms of hypoglycaemia?
tremors, palpitations, sweating , hunger | drowsiness, confusion, uncoordinated, seizures
297
how is hypoglycaemia treated?
glucose administartion - alert - oral - drowsy - buccal - unconscious - IV
298
when is hypoglycaemia problematic?
excessive/recurrent severe → tolerance so you become less able to detect low blood glucose nocturnal hypoglycaemia
299
risks of hypoglycaemia?
seizures, coma, death | impacts well-being, driving, cognition, day to day function
300
what are the risk factors for hypoglycaemia in t1dm?
``` exercise missing meals inappropriate insulin regime alcohol intake lower HbA1c lack of training ```
301
when is pre-diabetes diagnosed?
HbA1C is between 42 and 48
302
how is impaired glucose tolerance diagnosed?
2 hour OGTT between 7.8 and 11.1 mmol/L
303
how is impaired fasting glycaemia diagnosed?
fasting glucose levels between 6 and 7mmol/L
304
what is meant by a relative insulin deficiency in t2dm?
insulin is still produced by beta cells but not enough to overcome the insulin resistance at tissues
305
why does dka not normally occur in t2dm?
theres enough insulin being produced to inhibit ketogenesis
306
how can you measure and compare insulin levels?
using a hyperglycaemic clamp - give patients variable amount of glucose to get and maintain the same glucose level and then compare insulin response
307
via what mechanisms does hyperglycaemia occur in t2dm?
↓ insulin → ↓ glucose uptake into skeletal muscle | ↓ insulin and ↑ glucagon → ↑ HGO
308
what are the genetics of t2dm?
``` monogenic = single gene mutation → if born with it then definitely will develop diabetes - MODY polygenic = polymorphisms which increase the risk of developing diabetes → environmental triggers ```
309
how is obesity related to t2dm?
risk factor | ↑ fatty acids and adipocytokines can lead to insulin resistance, lipolysis, reduced B cell function
310
what are 2 other associations with t2dm?
perturbations in gut microbiota | intra-uterine growth retardation
311
how can t2dm present?
``` hyperglycaemia overweight dyslipidaemia diabetic complications insulin resistance and later deficiency ```
312
risk factors for t2dm?
``` age ↑BMI ethnicity PCIS family hx inactivity ```
313
how is t2dm diagnosed?
1 x hba1c ≥48 with osmotic symptoms OR 2 x hba1c ≥48 wihtout symptoms can be san incidental finding if patent presents with a complication eg retinopathy
314
what is a hyperosmolar hyperglycaemic state? treatment?
presents often w renal failure or infection insufficient insulin to prevent hyperglycaemia but enough to prevent dka severe dehydration, high plasma osmolarity and altered consciousness give iv fluids immediately and then insulin if neccessary
315
how is t2dm managed?
diet and structured education oral medication eg. metformin insulin later
316
what is checked in a t2dm consultation?
``` HbA1C levels medication review weight blood pressure dyslipidaemia - cholesterol profile complication screening - feet, retinas ```
317
how should diet change in t2dm?
↓ fat and refined carb calories ↑ complex carb calories ↓ sodium ↑ soluble fibre
318
how does metformin work?
insulin sensitiser reduces insulin resistance and HGO increases peripheral glucose disposal
319
what class of drug is metformin?
biguanide
320
what drugs can improve insulin sensitivity?
metformin | pioglitazone
321
what drug class is pioglitazone?
thiozolidinedione
322
what is GLP-1?
glucagon like peptide 1 gut hormone secreted in response to nutrients in gut stimulates insulin and suppresses glucagon increases satiety
323
why does glp-1 have such a short half life?
rapidly degraded by DPP4 enzyme (dipeptidyl peptidase-4)
324
what drugs can boost insulin secretion?
dpp4-inhibtors glp-1 agonists sulphonylureas
325
what drugs can reduce excess glucose in circulation?
alpha glucosidase inhibitor SGLT-2 inhibitor (reduce gut and renal absorption of carbs and glucose)
326
what is the incretin effect?
when glucose is given orally as opposed to intravenously plasma insulin levels rise much more
327
what drug class are dpp4-inhibitors?
gliptins
328
what effects do GLP-1 agonists have?
decrease glucose and glucagon concentrations → weight loss
329
give 2 examples of glp-1 agonists?
liraglutide | semaglutide
330
how do dpp4 inhibitors work?
increase half life of exogenous glp-1 and glp-1 concentartion decrease glucose and glucagon concentration
331
how do sglt-2 inhibitors work?
inhibit the sodium glucose transported in the kidney → glycosuria → ↓ glucose levels can improve CKD, lower risk of heart failure
332
examples of sglt-2 inhibitors?
empa- , dapa- and canagliflozin
333
what can potentially induce remission in t2dm patients?
gastric bypass surgery | very low calorie diet
334
what other 2 aspects need to be managed in t2dm?
blood pressure - ACE inhibitors | lipids - statins
335
what is an acute complication of t2dm?
hyperglycaemic hyperosmolar state
336
microvascular complications of diabetes?
retino- neuro- and nephropathy
337
macrovascular complications of diabetes?
ischaemic heart disease cerebrovascular disease peripheral vascualr disease
338
what is the target HbA1c to reduce microvascular complictaions?
<53mmol/L
339
what two factors are the main risk factor for diabetic vascular complications?
high hba1c | high blood pressure
340
what are other risk factors for developing vascular complications?
``` smoking duration of diabetes hyperglycaemic memory genetic factors hyperlipidaemia ```
341
why is diabetic retinopathy screening important?
early stages are often asymptomatic aims to detect it early when its still treatable to prevent vision loss annual screening
342
what are the stages of retinopathy?
background - hard exudates, microaneurysms, blot haemorrhages pre-proliferative - soft exudates (ischaemia), haemorrhage proliferative - visible new vessels on disc or retina maculopathy - hard exudates and oedema near macula (same as background but near macula)
343
treatment for background retinopathy?
annual surveillance
344
treatment for pre-proliferative retinopathy?
early pan retinal photocoagulation
345
treatment for proliferative retinopathy?
pan retinal photocoagulation
346
treatment for maculopathy?
anti-vegf injections for oedema (reduce inflammation) | grid photocoagulation
347
how does pan retinal photocoagulation work?
it stops the formation of new blood vessels
348
what are the impacts of diabetic nephropathy?
can progress to end stage renal failure requiring haemodialysis healthcare burden increases risk of cvd events
349
what are diagnostic signs of nephropathy?
progressive proteinuria - increased ACR (≥30) increased blood pressure deranged eGFR peripheral oedema
350
what is the earliest feature of nephropathy?
microalbuminuria ≥2.5mg/mmol
351
what is the mechanism of diabetic nephropathy?
diabetes → hypertension and hyperglycaemia → glomerular hypertension → proteinuria → glomerlualr and interstitial fibrosis → ↓ eGFR → renal failure
352
2 drugs to control blood pressure?
ace inhibitors - inhibit the production of angiotensin II (-pril) angiotensin receptor blockers - reduce action of angiotensin (-sartan)
353
when should diabetes patients be given an antihypertensive?
if they have microalbuminuria/proteinuria even if normotensive
354
management of nephropathy?
``` tighter glycemic control ACEi/ARB if microalbuminuria reduce BP stop smoking SLGT-2 inhibitor if t2dm ```
355
what are the small blood vessels supplying nerves called?
vasa nervorum
356
how does neuropathy arise?
when vasa nervorum get blocked → loss of sensation → potential amputation eg. not sensing an injury
357
what are the risk factors for diabetic neuropathy?
``` age duration of diabetes retinopathy poor glcyaemi control height (tall = longer nerves) smoking ```
358
why is neuropathy more common in the feet?
longest nerves supply feet
359
what should be assessed in annual foot check?
ulceration , foot deformity sensation foot pulses
360
what increases the risk of foot ulceration?
peripheral neuropathy - loss of sensation | peripheral vascular disease - poor blood supply
361
what is mononeuropathy?
damage to single nerve → sudden motor loss | eg. 3rd nerve palsy → down and out
362
what happens in autonomic neuropathy?
damage to SNS/PSNS nerves innervating GI tract, bladder, cardiovascular system
363
risk factors for macrovascular diseases?
age sex birth weight fhx/genes ``` dyslipidaemia hypertension smoking DM central obesity ```

BRS 2 (12 decks)

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