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BRS 2 > Endo > Flashcards

Endo Flashcards

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
Q

When and how is GH deficiency treated?

A

If QoL is low

Daily GH injections

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26
Q

How is GH injection response measured?

A

QoL improvement?

plasma IGF-1 levels?

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27
Q

How is TSH deficiency treated? And how is dose adjusted?

A

Levothyroxine daily tablet
Dose adjusted to fT4 levels
Should be above mid reference range

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28
Q

What are 2 treatment options for ACTH deficiency?

A

Prednisolone - 3mg once daily

Hydrocortisone - 3x/day - 10/5/2mg

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29
Q

How can adrenal crisis present? What can trigger it?

A

dizziness, hypotension, vomitting, weakness, collapse

Intercurrent illness

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30
Q

What are the sick day rules for ACTH deficient patients?

A

Double steroid dose when feverish/intercurrent illness
Wear steroid alert bracelet
Vomitting → inject steroids IM or go to a&e

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31
Q

What are the treatment options for fsh/lh deficiency in men?

A

topical/IM testosterone

gonadotropin injections if fertility is needed → spermatogenesis (takes 6-12 months)

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32
Q

What are the treatment options for fsh/lh deficiency in women?

A

Oestrogen - oral/topical
progesterone (sometimes)
gonadotropin injections if fertility is needed (IVF) → ovulation

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33
Q

When is progesterone needed to treat fsh/lh deficiency and why?

A

If uterus is intact

Prevents endometrial hyperplasia

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34
Q

Which neurone contain AVP and oxytocin?

A

Magnocellular neuons

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35
Q

Where do magnocellular neurones originate?

A

Paraventricular and supraoptic hypothalamic nuclei

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36
Q

What are the actions of vasopressin?

A

Stimulate water reabsorption in the renal CD (concentrates urine)
Vasocontrictor
Stimulates ACTH release

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37
Q

which receptors does vasopressin act on>

A

V2 in CD

V1 in vasoconstriction

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38
Q

how does vasopressin lead to increase reabsorption in the CD?

A

acts on v2 receptors → cAMP → protein kinase A → vesicles containing aquaporins move to apical membrane
more aquaporins = more water reabsorption

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39
Q

Describe the two stimuli for vasopressin release

A

osmotic - osmorecptors detect high plama osmolality

non-osmotic - atrial stretch receptors detect low atrial pressure

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40
Q

where are the osmoreceptors found?

A

Subfornical organ

Organum vasculosum

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41
Q

How are the SO and OV suited to their function?

A

Around 3rd ventricle → no BBB → can respond to changes in systemic circulation
Highly vascularised
Project to supraoptic nuclei with vasopressinergic neurons

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42
Q

how do osmoreceptors regulate vasopressin release`se?

A

high plasma osmolality → water leaves osmoreceptor → shrinks→ increased firing rate to hypothalamic neurone→ ↑ avp released

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43
Q

what is the function of atrial stretch receptors?

A

detect pressure in RA

normal pressure → stretch → inhibition of avp release via vagal afferents to hypothalamus

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44
Q

mechanism of vasopressin after a haemorrhage?

A

haemorrhage → less stretch → less inhibition of avp release → ↑ circulating volume → ↑ BP
vasoconstriction via V1r

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45
Q

mechanism of vasopressin in water deprivation?

A

↑ plamsa osmolality → osmoreceptors stimulated → ↑ avp release → ↑ water reabsorption in CD → ↓ urine and ↑ urine osmolality → ↓ plasma osmolality

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46
Q

3 symptoms associated with diabetes insipidus?

A

polyuria
nocturia
polydipsia

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47
Q

most common cause of polyuria
nocturia
polydipsia?

A

diabetes mellitus

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48
Q

explain the two types of diabetes insipidus

A

Cranial - hypothalamus/post pit cannot make avp - insufficiency
Nephrogenic - kidney CD unable to respond to avp - resistance

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49
Q

causes of cranial diabetes insipidus? (7)

A 
TBI
pit surgery
pit tumours
metastasis to pit 
granulomous infiltration
autoimmune
congenital
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50
Q

causes of nephrogenic diabetes insipidus?

A

congenital - mutation in gene coding for v2 receptor/aquaporin
drugs - lithium

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51
Q

what drug can cause nephrogenic DI?

A

lithium

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52
Q

how do patients with DI present?

A

very dilute, large volumes of urine
high plasma osmolality
hypernatraemia
normal glucose

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53
Q

why do DI patients have polydipsia?

A

avp problem → no water reabsorption in CD → ↑ dilute urine → ↑ plasma osmolality + Na → osmoreceptors stimulated → thirst → water intake → maintains circulating volume

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54
Q

when can DI lead to death?

A

if patient has no access to water

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55
Q

what are two differentials for DI?

A

DM

Psychogenic polydipsia

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56
Q

what happens in psychogenic polydipsia?

A

↑ water intake → ↓ plasma osmolality → less avp by post pit → ↓ water reabsorption in CD → ↑ volume of hypotonic urine → plasma osmolality normalises

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57
Q

what test is used to distinguish between DI and PP? what 4 things are measured?

A

water deprivation test
no access to fluids
measure urine volume, urine osmolality, plasma osmolatiy, weight

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58
Q

why should you weigh patients regularly in the water deprivation test?

A

> 3% body weight indicates significant dehydration which can happen in DI

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59
Q

how does DI differ to PP in the water deprivation test?

A

urine osmolality increase in PP but remains the same in DI

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60
Q

how do you distinguish cranial DI and neprhogenic DI?

A

give ddAVP
CDI - urine will concentrate
NDI - urine remains concentrated as kidneys do not respond

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61
Q

what is approx normal plasma osmolality range? what do above and below mean?

A

270-290 mOsm/kg H20

above = DI
below = PP
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62
Q

How do you treat cranial DI?

A

give desmopressin as tablets or intranasal

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63
Q

What receptor is desmopressin selective for and why?

A

the v2 receptor

v1 receptor activation would lead to unhelpful vasoconstriction

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64
Q

Treatment for nephrogenic DI?

A

Thiazide diuretics - eg bendrofluazide

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65
Q

What is SIADH?

A

Syndrome of inappropriate adh

Too much vasopressin released

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66
Q

Presentations of SIADH? and mechnaism?

A

↑ ADH → ↓ urine output and ↑ water retention → ↑ urine osmolality and ↓ plasma osmolality
Dilutional hyponatraemia

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67
Q

Causes of SIADH? (6)

A 
CNS - head injury, stroke, tumour
Pulmonary - pneumonia, bronchiestatis 
Malignancy - lung cancer
Drugs - carbamazepine, serotonin reuptake inhibitors
Idiopathic
Hypothyroidism/pituitarism
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68
Q

How can lung cancer lead to SIADH?

A

Ectopic production of ADH

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69
Q

SIADH management?

A

Fluid restrictions

Vaptan (vasopressin antagonist on v2 receptor)

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70
Q

What is the purpose of fluid restriction in SIADH?

A

to raise plasma sodium levels whilst looking for underlying cause

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71
Q

most common functioning pituitary tumour?

A

prolactinoma

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72
Q

three ways to classify pituitary tumours

A

MRI - size (micro or macro, sellar or suprasellar)
functioning (excess hormone secretion) or non-functioning
benign or malignant (v rare)

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73
Q

how does hyperprolactinaemia lead to hypoginadism?

A

excess prolactin → binds to kisspeptin neurons in hypothalamus → inhibits kisspeptin release → decreased downstream release of GnRH, LH, FSH, testosterone, oestrogen → hypogonadism

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74
Q

what serum prolactin is normally indicative of a prolactinoma?

A

> 5000 mU/L

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75
Q

how does a prolactinoma present?

A 
menstrual disturbance
erectile dysfunciton
reduced libido
glactorhhea 
subfertility
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76
Q

what else can cause an elevated prolactin aside from prolactinoma?

(physiological, pathological, iatrogenic)

A

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
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77
Q

what can cause a false serum prolactin elevation?

when would you suspect this?

A

macroprolactin
venepuncture
consider when patient has mild elevation and no clinical symptoms

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78
Q

what is macroprolactin?

A

polymeric form of prolactin → antigen-antibody complex of monomeric prolactin with IgG
on assay it’s recored as elevated prolactin levels

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79
Q

how can you measure prolactin if you suspect stress of venipuncture is causing elevated levels?

A

a cannulated prolactin series

measure serum prolactin 20 mins apart with an indwelling catheter to reduce stress

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80
Q

if serum prolactin is truly high what would you do next?

A

arrange pituitary MRI

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81
Q

what is the first line treatment for a prolcatinoma? how does it work?

A

cabergoline

dopamine agonist → binds to D2 receptors on tumour → inhibit prolactin release → prolcatinima shrinks

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82
Q

acromegaly has an insidious presentation, what does this mean?

A

a long time from onset of symptoms to diagnosis, ~10yrs

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83
Q

symptoms of acromegaly?

A

sweating
headaches
macroglossia, prominent nose, prognathism
big hands and feet
snoring, OSA
hypertension
imparted glucose tolerance/dibetes mellitus

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84
Q

which two places does somatotrophin act? what are its effects?

A

body tissue → metabolic actions → growth & development

liver → IGF-1 → body tissue

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85
Q

how is GH secreted?

A

pulsatile

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86
Q

what two ways can you diagnose acromegaly?

A

elevated serum IGF-1
OR
oral glucose tolerance test with a paradoxical rise in growth hormone

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87
Q

what other hormone can be raised in acromgealy?

A

prolactin (cosecreted with GH)

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88
Q

what is a complication untreated acromegaly?

A

increased CVD risk

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89
Q

what is the first line treatment in acromegaly?

A

trans-sphenoidal pituitary surgery

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90
Q

what can be done before surgery to shrink acromegaly tumours? (or if resection is incomplete)

A

somatostatin analogues eg. octretotide
dopamine agonists eg. cabergoline
radiotherapy (slow)

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91
Q

symptoms of Cushing’s syndrome?

A 
proximal myopathy
buffalo hump (inter scapular fat)
red/purple striae
moon face
red cheeks
thin skin
pendulous abdomen - centripetal obesity
depression
easy bruising
hypertension
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92
Q

4 causes of cushing syndrome?

A

ACTH independent
excess corticosteroids
adrenal adenoma/carcinoma

ACTH dependent
pituitary corticotroph adenoma
lung cancer - ectopic ACTH

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93
Q

what causes cushings disease?

A

pituitary adenoma securing excess ACTH

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94
Q

what 3 investigations would indicate cushings syndrome?

A

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)

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95
Q

what is dexamethasone? how does it work?

A

exogenous glucocorticoid → body should recognise cortisol levels are increased → ACTH levels decrease → cortisol levels should fall to zero

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96
Q

how can non-functioning pituitary tumours present?

A

bitemporal hemianopia → compression of optic chiasm
hypopituitarism and hyperprolactinoma → releasing hormones and dopamine cannot travel from hypothalmus down pituitary stalk to ant pit

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97
Q

how can you treat non-functioning pituitary tumours?

A

trans-sphenoidal pituitary surgery

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98
Q

explain graves disease?

A

graves disease - autoimmune

antibodies bind to and stimulated the TSH receptors in the thyroid

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99
Q

symptoms of graves disease?

A 
smooth goitre
sweating
weight loss with increased appetite
tachycardia, breathlessness
oligo/amenhorrea
exopthalmus
pretibial myxoedema
tremor
myopathy
insomnia, restlessness, excitability
heat intolerance
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100
Q

how does exophthalmus arise in graves disease?

A

antibodies bind to muscles behind the eyes

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101
Q

how does pretibial myxoedema arise in graves? what will you observe?

A

antibodies stimulate the uncontrolled growth of soft tissue (hypertrophy)
non-pitting swelling on the patient’s shins

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102
Q

what scan can be used to visualise a goitre? what will be seen in graves disease?

A

radioiodine uptake scan

diffuse enlargement and engorgement of thyroid,uniform radio iodine uptake

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103
Q

two main causes of hyperthyroidism?

A

graves disease

toxic multinodular goitre

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104
Q

how does a toxic nodular goitre form?

A

iodine definciency → ↑ no of follicular cells in attempt to make more thyroid hormones
mutation → permanently stimulated TSH receptor → follicular cells contstanly dividing (adenomatous) → nodules

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105
Q

what two symptom will you not see in toxic nodular patients when compared to graves disease patients?

A

no pretibial myoxoedam nor exophthalmus (no antibodies)

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106
Q

what will you see in a radioiodine uptake scan if there us a toxic nodular goitre?

A

only ‘hot nodules’ show up as rest of thyroid atrophies

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107
Q

what is the effect off thyroxine on the SNS? what symptoms does this lead to if its in excess?

A

sensitises beta adrenoreceptors to ambient levels of adrenaline and NA
→ excess → apparent sympathetic activation → tachycardia, palpitations, tremor, lid lag

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108
Q

what is a medical emergency in hyperthyroidism patents? what are the features?

A 
thyroid storm
heat intolerance → hyperpyrexia
tachycardia → arrhythmia
cardiac failure
delirium/frank psychosis
jaundice
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109
Q

what are the three main treatment options for hyperthryodism?

A

thyroidectomy surgery
radioiodine
drugs

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110
Q

why would you give beta blockers to hyperthyroidism patients? give an example of one

A

to help symptoms whilst waiting for thyroid hormones to decrease, eg reduce tachycardia, tremors
propanalol - non-selective

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111
Q

what re the two thionamides that can be used in hyperthyroidism?

A

propylthiouracil PTU

carbimazole CBZ

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112
Q

how does potassium iodide work in hyperthryoidism? what is the effect called?

A

↑ iodine → ↓ thyroid hormone synthesis
hyperthyroid symptom reduce in 1-2 days
gland sizes reduces in 10-14 days
Wolff-Chaikoff effect

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113
Q

what is the mechanism of thionamides?

A

inhibit thyroid peroxidase → less t3/4 synthesis and secretion

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114
Q

why does it take time to see clinical effects of thionamides?

A

takes a few weeks for the body to use up the excess t3/4

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115
Q

two unwanted actions of thionamides?

A

agranulocytosis (↓ neutrophils) (rare and reversible)

rashes

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116
Q

when would you give potassium ioidine in hyperthyroidism?

A

in preparation for surgery

thyroid storm

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117
Q

4 risks of a thyroidectomy?

A

voice change
losing parathyroid glands
scar
anaesthetic

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118
Q

what are the symptoms of viral thyroiditis?

A

painful dysphagia
fever
hyperthyroidism symptoms
thyroid inflammation, tender and palpable

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119
Q

explain viral thyroiditis

A

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

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120
Q

what can have similar features to viral thyroiditis without the pain?

A

postpartum thyroditis

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121
Q

what steroids do the three layers of the adrenal cortex secrete?

A

zona glomerulosa - aldosterone
zona fasiculata - cortisol
zona reticularis -androgens

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122
Q

what enzymes does angiotensin II activate in the adrenals?

A

side chain cleavge
3 hydrozysteroid dehydrogenase
21, 11, 18 hydroxylase

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123
Q

what is the action of aldosterone?

A

increases blood pressure by increasing sodium levels and decreasing potassium levels

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124
Q

what enzymes does ACTH activate in the adrenals?

A

side chain cleavage
3 hydrozysteroid dehydrogenase
17, 21, 11 hydroxylase

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125
Q

what enzyme do the cortisol and androgen production pathways share?

A

17 hydroxylase

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126
Q

what are two commonest causes of Addison’s disease?

A

autoimmune - uk

TB - worldwide

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127
Q

signs and symptoms of Addisons disease?

A 
vitiligo
weight loss
low BP
nausea, vomitting, diarrhoea, constipation
muscular weakness
hyperkalaemia
loss of salt in urine
low glucose due to glucocorticoid deficiency
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128
Q

explain the increased pigmentation seen in patients with Addisons

A

high levels of ACTH
precursor of which is pro-opio melanocortin which is also the precursor to MSH
therefore ↑ ACTH → ↑ MSH

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129
Q

name another cause of adrenocortical failure

A

congenital adrenal hyperplasia

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130
Q

what three tests can you do if you suspect Addison’s disease?

A

9am cortisol → low
ACTH → high
synACTHen test → 250 ug IM → measure cortisol → still low = Addisons

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131
Q

why is fludrocortisone used instead of aldosterone in treating Addisons?

A

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

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132
Q

in what pattern is cortisol secreted?

A

diurnally , high in the morning, low at night

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133
Q

why is prednisolone given instead of hydrocortisone in treating Addisons?

A

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

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134
Q

what are the two main drugs used in treating Addisons disease?

A

fludrocortisone 50-100 mcg/day (adjust for potassium levels and hypertension)
prednisolone 3mg/day

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135
Q

what is the commonest cause of congenital adrenal hyperplasia?

A

21 hydroxylase deficiency (complete or partial)

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136
Q

what effects does the absence of 21 hydroxylase have on the adrenal steroids pathways?

A

no aldosterone and cortisol

↑ androgens and oestrogen

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137
Q

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?

A

24 hours
give IV saline for salt losing addisonian crisis
in utero foetus gets steroids from mother across placenta

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138
Q

how might babies with complete 21 hydroxylase deficiency present?

A

with ambiguous genitalia (could be variety of causes but treat immediately as CAH just in case)

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139
Q

what is the age of presentation in partial 21 hydroxylase deficiency? how will they present?

A

any age as they survive
hirsutism and virilisation in girls
precocious puberty in boys

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140
Q

what is the second most common cause of CAH?

A

11 hydroxylase deficiency

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141
Q

what effects does the deficiency of 11 hydroxylase have on the adrenal steroids pathways?

A

deficient cortisol and aldosterone
ALSO increase 11-deoxycorticosterone
excess sex steroids

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142
Q

how can 11 hyrdroxylase deficiency present? (relate to excess steroids)

A

virilisation from excess sex steroids

hypokalaemia and hypertension as 11-deoxycorticosterone behaves like aldosterone

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143
Q

what effects does the deficiency of 17 hydroxylase have on the adrenal steroids pathways?

A

deficient cortisol and sex steroids

excess aldosterone

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144
Q

what are the problems seen in 17 hydroxylase deficiency?

A

hypertension
hypokalaemia
low glucose from glucocorticoid deficiency
sex steroid deficiency

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145
Q

what happens in the low does dexamethasone test?

A

give 0.5mg 6 hourly for 48 hours → cortisol should be supressed to zero

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146
Q

what 2 drugs can be used to treat cushings? what is their action?

A

metyrapone
ketoconazole (no longer used)
inhibit steroid biosynthesis

147
Q

what is the mechanism of action for metyrapone?

A

inhibits 11b-hydroxylase → no cortisol → ↑ deoxycortiol (no negative feedback on HPA) → ACTH ↑

148
Q

how should metyrapone be adjusted?

A

according to cortisol levels , aim for 150-300 nmol/L

149
Q

why is metyrapone given in cuhsings patients prior to surgical intervention/after radiotherapy?

A

improves patients symptoms and leads to better post op outcomes

150
Q

what are 2 unwanted actions of metyrapone? explain

A

hypertension and hypokalaemia - inhibition of 11b-hydroxylase leads to excess 11-deoxycorticosterone → aldosterone-like effects
hirsutism in women → ↑ androgens

151
Q

what enzyme does ketoconazole inhibit?

A

17a-hydroxylase → ↓ cortisol

152
Q

why is ketoconazole no longer used?

A

hepatotoxicity , possibly fatal

153
Q

treatment options for cushings syndrome?

A 
transphenoidal pituitary surgery for pituitary adenoma
bilateral adrenalectomy
unilateral adrenalectomy for mass
metyrapone
(ketoconazole)
154
Q

what is Conns syndrome? what causes it?

A

excess aldosterone

benign adrenal adenoma in zona glomerulosa (primary hyperaldosteronism)

155
Q

what are two signs of conns syndrome?

A

hypertension and hypokalaemia

156
Q

How can you confirm primary hyperaldosteronism? (as opposed to secondary)

A

suppression of renin-angiotensin system

157
Q

what 2 drugs can be used to treat conns syndrome? what is their action?

A

spironolactone
epleronone
mineralcorticoid receptor antagonists

158
Q

what is the mechanism of action of spironolactone?

A

converted to canrenone → competitive antagonist of mineralocorticoid receptor → inhibits na resorption and k excretion in kidney tubules

159
Q

how is spironolactone administered and where is it metabolised?

A

orally

in liver

160
Q

2 unwanted actions of spironolactone?

A

menstrual irregularities

gynaecomastia

161
Q

mechanism of action of epleronone?

A

mineralocorticoid antagonist similar to spironolactone

162
Q

why is epleronone better tolerated compared to spironolactone?

A

less binding to androgen and progesterone receptors → less menstrual irregularities and gynacomastia

163
Q

what is a phaeochromocytoma?

A

adrenal medulla tumours that secrete catecholamines (adrenaline and NA)

164
Q

what are the clinical features of phaeochromocytoma?

A

episodic severe hypertension (especially in young people)
palpatations
sweating
headache

165
Q

why is hypertension intermittent in phaeochromocytoma?

A

cells degranulate all at once and release a load of adrenaline → hypertension

166
Q

what are some complications of phaeochromocytoma?

A

MI
stroke
ventricular fibrillation

167
Q

why does a patient with a phaeochromocytoma need careful management prior to surgery?

A

anaesthetic can precipitate a hypertensive crisis

168
Q

what are the steps in managing a phaeochromocytoma?

A

alpha blockade
IV fluids
beta blockade to prevent tachycardia

169
Q

what hormones increase serum calcium?

A

vitamin D

parathyroid hormone

170
Q

what hormone decreases calcium?

A

calcitonin from parathyroid follicular cells

171
Q

what are the 2 forms of vitamin d and their sources?

A

D2 from the diet

D3 - UVB → 7-dehydrocholestrol → pre vitamin D3 → vitamin D3

172
Q

how does vitamin D3 get converted to calcitriol?

A

vitamin D3 → liver → 25-hydroxylase converts it to 25(OH)cholecalciferol → kidney → 1-alpha hydroxylase converts it to 1,25(OH)2cholcalciferol (calcitriol)

173
Q

what is the active form of vitamin D?

A

calcitriol

174
Q

how does calcitriol regulate its own synthesis?

A

negative feedback on 1-alpha-hydroxylase

175
Q

what are the effects of calcitriol on the body?

A

↑ osteoblast activity → ↑ca2+
↑ ca2+ and PO43- absorption in gut
↑ ca2+ and PO43- reabsorption in kidney

176
Q

what are the effects of PTH on the body?

A

↑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
Q

how is serum phosphate regulated bye FGF-23?

A

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
Q

what two hormones inhibit the sodium phosphate cotransporter in the PCT?

A

FGF-23

PTH

179
Q

What are the signs and symptoms of hypocalcaemia?

A 
paraesthesisa
convulsions
arrhythmias
tetany (involuntary muscle contraction)
muscle cramps
chvosteks and trousseau's signs
180
Q

what are chvostek’s and trousseau’s signs? when are they seen?

A

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
Q

what are 5 causes of hypocalcaemia?

A 
↓ PTH 
-surgery
-autoimmune
-magnesium deficiency
-congenital
↓ vit D levels
-diet, malabsorption, low UVB, retail failure
182
Q

how can renal failure lead to hypocalcaemia?

A

→ no 1-alpha-hydroxylase → impaired production of calcitriol

183
Q

what are the signs and symptoms of hypercalcaemia?

A

stones, GI moans and psychic groans

  • nephrocalcinosis → kidney stones & renal colic
  • anorexia, nausea, dyspepsia, constipation, pancreatitis
  • fatigue, depression, impaired concentration, coma (≥3mmmol/L)
184
Q

what are 4 causes of hypercalcaemia?

A
  • 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
Q

why is phosphate low in primary hyperparathyroidism?

A

↑ PTH inhibits sodium phosphate transporter in kidney PCT → ↑ phosphate secretion

186
Q

what is another complication of hyperparathyroidism aside from those seen with the hypercalcaemia?

A

osteoporosis

187
Q

what is the first line treatment for primary hyperparathyroidsim?

A

parathyroidectomy

188
Q

why does secondary hyperparathyroidism occur?

A

as a normal physiological response to hypocalcaemia

PTH is high secondary to low calcium

189
Q

what is the commonest cause of secondary hyperparathyroidism?

A

vitamin d deficiency (diet, ↓ sunlight, renal fialure)

190
Q

what are the treatment options for secondary hyperparathyroidism?

A

normal renal function:
give 25 hydorxyvitamin D (ergo or cholecalciferol)

renal failure:
give alfacalcidol (1a-hydroxycholecalciferol)
191
Q

what drug would you give to a patient in renal failure who has high levels of PTH and low calcium?

A

alfacalcidol (secondary hyperparathyroidism)

192
Q

when does tertiary hyperparathyroidism occur?

A

in chronic renal failure/vit D deficiency

193
Q

what happens in tertiary hyperparathyroidism?

A

chronic renal failure → ↓ calcitriol → ↓ calcium → chronic ↑ PTH → parathyroid glands enlarge (hyperplasia) → become autonomous → ↑↑ calcium

194
Q

treatment for tertiary hyperparathyroidism?

A

parathyroidectomy

195
Q

how is vitamin d measured?

A

as 25(OH)vitamin D because calcitriol is very difficult to measure

196
Q

How is infertility defined?

A

failure to achieve clinical pregnancy after more than 12 months of regular unprotected sexual intercourse

197
Q

primary vs secondary infertility?

A 
primary = not had a live birth previousoly
secondary = had a live birth more than 12 months ago
198
Q

what is cryptorchidism?

A

when testis do not descend through the inguinal canal

199
Q

what is endometriosis?

A

presence of functioning endometrial tissue outside of the uterus that resounds to oestrogen

200
Q

what are the symptoms of endometriosis?

A

irregular menstruation
↑ menstrual pain
deep dyspareunia (painful intercourse)
infertility

201
Q

what are the 4 treatment options for endometriosis?

A

hormones eg. continuous OCP/progesteorone
laparascopic ablation
hysterectomy
bilateral salpingo-oophorectomy

202
Q

what are fibroids?

A

benign tumours of the myometrium that respond to oestrogen

203
Q

symptoms of fibroids?

A 
usually asymptomatic 
irregular menstruation
↑ menstrual pain
deep dyspareunia (painful intercourse)
infertility
204
Q

fibroid treatments?

A

hormones eg.. ocp, prog, GnRH agonists

hysterectomy

205
Q

what are 4 pretesticular causes of male infertility?

what will be low in all 4?

A

congenital hypogonadotrophic hypogonadism (Kallman syndrome)
acquired hypogonadotrophic hypogonadism (stress, exercise, low bmi)
hyperprolactinaemia
hypopituitarism (tumour, apoplexy, radiation, surgery)

↓ LH, FSH, T

206
Q

what are 2 causes of testicular infertility?

A

congenital primary hypogonadism - kleinfelters syndrome 47XXY
acquired primary hypogonadism - trauma, radiation, cryptorchidism, chemo

207
Q

how does kallmann syndrome arise?

A

congenital

failure of migration of GnRH neurones to migrate with olfactory fibres from olfactory placed to hypothalamus

208
Q

what are the signs & symptoms of kallmann syndrome?

A 
↓Lh, FSH, T
cryptorchidism 
failure of puberty - micropenis, lack of testiuclar development 
primary amenorrhea
infertility
209
Q

what does 47XXY indicate?

A

kleinfelters syndrome

210
Q

how does kleinfelters syndrome present?

A 
tall stature
↓ facial and chest hair
gynacomastia
small penis & testes
narrow shoulders and wide hips
mildly impaired iq
infertility
211
Q

how will HPA hormones present in Klinefelters?

A

↑ FH and LSH

↓ T

212
Q

what are the 4 main investigations carried out for male infertility?

A

semen analysis
blood tests
microbiology (urine test and chlamydia swab)
Imaging (scrotal US and MRI pituitary)

213
Q

what levels are looked at in blood tests for male infertility?

A 
LH, FSH, PRL
morning fasting testosterone
SHBG
albumin
iron
pituitary/thyroid profile
karyotyping
214
Q

what are the treatment options for male infertility?

A

lifestyle - reduce bmi, smoking cessation, alcohol redution
dopamine agonist for hyperPRL
gonadotrophin for fertility
testosterone hrt if no fertility required
surgery

215
Q

what is primary ovarian insufficniency? how is it diagnosed?

A

early menopause
high FSH≥25iU/L (2 measurements at least 4 weeks apart)
(low E2)

216
Q

what are 3 causes of premature ovarian insufficiency?

A

autoimmune
Turners syndrome
cancer treatment - radio/chemotherapy

217
Q

what are causes of hypergonadotrophic hypogonadism in women?

A

↑ FSH & LH, ↓ E2

POI, turners syndrome, surgery, chemo, radiation, trauma

218
Q

what are the Rotterdam PCOS diagnostic criteria? how many re required for a diagnosis?

A

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
Q

what is the worst metabolic risk combination of the Rotterdam criteria?

A

hyperandrogegism and oligomenorrhoea

220
Q

what is the first line treatment for PCOS in someone who wants children? other treatments?

A

metformin

letrozole, clomiphene, IVF

221
Q

what can be used to treat the amenhorrea in PCOS?

A

metformin

OCP

222
Q

why is it imortamt to give lifestyle advice to PCOS patients?

A

they are at a higher risk of developing t2dm and gestational diabetes due to an increased insulin resistance

223
Q

what are treatment options for hirsutism?

A

creams, waxing, laser, spironolactone (anti-andorgen)

224
Q

which cancer is PCOS associated with a risk of developing? what can be given to reduce this risk?

A

endometrial cancer

give progesterone

225
Q

what does 45X0 indicate?

A

turners syndrome

226
Q

what are the symptoms of turners syndrome?

A 
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
Q

what type of hypogonadism is turners syndrome? what are HPA hormone levels?

A

hypergonadotrophic

↑ FSh & LH, ↓ E2

228
Q

what are the tubal causes of female infertility?

A

infection
trauma
endometriosis

229
Q

what are the uterine causes of female infertility?

A

chronic endometriosis
fibroids
adhesions
congenital malformation

230
Q

what disease can cause chronic endometriosis?

A

TB

231
Q

what are the cervical causes of female infertility?

A

chronic cervicitis
antisperm antibodies
(lead to ineffective sperm penetration)

232
Q

what are the ovarian causes of female infertility?

A

anovulation due to endocrine problems

corpus lute insufficiency

233
Q

when would you give testosterone replacement?

A

in a man who has hypogonadism but doesn’t desire fertility

used to treat symptoms

234
Q

what are the symptoms of male hypogonadism?

A

decreased shaving
less energy
loss of early morning erections
decreased libido

235
Q

how are testosterone levels measured?

A

2 serum T measurements before 11 am (should be highest in the morning)

236
Q

what are the options for testosterone replacement?

A

daly gel (risk if contamination)
3 weekly/ 3 monthly IM injections
implants/oral preparations

237
Q

what needs to be regularly monitored and why in testosterone HRT?

A

Haematocrit → ↑ RBCs → hyperviscosity → stroke (T increases EPO production)
PSA levels for prostate cancer

238
Q

how do you treat secondary hypogonadism in terms of fertiltiy? in males

A

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
Q

what cells does LH stimulate in males? what increases?

A

leydig cells

intratesticular testosterone

240
Q

what does FSH stimulate in men?

A

seminiferous tubule development and spermatogenesis

241
Q

why is testosterone not given to men wanting fertility?

A

testosterone would lower LH and FSH levels and further reduce spermatogenesis

242
Q

what are the 4 options for retiring ovulation in pcos patients?

A
  1. lifestyle and metformin
  2. letrozole
  3. clomiphene
  4. IVF
243
Q

how does letrozole work?

A

aromatase inhibitor so inhibits conversion of androgens to oestradiol
↓ E2 → less negative feedback on HPA→ ↑ GnRH → ↑ FSH & LH → stimualtion of follicle growth

244
Q

how does clomiphene work?

A

oestradiol receptor antagonist in hypothalamus → reduced negative feedback → ↑ FSH & LH → stimulation of follicle growth

245
Q

what are the steps in IVF?

A
  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
Q

what is ICSI and when is it done?

A

intra-cytoplasmic sperm injection done in male factor infertility

247
Q

what are the positives and negatives of condoms?

A

+ves : protect against STIs, easy to obtain, no contraindications
-ves : can internet sex, reduce sensation, interfere w erections

248
Q

how does the oral contraceptive pill work? 3 ways

A
  1. ↑ oestrogen and prog. → negative feedback → ↓ FSH & LH → anovulation
  2. thickens cervical mucus
  3. thins endometrial lining to reduce implantation
249
Q

what are the positives and negatives of OCP?

A

+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
Q

what are some side effects of the OCP?

A 
spotting
nausea
sore breasts
changes in mood/libido
more hungry
blood clot (v rare)
251
Q

what are non-contraceptive uses of the OCP?

A

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
Q

what are two differences with the POP compared to the OCP?

A

can be used when breastfeeding

shorter acting so needs to be taken at same time each day

253
Q

what are the long-acting reversible contraceptives?

A

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
Q

what are the emergency contraception options?

A

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
Q

3 side effects of emergency contraceptives?

A

headache, nausea, abdominal pain

256
Q

what can make emergency contraception less effective?

A

liver P450 enzyme inducer medications

257
Q

when should the OCP be avoided and why?

A

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
Q

what 4 things should be considering when choosing contraception?

A
  • 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
Q

why do oral oestrogens have a higher risk of VTE compared to transdermal oestrogens?

A

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
Q

when should transdermal oestrogens be given as opposed to oral?

A

BMI ≥ 30

261
Q

what cancers are associated with HRT?

A

breast, ovarian , endometrial

262
Q

when should progestogens be given in HRT and why?

A

if the woman has an endometrium otherwise endometrial hyperplasia can occur and lead to cancer

263
Q

when should HRT safety and efficacy be assessed?

A

at 3 months and then annually

264
Q

what can indicate endometrial cancer?

A

postmenopausal bleeding

265
Q

Is there cvd risk with hrt?

A

only if started more than 10 yrs after menopause

no increased risk if started before 60

266
Q

which HRT forms have a higher risk of stroke?

A

oral as opposed to transdermal

combined as opposed to oestrogen only

267
Q

what are 2 main benefits of hrt?

A

relief of menopausal symptoms eg. flushing, disturbed sleep, reduced libido
less osteoporosis related fractures

268
Q

what hormones can be given to transgender prepubertal young people?

A

GnRH agonists to suppress puberty and then sex steroids

269
Q

what hormones can be given to transgender men?

A

testosterone

progesterone to suppress menstrual bleeding

270
Q

what changes will occur in trasngender men after commencing hormone treatments?

A 
balding
deeper voice, acne, more hair
changes in body fat distrubution
clitoris enlargement
menstruation stops
increased muscle mass and strenght
(1-6 months)
271
Q

what hormones can be given to transgender women?

A

estrogen 4-5mg/day to increase oestradiol to about 734pmol/L

GnRH agonists and anti-androgen medication to reduce testosterone

272
Q

give an example of an anti-androgen medication? (what else can it be used for?)

A

spironolactone (also used for conns)

273
Q

what changes will occur in trasngender women after commencing hormone treatments?

A 
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
Q

in what ways can T2DM be similar to T1DM?

A

can present in childhood

DKA can occur

275
Q

what is T1DM that presents in adults called?

A

LADA - latent autoimmune diabetes in adults

276
Q

what are the 2 triggers for T1DM?

A

environmental and genetics (polygenic)

277
Q

how is insulin measured in the blood?

A

via c-peptide

pro-insulin → insulin + c-peptide

278
Q

online the immune response in T1DM

A

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
Q

what are 4 auto-antibodies associated with T1DM?

A

insulin antibodies - IAA
glutamic acid decarboxylase antibodies - GAD65
insulinoma-assoictaed-2-autoantibodies - IA-2A
zinc transporter 8 - ZnT8

280
Q

signs and symptoms of t1dm?

A

polyuria, nocturia, polydipsia, blurred vision, recurrent infections, weight loss, fatigue

dehydration, cachexia, hyperventialtion, smell of ketones, glycosuria, ketonuria

281
Q

what are 3 metabolic effects of reduced insulin?

A

↑ proteinolysis, HGO and lipolysis → ↑ amino acids, glucose and NEFA

282
Q

why and how do ketone bodies form in t1dm?

A

no insulin to inhibit the conversions of fatty acyl coA → acetyl coA, → acetoacetate → acetone and 3-OH beta → ketone bodies

283
Q

what are the 4 aims of t1dm treatment?

A

maintain glucose levels
restore close to physiological insulin profile
prevent acute metabolic decompensation
prevent vascular complications

284
Q

what are the complications of t1DM?

A

acute - dka
chronic - retino, neuro and nephropathy | ischaemic hd , cerbrovascular disease , peripheral vascular disease
treatment - hypoglycaemia

285
Q

4 management options for t1dm?

A

insulin
structured education programme and diet support
technology
transplant

286
Q

what are the types of insulin?

A

short-acting taken with meals

  • human insulin
  • insulin analogue

long-acting basal insulin

  • bound to zinc/protamine
  • insulin analogue
287
Q

what is the typical basal bolus regime?

A

short-acting insulin 3xday

once/twice daily long-acting

288
Q

how does insulin pump therapy work?

A

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
Q

how does an artificial pancreas work?

A

real-time continuous glucose sensor to monitor glucose levels
insulin pump delivers insulin based on glucose levels

290
Q

what are the transplant options for t1dm?

A

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
Q

what guides insulin doses?

A

self-monitoring of glucose levels (capillary or continuous) and HbA1c levels every 3 months

292
Q

when can DKA occur?

A

new onset t1dm
acute illness
missed/inadequate insulin doses

293
Q

how is dka diagnosed?

A

ph<7.3
increased plasma/urine ketones
HCO3- <15mmol/L
glucose ≥11mmol/L

294
Q

how is hypoglycaemia defined in terms of glucose levels?

A

~<3.6mmol/L

295
Q

how is severe hypoglycaemia defined?

A

when 3rd party assistance is required

296
Q

what are the symptoms of hypoglycaemia?

A

tremors, palpitations, sweating , hunger

drowsiness, confusion, uncoordinated, seizures

297
Q

how is hypoglycaemia treated?

A

glucose administartion

  • alert - oral
  • drowsy - buccal
  • unconscious - IV
298
Q

when is hypoglycaemia problematic?

A

excessive/recurrent severe → tolerance so you become less able to detect low blood glucose
nocturnal hypoglycaemia

299
Q

risks of hypoglycaemia?

A

seizures, coma, death

impacts well-being, driving, cognition, day to day function

300
Q

what are the risk factors for hypoglycaemia in t1dm?

A 
exercise
missing meals
inappropriate insulin regime
alcohol intake
lower HbA1c
lack of training
301
Q

when is pre-diabetes diagnosed?

A

HbA1C is between 42 and 48

302
Q

how is impaired glucose tolerance diagnosed?

A

2 hour OGTT between 7.8 and 11.1 mmol/L

303
Q

how is impaired fasting glycaemia diagnosed?

A

fasting glucose levels between 6 and 7mmol/L

304
Q

what is meant by a relative insulin deficiency in t2dm?

A

insulin is still produced by beta cells but not enough to overcome the insulin resistance at tissues

305
Q

why does dka not normally occur in t2dm?

A

theres enough insulin being produced to inhibit ketogenesis

306
Q

how can you measure and compare insulin levels?

A

using a hyperglycaemic clamp - give patients variable amount of glucose to get and maintain the same glucose level and then compare insulin response

307
Q

via what mechanisms does hyperglycaemia occur in t2dm?

A

↓ insulin → ↓ glucose uptake into skeletal muscle

↓ insulin and ↑ glucagon → ↑ HGO

308
Q

what are the genetics of t2dm?

A 
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
Q

how is obesity related to t2dm?

A

risk factor

↑ fatty acids and adipocytokines can lead to insulin resistance, lipolysis, reduced B cell function

310
Q

what are 2 other associations with t2dm?

A

perturbations in gut microbiota

intra-uterine growth retardation

311
Q

how can t2dm present?

A 
hyperglycaemia
overweight
dyslipidaemia
diabetic complications
insulin resistance and later deficiency
312
Q

risk factors for t2dm?

A 
age
↑BMI
ethnicity
PCIS
family hx
inactivity
313
Q

how is t2dm diagnosed?

A

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
Q

what is a hyperosmolar hyperglycaemic state? treatment?

A

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
Q

how is t2dm managed?

A

diet and structured education
oral medication eg. metformin
insulin later

316
Q

what is checked in a t2dm consultation?

A 
HbA1C levels
medication review
weight
blood pressure
dyslipidaemia - cholesterol profile
complication screening - feet, retinas
317
Q

how should diet change in t2dm?

A

↓ fat and refined carb calories
↑ complex carb calories
↓ sodium
↑ soluble fibre

318
Q

how does metformin work?

A

insulin sensitiser
reduces insulin resistance and HGO
increases peripheral glucose disposal

319
Q

what class of drug is metformin?

A

biguanide

320
Q

what drugs can improve insulin sensitivity?

A

metformin

pioglitazone

321
Q

what drug class is pioglitazone?

A

thiozolidinedione

322
Q

what is GLP-1?

A

glucagon like peptide 1
gut hormone secreted in response to nutrients in gut
stimulates insulin and suppresses glucagon
increases satiety

323
Q

why does glp-1 have such a short half life?

A

rapidly degraded by DPP4 enzyme (dipeptidyl peptidase-4)

324
Q

what drugs can boost insulin secretion?

A

dpp4-inhibtors
glp-1 agonists
sulphonylureas

325
Q

what drugs can reduce excess glucose in circulation?

A

alpha glucosidase inhibitor
SGLT-2 inhibitor
(reduce gut and renal absorption of carbs and glucose)

326
Q

what is the incretin effect?

A

when glucose is given orally as opposed to intravenously plasma insulin levels rise much more

327
Q

what drug class are dpp4-inhibitors?

A

gliptins

328
Q

what effects do GLP-1 agonists have?

A

decrease glucose and glucagon concentrations → weight loss

329
Q

give 2 examples of glp-1 agonists?

A

liraglutide

semaglutide

330
Q

how do dpp4 inhibitors work?

A

increase half life of exogenous glp-1 and glp-1 concentartion
decrease glucose and glucagon concentration

331
Q

how do sglt-2 inhibitors work?

A

inhibit the sodium glucose transported in the kidney → glycosuria → ↓ glucose levels
can improve CKD, lower risk of heart failure

332
Q

examples of sglt-2 inhibitors?

A

empa- , dapa- and canagliflozin

333
Q

what can potentially induce remission in t2dm patients?

A

gastric bypass surgery

very low calorie diet

334
Q

what other 2 aspects need to be managed in t2dm?

A

blood pressure - ACE inhibitors

lipids - statins

335
Q

what is an acute complication of t2dm?

A

hyperglycaemic hyperosmolar state

336
Q

microvascular complications of diabetes?

A

retino- neuro- and nephropathy

337
Q

macrovascular complications of diabetes?

A

ischaemic heart disease
cerebrovascular disease
peripheral vascualr disease

338
Q

what is the target HbA1c to reduce microvascular complictaions?

A

<53mmol/L

339
Q

what two factors are the main risk factor for diabetic vascular complications?

A

high hba1c

high blood pressure

340
Q

what are other risk factors for developing vascular complications?

A 
smoking
duration of diabetes
hyperglycaemic memory
genetic factors
hyperlipidaemia
341
Q

why is diabetic retinopathy screening important?

A

early stages are often asymptomatic
aims to detect it early when its still treatable to prevent vision loss
annual screening

342
Q

what are the stages of retinopathy?

A

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
Q

treatment for background retinopathy?

A

annual surveillance

344
Q

treatment for pre-proliferative retinopathy?

A

early pan retinal photocoagulation

345
Q

treatment for proliferative retinopathy?

A

pan retinal photocoagulation

346
Q

treatment for maculopathy?

A

anti-vegf injections for oedema (reduce inflammation)

grid photocoagulation

347
Q

how does pan retinal photocoagulation work?

A

it stops the formation of new blood vessels

348
Q

what are the impacts of diabetic nephropathy?

A

can progress to end stage renal failure requiring haemodialysis
healthcare burden
increases risk of cvd events

349
Q

what are diagnostic signs of nephropathy?

A

progressive proteinuria - increased ACR (≥30)
increased blood pressure
deranged eGFR
peripheral oedema

350
Q

what is the earliest feature of nephropathy?

A

microalbuminuria ≥2.5mg/mmol

351
Q

what is the mechanism of diabetic nephropathy?

A

diabetes → hypertension and hyperglycaemia → glomerular hypertension → proteinuria → glomerlualr and interstitial fibrosis → ↓ eGFR → renal failure

352
Q

2 drugs to control blood pressure?

A

ace inhibitors - inhibit the production of angiotensin II (-pril)
angiotensin receptor blockers - reduce action of angiotensin (-sartan)

353
Q

when should diabetes patients be given an antihypertensive?

A

if they have microalbuminuria/proteinuria even if normotensive

354
Q

management of nephropathy?

A 
tighter glycemic control
ACEi/ARB if microalbuminuria 
reduce BP
stop smoking
SLGT-2 inhibitor if t2dm
355
Q

what are the small blood vessels supplying nerves called?

A

vasa nervorum

356
Q

how does neuropathy arise?

A

when vasa nervorum get blocked → loss of sensation → potential amputation eg. not sensing an injury

357
Q

what are the risk factors for diabetic neuropathy?

A 
age
duration of diabetes
retinopathy
poor glcyaemi control
height (tall = longer nerves)
smoking
358
Q

why is neuropathy more common in the feet?

A

longest nerves supply feet

359
Q

what should be assessed in annual foot check?

A

ulceration , foot deformity
sensation
foot pulses

360
Q

what increases the risk of foot ulceration?

A

peripheral neuropathy - loss of sensation

peripheral vascular disease - poor blood supply

361
Q

what is mononeuropathy?

A

damage to single nerve → sudden motor loss

eg. 3rd nerve palsy → down and out

362
Q

what happens in autonomic neuropathy?

A

damage to SNS/PSNS nerves innervating GI tract, bladder, cardiovascular system

363
Q

risk factors for macrovascular diseases?

A

age
sex
birth weight
fhx/genes

dyslipidaemia
hypertension
smoking
DM
central obesity

BRS 2 (12 decks)

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