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Medicine MBBS year 2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

primary hypopituitarism is a problem with the ____ itself

A

gland. eg destruction

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2
Q

secondary hypopituitarism is a problem with _____

A

pituitary gland or hypothalamus e.g. tumor

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3
Q

in primary hypoadrenalism ___ decreases and __ increases. ___ also decreases

A

cortisol
ACTH
aldosterone
(Primary hypoadrenalism = Addison’s disease)

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4
Q

describe secondary hypoadrenalism and its features

A

pituitary tumor damaging corticotrophs

  • ACTH low
  • cortisol low
  • no effect on aldosterone
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5
Q

what happens to T4, T3 and TSH in secondary hypothyroidism?

A

all low

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6
Q

in primary hypothyroidism what happens to T3, T4 and TSH ?

A

T3 and T4 decrease

TSH increases

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7
Q

state 5 causes of hypopituitarism

A
  1. non-secreting pituitary adenoma
  2. sheehans syndrome
  3. pituitary apoplexy
  4. brain injury
  5. radiation
  6. infection, inflammation
  7. pituitary surgery
  8. congenital
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8
Q

Total loss of anterior and posterior pituitary function

= ?

A

panhypopituitarism

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9
Q

What are the results of radiation induced hypopituitarism?

A

GH and gonadotrophins most sensitive - reduction

Prolactin can increase after radiotherapy due to loss of dopamine

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10
Q

effect of low FSH/LH?

A

Reduced libido, Secondary amenorrhea, erectile dysfunction, reduced pubic hair

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11
Q

effect of low ACTH?

A

Fatigue, weight loss

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12
Q

effect of low TSH?

A

fatigue

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13
Q

effect of low prolactin?

A

inability to breastfeed

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14
Q

effect of low GH?

A

short stature in children

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15
Q

post-partum hypopituitarism secondly to blood loss during pregnancy is known as??

A

sheehans syndrome

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16
Q

state 4 symptoms of sheehans syndrome and the hormone(s) that cause it

A
  1. Difficulty breastfeeding or inability to breastfeed - prolactin deficiency
  2. Failure to resume menses - FSH and LH deficiency
  3. Cold intolerance - TSH deficiency
  4. Fatigue - ACTH, TSH and GH deficiency
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17
Q

Intro-pituitary hemorrhage of a pituitary Adenoma or less commonly infarction is known as?

A

pituitary apoplexy

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18
Q

pituitary apoplexy can be precipitated by __?

A

anticoagulants

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19
Q

state 3 key features of pituitary apoplexy

A
  1. Severe sudden onset headache
  2. Visual field defect - bitemporal hemianopia
  3. Cavernous sinus involvement may lead to diplopia and ptosis

(+ low pituitary hormones)

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20
Q

how do you diagnose hypopituitarism?

A
  1. Give insulin injection (insulin stress test) making blood glucose go low. This causes the stress hormones, GH and ACTH to be released.these hormones raise blood glucose. (cortisol measured)
    Hypoglycaemia (<2.2mM) = ‘stress’
  2. Give TRH to stimulate TSH release
  3. Give GnRH to stimulate FSH and LH release

If the release of hormones in each case is slight or not present = hypopituitarism/problem with the pituitary

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21
Q

what is used to replace each hormone in hypopituitarism

A

ACTH - replace with CORTISOL - hydrocortisone or prednisolone

TSH - replace with thyroxine

GH - synthetic GH

cant replace prolactin

FSH & LH - testosterone/ oestrogen + progesterone if no fertility required. if required give FSH and LH instead

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22
Q

if unwell/ has fever , what must patients with ACTH deficiency do? why?

A

double steroid dose

patient at risk of an adrenal crisis

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23
Q

what is an adrenal crisis? what are the features?

A

low cortisol

  • postural hypotension, nausea, weakness
  • abdominal pain, hypogylceamia
  • can result in collapse/ death
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24
Q 
Woman with bitemporal hemianopia. Pituitary MRI shows a pituitary tumour. 
vision.
9AM cortisol 650 nmol/L (>350)
fT4    8.1 pmol/L    (9-23)
TSH    0.2 mU/L    (0.3 – 4.2)
What is the diagnosis?
A

Low fT4. And low TSH.

= secondary hypothyroidism

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25
Q

state 3 differentials for sheehans syndrome

A
  • post-natal depression
  • anemia
  • Primary Hypothyroidism -after pregnancy effects on immunity - autoimmune disorders may be triggered
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26
Q

identify the organum vasculosum & subfornical organ on a diagram of the brain. what do they contain?

A

osmoreceptors

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27
Q

How do osmoreceptors regulate AVP

A
  1. Increase in extracellular Na+
  2. Water flows out of osmoreceptor in organum vasculosum and subfornical organ
  3. The receptor shrinks leading to receptor firing
  4. AVP release from supraoptic nucleus
  5. Osmoreceptors also cause thirst
  6. Reduced urine volume and plasma conc
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28
Q

How does non-osmotic stimulation of vasopressin occur?

A

Reduction in volume/ Hemorrhage - less stretch - less inhibition of atrial stretch receptors in RA - more AVP release

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29
Q

give two reasons why AVP release is good following hemorrhage

A
  • vasocontrictor via V1 receptor

- helps reasorb water

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30
Q

state the symptoms of diabetes insipidus

A

polyuria, polydipsia, nocturia

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31
Q

____ is a condition where there is a lack of vasopressin

A

CDI

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32
Q

state causes of CDI

A

Pituitary tumour, trauma, autoimmune

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33
Q

state the findings you would expect in CDI

A

Reduction in Vasopressin/ADH
Reduction in urine Osmolality
increase in plasma osmolality - hypernatraemia

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34
Q

____ is a condition where there is a lack of response to circulating ADH

A

nephrogenic DI

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35
Q

State causes of NDI

A
  • mutation in V2 receptor

- lithium

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36
Q

state the findings you would expect in NDI

A

Increase in Vasopressin/ADH
Reduction in urine Osmolality
increase in plasma osmolality - hypernatraemia

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37
Q

unlike DI, plasma osmolality is ____ in psychogenic polydipsia

A

low

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38
Q

what goes on the x and y axis in a water deprivation test?

A

y axis = urine osmolality

x axis = hours of water deprivation

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39
Q

How do we distinguish between cranial and nephrogenic DI?

A

Give Synthetic vasopressin/ desmopressin/ddAP

CDI - urine concentrates

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40
Q

how does desmopressin work?

why is it used instead of AVP?

A
  • a selective V2 receptor agonist

- AVP is unstable, would stimulate V1 receptors in blood vessels, is IV drug

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41
Q

drug for NDI?

A

Hydrochlorothiazide

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42
Q

features of SIADH?

A
  • too much ADH

- reduced urine output

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43
Q

state 4 causes of SIADH

A
  1. CNS •Head injury, stroke, tumour,
  2. Pulmonary disease - pneumonia, bronchiectasis
  3. Ectopic ADH - e.g small cell lung cancer
  4. Drugs - carbamazepine, cyclophosphamide, SSRIS
  5. Idiopathic
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44
Q

how do you treat SIADH?

A 
Restrict fluid
 vasopressin antagonist (Vaptan)
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45
Q

what tests should be carried out when you have the following differentials:
- Diabetes mellitus , diabetes insipidus, psychogenic polydipsia,

A

glucose
sodium levels
random plasma and urine osmolality
water deprivation test

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46
Q

State the 5 types of anterior pituitary cells and the result of a functioning pituitary tumor.

A 
Somatotrophs  - Acromegaly 
lactotrophs -      prolactinoma
thyrotrophs  -     TSHoma
gonadotrophs -   gonadotrophinoma
corticotrophs  -    cushings disease
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47
Q

serum prolactin may be ___ due to a non-functioning pituitary adenoma

A

raised.

dopamine cant travel down the stalk

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48
Q

serum prolactin may be ___ due to a non-functioning pituitary adenoma because ____

A

raised.

dopamine cant travel down the stalk

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49
Q

effects of hyperprolactineamia?

A
  • Shut down of GnRH axis (oligo-amenhhorea, low libido, infertility)
  • galactorrhoea
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50
Q

describe the mechanism by which hyperprolactineamia causes its effects

A

prolactin binds to kisspeptin neurons in hypothalamus
inhibits kisspeptin release
decrease in GnRH, FSH, LH, T, Oest

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51
Q

____ is the most common functioning pituitary adenoma

A

prolactinoma

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52
Q

state 3 pysiological causes of elevated prolactin

A

Pregnancy/breastfeeding
Stress: exercise, seizure, venepuncture
Nipple/chest wall stimulation

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53
Q

Excluding prolactinomas, state 3 pathological causes of elevated prolactin

A
  1. Primary Hypothyroidism - Elevated TRH can increase prolactin
  2. Polycystic ovarian syndrome
  3. Chronic renal failure
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54
Q

____ are an iatrogenic cause of elevated prolactin

A

antipsychotics (also oestrogens/OCP)

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55
Q

How do you determine a “true” elevation in serum prolactin?

A

no diurnal variation in serum prolactin and no effect from food

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56
Q

If a patient has a mild elevation in prolactin, no clinical features consistent with prolactinoma and you have reviewed medication list, what else could be causing elevation?

A
  1. macroprolactin - complex of monomeric prolactin and IgG

2. stress of venepuncture- exclude by a cannulated prolactin series.

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57
Q

How do you investigate a prolactinoma?

A

mRI once you’ve ruled out other causes

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58
Q

treatment for prolatinoma?

A

dopamine receptors AGONIST - binds to D2 receptors - CABERGOLINE

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59
Q

state 4 features of acromegaly

A
  1. Sweatiness, headache
  2. coarsening of facial features
  3. increased hand and feet size
  4. hypertension
  5. impaired glucose tolerance
  6. macroglossia
  7. obstructive sleep apneoa
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60
Q

how do you diagnose acromegaly?

A
  • elevated serum IGF-1
  • Oral glucose tolerance test - Failed suppression of GH following oral glucose load
  • +ve MRI
  • prolactin may be raised due to co-secretion
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61
Q

how do you treat acromegaly?

A
  1. first line = surgical- trans-sphenoidal pituitary surgery
  2. somatostatin analogues - octreotide
  3. dopamine agonists
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62
Q

Distinguish between Cushing’s syndrome and Cushing’s disease

A

Too much cortisol for any reason = Cushing’s syndrome

Too much cortisol due to corticotroph Adenoma = cushings disease

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63
Q

state 2 ACTH independent causes of Cushings syndrome

A

Taking steroids by mouth (common)

•Adrenal adenoma or carcinoma

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64
Q

How do you investigate someone with Cushing’s DISEASE?

A

First establish cushings syndrome:

  • elevated 24 hour urine free cortisol
  • elevated late night glucose
  • Failure to suppress cortisol after LOW dose oral dexamethasone - increased cortisol secretion

then establish cushings DISEASE
- ACTH will be high
- High does dexamethosone = cortisol suppression
+ve pituitary MRI

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65
Q

describe symptoms of hyperthyroidism

A
  • weight loss despite increased appetite
  • diarrhoea
  • tachycardia, palpitations, tremors and lid lag (sensitised Beta adrenoreceptors)
  • heat intolerance
  • hypercalceamia (T3 directly stimulates bone resorption)
  • pretibial myxedema in graves disease
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66
Q

state 3 presentations in a patient with thyroid storm

A
  • delirium
  • fever
  • tachyarrhythmia (cause of death)
  • jaundice (hepatocellular dysfunction)
  • cardiac failure
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67
Q

thyroid storm is extreme hyperthyroidism. It is hyperthyroidism that worsens in the setting of acute stress such as ___, ____, or _____.

A

trauma
infection
surgery

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68
Q

state 3 causes of primary hyperthyroidism

A

Graves Disease
Toxic multinodular goiter/ Plummer’s disease
Viral thyroiditis/ de Quervains

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69
Q

the most common cause of hyperthyroidism is?

A

graves disease

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70
Q

describe the pathology of graves disease

A

antibodies bind to TSH Receptor
TSH levels itself are low

  • smooth goitre
  • pretibial myxeodema
  • exophthalamos
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71
Q

a thyroid scan in Graves disease will show…..?

A

smooth iodine uptake

all black

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72
Q

describe the pathophysiology of toxic multinodular goitre

A

Benign adenoma that is overactive at making thyroxine.

Tumor grows whist thyroid gland shrinks

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73
Q

a thyroid scan in toxic multinodular goitre shows…?

A

tumor taking up the iodine. not smooth uptake

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74
Q

describe the pathophysiology of Viral thyroiditis/ de Quervain

A
  • Virus attacks the thyroid gland

- Thyroid stops making thyroxine and makes viruses instead

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75
Q

state some features of de Quervain

A
  • pain
  • dysphagia
  • hyperthyroidism followed by hypothyroidism
  • pyrexia
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76
Q

what would a thyroid scan in de Quervains look like?

A
  • blank

- no iodine uptake as no thyroxine

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77
Q

state 3 different treatments for hyperthyroidism

A
  • thyroidectomy
  • radioiodine
  • drugs
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78
Q

state 3 classes of drugs used to treat hyperthyroidism

A
  • thionamides
  • potassium iodide
  • beta blockers - e.g. propanolol
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79
Q

state 2 thionamide drugs

what are their mechanisms?

A

PTU (propylthiouracil) and carbimazole

Inhibits the enzyme thyroid peroxidase and hence T3 and T4 synthesis

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80
Q

what is a key side effect of thionamides?

A

agranulocytosis

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81
Q

state 2 uses of potassium iodide in hyperthyroidism

what is its mechanism

A
  1. Use to prepare patients for surgery - thyroid atrophies and is less vascularized during surgery
  2. Use during thyroid storm

inhibits thyroid peroxidase

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82
Q

what are the causes of primary adrenal insufficiency?

A

chronic causes include TB and Addison Disease

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83
Q

what are some consequences of adrenocortical failure ?

A

In primary only:

  1. fall in aldosterone - low bp, hyperkalemia, hyponatremia/salt craving, H+ retention an acidosis
  2. high ACTH and MSH (skin/mucosal hyperpigmentation)

In primary, secondary and tertiary:
3. fall in cortisol - postural hypotension, abdominal pain, diarrhea, hypoglyceamia, weakness, fatigue

84
Q

what tests are carried out for Addisons and what are the results?

A
  1. 9am cortisol - low OR synthetic ACTH stimulation (failure of cortisol to rise)
  2. then follow up with ACTH blood test - high
85
Q

medication for adrenal failure?

A

fludrocortisone - aldosterone replacement

hydrocortisone or prednisolone - cortisol replacement

86
Q

most common cause of congenital adrenal hyperplasia?

A

21-hydroxylase deficiency.

87
Q

What is the effect of complete 21-hydroxylase deficiency?

A

high sex hormones - male with precocious puberty, female with virilization.

  • low cortisol
  • low aldosterone - low bp, hyperkalemia
88
Q

which congenital adrenal hyperplasia is marked by increase in 17-hydroxyprogesterone?

A

21-hydroxylase deficiency

89
Q

all congenital adrenal hyperplasias are characterised by ___ ____ and ____ adrenal gland _____ due to ACTH stimulation.

A 
skin hyperpigmentation (high ACTH, high MSH) 
bilateral adrenal gland enlargement
90
Q

difference between partial and complete hydroxylase deficiency?

A

in complete, survival is less than 24 hrs

91
Q

What is the effect of an 11 hydroxylase deficiency?

A
  • low aldosterone
  • high 11-deoxycorticosterone -> high bp, hypokalemia
  • low cortisol
  • high sex hormones (XX virilization, precocious puberty in men)
92
Q

What is the effect of a 17 hydroxylase deficiency?

A
  • high aldosterone -> high bp, hypokalemia
  • low cortisol
  • low sex hormones -> XY have female type genitalia, XX lack secondary sexual development (primary amenorrhea)
93
Q

state 3 causes of adrenal hyperfunction

A
  1. cushings disease
  2. conns syndrome
  3. pheochromocytoma
94
Q

state different treatments for cushings syndrome?

A

depends on cause. primary treatment is surgery

  • pituitary surgery
  • unilateral adrenalectomy for mass
  • medication
  • bilateral adrenalectomy
95
Q

what 2 medications are given for cushings syndrome?

state their functions

A

Metyrapone - inhibits 11-B hydroxylase

ketoconazole - inhibits 17-a hydroxylase

96
Q

state 2 side effects of Metyrapone

A
  1. accumulation of 11- deoxycorticosterone - hypertension, hypokalemia
  2. Increased production of androgens - hirsutism in women
97
Q

why are metyrapone and ketoconazole used?

A

to control cushings syndrome before surgery

98
Q

how do you diagnose conn syndrome/primary hyperaldosteronism?

A
  • increase in aldosterone
  • decrease in renin
  • adrenal adenoma
99
Q

medication for conns syndrome?

A

spironolactone, epleronone

100
Q

mechanism of spironolactone action?

A
  • blocks Na+ resorption and K+ excretion in the kidney tubules
101
Q

pheos can cause severe ____ hypertension. the high adrenaline can cause death via ___

A

episodic

VF

102
Q

treatment for pheaos?

A

SURGERY.

pre-operative - alpha blockade + IV fluid, followed by B-blockers

103
Q

lab test results in primary hyperparathyroidism?

A
  • high PTH
  • high calcium (or normal)
  • low phosphate
104
Q

what is the treatment for primary hyperparathyroidism

A

parathyroidectomy (as it usually due to adenoma)

105
Q

symptoms in primary hyperparathyroidism?

A

stones, thrones, bones, groans and psychiatric overtones

osteoporosis - PTH activation of osteoclasts

106
Q

what do lab tests show in secondary hyperparathyroidism?

A

Due to vitamin D deficiency:
- low Ca2+, low phosphate, high PTH

Due to chronic kidney disease:

  • low Ca+, HIGH phosphate, high PTH
  • low vitamin D
107
Q

treatment for secondary hyperparathyroidism?

A

Vitamin D replacement - Give 25 hydroxy vitamin D. D2= ergocalciferol. D3 = cholecalciferol

In patients with renal failure - give 1a hydroxycholecalciferol

108
Q

give the lab values for tertiary hyperparathyroidism. when does this occur?

A
  • Very high PTH
  • high calcium
  • in the setting of CHRONIC KIDNEY DISEASE
  • parathyroid gland autonomously secretes PTH
109
Q

state 4 causes of hypercalceamia

A
  1. primary hyperparathyroidism
  2. tertiary hyperparathyroidism
  3. bony metastases
  4. Vitamin D excess
110
Q

what are the lab values in hypercalceamia caused by metastatic cancer?

A
  • high calcium

- LOW PTH

111
Q

treatment for hypercalceamia of malignancy?

describe the mechanism

A 
First line = IV fluids 
Then bisphosphonates (inhibits osteoclasts)
112
Q

infertility is failure to achieve pregnancy after __ months of regular unprotected sexual intercourse

A

12

113
Q

secondary infertility is?

A

live birth > 12 months previously

114
Q

What are the causes of infertility and what percentage do they each carry?

A

30% combined, 30% male, 30% female, 10% unknown

115
Q

state 2 post-testicular causes of male infertility

A

congenital absence of vas deferens

erectile dysfunction

116
Q

state 4 pre-testicular causes of male infertility

A
  1. Congenital and acquired endocrinopathies
  2. Klinefelters 47 XXY
  3. HPG, PRL
117
Q

state 2 ovarian causes of female infertility

A

anovulation

corpus luteum insufficiency

118
Q

state 2 cervical causes of female infertility

A

chronic cervicitis

immunological

119
Q

treatments for endometriosis?

A

Hormonal - OCP, prog, Laparoscopic ablation, Hysterectomy

120
Q

what are fibroids?

A

Benign tumours of the myometrium

121
Q

treatment for fibroids?

A

Hormonal - OCP, prog, continuous GnRH agonists

Hysterectomy

122
Q

kallmann syndrome, acquired hypogonadotrophic hypogonadism (low BMI, Excess exercise, stress), and hyperprolactineamia all result in a reduction in ___ in both sexes

A

GnRH

123
Q

____ is an example of congenital primary hypogonadism in men.

A

klinefelters

124
Q

____ and ___ are examples of congenital primary hypogonadism in women.

A
  • Turners (45X0)

- POI (can also be aquired)

125
Q

surgery, trauma, chemo, radiation are all ___ causes of primary hypogonadism in both sexes.

A

acquired

126
Q

hyperthyroidism and hypothyroidism can cause infertility by reducing bioavailable _____

A

oestrogen/testosterone

127
Q

what is kallmann syndrome?

features?

A

Failure of migration of GnRH neurons into hypothalamus

  • low GnRH
  • low FSH/LH
  • low testosterone/oestrogen
  • anosmia

(thus amennorrhea in women,
low sperm count, small testes, cryptorchidism in men)

128
Q

state 4 features of klinefelters syndrome

A
  • small penis and testes
  • wide hips
  • gynecomastia
  • tall with long extremeties
  • female hair distribution
  • may have mildly impaired IQ
129
Q

Describe the initial history, examination and investigation for Male Infertility

A

refer to table in notes

130
Q

what happens in POI?

A

Premature atresia of ovarian follicles - Estradiol decreases, LH and FSH increase

131
Q

state 3 causes of POI

A
  1. turners syndrome
  2. fragile x
  3. cancer therapy
132
Q

What is the most common endocrine disorder and most common cause of infertility in women?

A

PCOS

133
Q

How do you diagnose PCOS?

A

Must have two of the following:

  1. Oligo or anovulation - anovulation proven using ultrasound or lack of progesterone rise
  2. Clinical and or Biochemical Hyperandrogenism.
    Clinical - acne, hirsutism, alopecia
    Biochemical - raised androgens e.g. testosterone
  3. Polycystic ovaries - greater or equal to 20 follicles
134
Q

what causes PCOS?

A

Hyperinsulinemia or insulin resistance.
This Increases LH:FSH ratio.
Associated with obesity

135
Q

Describe the initial history, examination and investigation for female Infertility

A

refer to table in notes

136
Q

How do you treat PCOS?

A

To induce regular periods - OCP with progesterone

For fertility - Clomiphene (estradiol receptor antagonist),
Letrozole ( inhibits aromatase in the ovary so it doesnt turn testosterone to oestradiol) Low oestradiol reduces negative feedback on GnRH and pituitary). Increased FSH and LH

Metformin and weight loss

anti-androgens

137
Q

state 4 features of turners syndrome

A 
short stature 
webbed neck 
shield chest 
coarctation of the aorta 
ovarian dysgenesis 
short 4th metacarpals
138
Q

how do you induce spermatogenesis?

A

hCG injections which act on LH receptors. If no response after 6 months, add FSH.

139
Q

Does Congenital Secondary Hypogonadism have better, same or worse prognosis than Acquired Secondary Hypogonadism eg due to a pituitary tumour?

A

Worse - Congenital Hypogonadotropic Hypogonadism (CHH) eg Kallmann syndrome have not had mini-puberty.

FSH during mini-puberty important for growing the pool of immature spermatogonia and germ cells

140
Q

adverse effects of testosterone replacement?

A 
Increased Haematocrit (risk of hyperviscosity and stroke)
Increased PSA
141
Q

state the 3 steps in IVF treatment

A
  1. FSH stimulation/ superovulation
  2. Prevent premature ovulation
  3. LH exposure to mature eggs - hcG to trigger maturation
142
Q

how do you prevent premature ovulation in IVF?

A

FSH first then later introduce GnRH antagonist in combination = SHORT PROTOCOL

GnRH agonist first then later introduce FSH = LONG PROTOCOL

143
Q

what are some symptoms of OHSS?

A

Pleural effusion, ascites, renal failure, ovarian torsion

144
Q

Which molecule plays a role in OHSS?

A

VEGF

145
Q

what does the OCP contain?

A

oestrogen and progesterone

146
Q

an IUD works by…..?

A

preventing implantation and sperm egg survival

copper coil

147
Q

an IUS works by

A

secreting progesterone e.g. mirena coil

148
Q

state 3 conditions in which you should avoid the OCP

A

migraine with aura
Diabetes with retinopathy/nephropathy/neuropathy
stroke or CVD history

149
Q

what is HRT used for

A

relief or prevention of menopausal symptoms

150
Q

HRT increases risk of ____ and there are concerns over _____ risk

A

endometrial cancer

cardiovascular

151
Q

_____ ___ is used to treat Prepubertal Young people to stop sexual development?

A

GnRH agonist

152
Q

a BMI of > than ____ is obese

A

30

153
Q

state 3 factors affecting obesity

A
  1. screen time
  2. poverty
  3. education
154
Q

state 3 comorbidities associated with obesity

A
  1. diabetes
  2. stroke
  3. MI
155
Q

state the 3 types of bariatric surgery

A
  1. sleeve gastrectomy
  2. gastric band
  3. gastric bypass
156
Q

describe the pathophysiology of Type 1 Diabetes

A

autoimmune destruction of Beta cells -> partial or complete insulin deficiency

157
Q

___ develops in diabetic patients when their body cant produce enough insulin. It is more common in type 1 but can rarely occur in type 2 also

A

DKA

158
Q

what happens as you go from early Type 1 diabetes to late

A

infiltration of immune cells -> they disappear and fibrosis occurs

159
Q

describe the immunology underpinning type 1 DM

A
  1. presentation of auto-antigen to autoreactive
  2. CD4+ T lymphocytes
    CD4+ cells activate
  3. CD8+ T lymphocytes
    CD8+ cells travel to islets and lyse beta-cells expressing auto-antigen
  4. Exacerbated by release of pro-inflammatory cytokines
160
Q

which type of diabetes is associated with HLA system?

A

-Type 1 diabetes
- HLA-DR4 and HLA-DR3 carry significant risk.
(4-3) = 1

161
Q

state environmental factors implicated in type 1 DM development

A

Enteroviral infections
Cows milk protein exposure
Seasonal variation
Changes in microbiota

162
Q

state 2 auto-antibodies found in type 1 diabetes mellitus

A
  • Insulin antibodies (IAA)
  • Glutamic acid decarboxylase (GADA)
  • d-2 autoantibodies (IA-2A)– Zinc-transporter 8 (ZnT8)
163
Q

what are the symptoms of T1DM?

A

Polyuria, nocturia, polydipsia, blurring of vision, recurrent infections, weight loss, fatigue

164
Q

what are some signs of T1DM?

A

Dehydration, cachexia, hyperventilation, smell of ketones, glycosuria, ketonuria

165
Q

How do you diagnose T1DM?

A
  • Clinical features, HBA1C
  • presence of ketones.
  • May check for autoantibodies (e.g. GADA, IA2) and c-peptide (should be low)
166
Q

describe some complications of hyperglycemia

A

acute - DKA

chronic microvascular - nephropathy(renal glomerular arterioles), retinopathy (retinal arteries), neuropathy(vasa nervorum)

chronic macrovascular - IHD, PVD, cerebrovascular disease, renal artery stenosis

167
Q

state 2 types of insulin given with meals/ bolus

how many times do you give bolus?

A
  • human insulin
  • insulin analogues
  • 3 times a day after meals
168
Q

state two types of insulin given as basal. how many times do you give basal?

A
  • insulin bound to zinc or protamine
  • insulin analogue
  • once a day
169
Q

how does insulin pump therapy work?

A

Continuous delivery of short-acting insulin analogue

Delivery of insulin into subcutaneous space

170
Q

how can transplantation work in type 1 DM?

A

Islet cell transplant - transplant into hepatic portal vein

Simultaneous pancreas and kidney transplants

171
Q

what are the lab values in DKA?

A
  • increase in H+: pH <7.3,
  • HCO3- <15 mmol/L
  • ketones increased (urine, capillary blood),
  • hyperglycemia: glucose >11 mmol/L
  • hyperkalemia
172
Q

what are the symptoms of DKA ?

A

DKA is D eadly

  • delIrium, psychosis
  • kussmaul respirations (rapid, deep breathing) - due to metabolic acidosis
  • Abdominal (pain, nausea, vomiting)
  • dehydration - due to polyuria
  • fruity breath odour
173
Q

what is the effect of excess alcohol intake in type 1 diabetes?

A

hypoglycemia

174
Q

what treatment do you give to a patient with DKA?

A

IV insulin, IV fluids, and K+ to replete intracellular stores as insulin drives potassium into cells

175
Q

describe some symptoms of hypoglycemia

A

Sweatiness, palpitations, hungry, tired, shakiness.

Confusion, loss of consciousness if severe

176
Q

describe the pathophysiology of Type 2 DM

A

insulin resistance + progressive beta-cell failure -> hyperglycemia

177
Q

how do you diagnose T2DM?

A

Fasting glucose > or equal to 7mmol/L

OGTT > or equal to 11mmol/L

HbA1C > or equal to 48mmol/mol

178
Q

what is the name of the model used to calculate beta cell function using fasting glucose and fasting insulin levels

A

HOMA model

179
Q

how do you treat type 2 DM

A
  1. oral agents “To Normalize Pancreatic Function” = “gliTs, gliNs, gliPs, gliFs”
  2. advanced stage = insulin replacement
180
Q

why do triglyceride levels rise in T2DM?

A

Insulin promotes the conversion of triglycerides in the blood to NEFA

181
Q

which SNP increases the risk of diabetes the most?

A

TCF7L2

182
Q

symptoms of T2DM?

A

Hyperglycaemia, overweight, dyslipidemia, fewer osmotic symptoms. PCOS= risk factor

183
Q

what is a common acute complication of T2DM? and what are its features?

A

Hyperosmolar hyperglycemic state

184
Q

In diabetes mellitus, what factors are associated with the development of microvascular complications?

A

High BP - most important
higher HBA1C
genetics
hyperglyceamic memory

185
Q

what are the stages of retinopathy?

describe the findings in each stage

A
  1. Background Retinopathy - hard exudates (cheese spots) + blot hemorrhages
  2. pre-proliferative retinopathy - soft exudates/cotton wool spots. represent retinal ischemia
  3. proliferative retinopathy - visible new vessel s
186
Q

__ can occur at any stage of retinopathy. It is characterised by hard exudates near the ___. This can threaten direct vision

A

maculopathy

macula

187
Q

on a picture of a normal retina, label the fovea (macula) and optic disc

A

check notes

188
Q

how is retinopathy treated?

A
  1. All types require improvement in HBA1C and better blood pressure control
  2. Pre-proliferative and proliferative require panretinal photocoagulation
  3. Maculopathy requires anti-VEGF injections for oedema and Grid photocoagulation
189
Q

what are the characteristics of diabetic nephropathy?

A

Decline in eGFR
urine albumin:creatinine ratio, >2.5 in men, >3.5 women shows microalbuminuria. ACR> 30 = proteinuria

advanced = peripheral oedema

190
Q

how do you treat diabetic nephropathy?

A

HBA1C and blood pressure management, stop smoking

ACE inhibitors (cause dilation of efferent arteriole and reduce hyperfiltration)

191
Q

what is the most common type of neuropathy

A

Peripheral sensory neuropathy

  • Others include mononeuritis multiplex and autonomic neuropathy
  • Or mononeuropathy- sudden motor loss, wrist drop, foot drop, cranial nerve palsy - double vision due to 3rd
192
Q

what factors contribute to macro vascular complications in diabetes

A
  1. dyslipedemia - most important
  2. high HBA1C
  3. hypertension
  4. central fat
193
Q

how do you assess neuropathy?

A

vibration, temp, fine touch sensation

ankle jerk reflex

194
Q

state and describe the different types of foot ulcers

A

Neuropathic foot - numb, warm, dry, ulcers at points of high pressure loading, palpable pulse

Ischaemic foot - cold, pulseless, ulcers at the foot margins

Neuroischaemic - numb, cold, dry, pulseless, ulcers at p high pressure and margins

195
Q

__ ___ are hyperpigmented plaques in intertriginous sites often associated with insulin ___. It is also rarely associated with malignancy

A

acanthosis nigricans

resistance

196
Q

state two mechanisms that lead to chronic complications in Diabetes mellitus

A
  1. non-enzymatic glycation and AGEs

2. Sorbitol accumulation

197
Q

State the actions and side effects of metformin

A

Activates AMPK in hepatocyte mitochondria -> inhibits ATP production -> blocks gluconeogenesis

Also blocks adenylate Cyclase -> promotes fat oxidation

Reduced hepatic glucose output
Increases insulin sensitivity,

GI side effects - contraindicated in liver, cardiac or renal failure
SEs: Lactic acidosis, weight loss

198
Q

State the actions and side effects of Glitazones/thiazolidinediones

A

E.g. pioglitazone

PPAR-gamma receptor agonist
Increases insulin sensitivity and levels of adiponectin -> Regulation of glucose metabolism and fatty acid storage

weight gain but it is mainly peripheral, heart failure, MI

199
Q

State the actions and side effects of Sulphonylureas

A

E.g. gliclazide

Close K+ channels in pancreatic B cell - depolarization - insulin release

SEs: weight gain, hypoglycemia

200
Q

State the actions and side effects of DPP-4 inhibitors

A

Gliptins group of drugs

Increases glucose-induced insulin secretion
Inhibits DDP4 enzyme in vascular endothelium tthat deactivates GLP-1

GLP1 can exert its effects

Satiety, URTIs, UTIs

201
Q

State the actions and side effects of SGLT-2 inhibitors

A

“Glifs” group of drugs - e.g canagliflozin

Decreases glucose absorption - blocks reabsorption in PCT

Glycosuria - UTIs

202
Q

How does metformin move across body compartments?

A

via OCT1

203
Q

what does the “To Normalize Pancreatic Function”

mnemonic mean?

A

gliTs - thiazolinodionses/glitazones

gliNs - meglitinides

gliPs - DDP4 inhibitors

gliFs - SGLT-2 inhibitors

204
Q

What is POI also known as?

What would lab results look like?

A

Acquired primary hypogonadism

Low oestradiol, high FSH and LH

205
Q

How do you treat POI?

A

IVF
Egg donation
Blood test for AMH - marker of ovarian reserve

206
Q

DKA is typically associated with which type of diabetes mellitus?

A

Type 1

207
Q

State the actions and side effects of GLP1 analogs

A

e.g Liraglutide

Responsible for incretin effect
Increase glucose induced insulin secretion
Inhibits glucagon and delays gastric emptying

Medicine MBBS year 2 (11 decks)

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