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Phase 4 - Katherine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is T1DM

A

Autoimmune destruction of pancreatic islet cells leading to
reduced insulin

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2
Q

What is T2DM

A

Hypersecretion of insulin by depleted beta cell mass.
Increasing insulin resistance

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3
Q

Main comps of diabetes

A

Retinopathy, neuropathy, nephropathy, skin infection (low immunity)

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4
Q

What do alpha cells produce in pancreas?

A

glucagon

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5
Q

What does insulin do to cells?

A

allows glucose to enter

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6
Q

pres of t1DM

A

Polyuria, polydipsia, weight loss, lethargy,
DKA problems… (dehydration, breathing, abdo pain)…

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7
Q

Initial Ix in DM

A

Urine dip, fasting glucose, random glucose, GTT, HbA1c

For comp:
Urine - protein
BP for HTN
Fasting lipid - hyperlipidaemia

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8
Q

Where is neuropathy in DM

A

glove and stocking

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9
Q

mx of nephropathy in DM

A

ACEi/ARB

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10
Q

How can you minimise CV risk in diabetes

A

BP control + diet + smoking + statin -> QRISK

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11
Q

How to reduce chest infections in DM

A

Pneumococcal vaccine and annual influenza

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12
Q

What causes diabetic foot

A

Peripheral artery disease, neuropathy + infection

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13
Q

How does diabetic food present?/

A

Ulcers (neuropathic painless and punched out or arterial), loss of pulses

*Charcot foot

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14
Q

Name 2 things you might see in diabetic eye?

A

Microaneurysm - from physical weakness

Hard exudates - lipoproteins from leakage

Haemorrhages - rupture of weakened capillaries small dots, blots or flame (track along nerves in superficial retinal haemorrhages)

Cotton wool spots - build up of axonal debris

Neovascularisation

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15
Q

How do diabetic eye present?

A

Painless, patch loss of vision

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16
Q

Mx of diabetic eye

A

Optimise glycaemic control
Blood pressure control
Lipid control
Laser photocoagulation

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17
Q

General non pharma mx of diabetes

A

Diabetes education

Diet and exercise - low sugar, low fat, high starchy carb

Exercise and smoking advice

Maximise glucose control - DAFNE for type 1

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18
Q

Name 3 things checked annually in diabetes

A

Educate + modifiable RFs

Check BMI

Check complications: hypos, HOHS, DKA

Assess CVS: BP, pulses, bruits
Inspect injection sites - lipodystrophy

Foot check - neuropathy and pulses

Urine dip - protein, nitrites, ketones

Check eyes - acuity and ophthalmoscopy -> refer opthalmology

Ask erectile dysfunction

Bloods: HbA1c and home capillary monitoring results, random lipids

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19
Q

What is the target hba1c

A

<48mmol

42-27 is pre-diabetes

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20
Q

Pharma control of type 2 diabetes

A

1- metformin
if hba1c >58

2- add Gliptin or sulfonylurea or pioglitazone

if hba1c >58

3- add another

if hba1c>58

4- insulin

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21
Q

how does metformin work

A

Increases insulin sensitivity (GLUT 4), decreases gluconeogenesis

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22
Q

Ci to metformin

A

CKD, eGFR < 30

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23
Q

common SE metformin

A

GI upset

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24
Q

How does gliptin work?

A

DPP-4 inhibitors (DPP-4 destroys incretin)

Raised incretin -> produce more insulin when needed

SE: pancreatitis

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25
Q

How does sulfonylurea work?
CI?
SE?

A

Increase panc insulin secretion
[Suuuuuplements insulin]

Pregnancy

*Hypo, weight gain

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26
Q

how does piaglitazone work? SE? CI?

A

Increases insulin sensitivity

Weight gain, fluid retention and osteoporosis

Heart failure and osteoporosis

[PIG - big full of water]

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27
Q

Eg of rapid acting insulin you can take before meals

A

Humalog or Novorapid

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28
Q

Eg of long acting insulin

A

detemir

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29
Q

Mx of concious hypo?

A

10-20g short acting carb e.g. glass of lucozade, x3 glucose tablets, glucogel

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30
Q

Mx unconcious hypo

A

IM glucagon

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31
Q

Why does being unwell increase risk of DKA

A

Stress response to illness -> increased cortisol
Cortisol increases blood sugars and decreases insulin

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32
Q

Triggers of DKA?
pres?

A

Missed insulin, infection, intoxication, ischaemia, infarction

n/v, GCS, abdo pain, kussmal, dehydration

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33
Q

What is kussmal respiration?

A

deep hyperventilation to correct acidosis

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34
Q

ECG of hypokalaemia

A

PRSTTU

PR prolonged
ST depression
Flattened/inverted T wave
Prominent U wave after T

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35
Q

3 Ix in DKA ? what are you expecting to see?

A

Plasma glucose: high >11 or known DM

Plasma ketones: high >3mmol/l

ABG: metabolic acidosis pH < 7.3

Bicarb <15

[Urine dip: ketones (++) and glucose ]

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36
Q

Mx of DKA ?
For acidaemia?

A

ABCDE sats etc… + catheterise

IV NaCl
IV insulin : 0.1U/kg/hr

Correct K as it falls

Acidaemia: IV bicarbonate

DKA complications - cerebral oedema, hypoK/hyperK, hypoG/hyperG, AKI

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37
Q

Monitoring in DKA

A

Electrolytes and bicarb - 1-2 hours,
pH,
fluid balance hourly,
glucose hourly,
ECG

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38
Q

Characteristic features of Hyperosmolar hyperglycaemic state

A

T2DM
very high blood glucose >40 + v.high serum osmolality

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39
Q

Triggers of HOHG

A

Infection, MI, dehydration, inability to take normal meds, thiazides + loop, poor con

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40
Q

What happens in untreated HOHG

A

Extreme dehydration + altered mental state ± seizures ± delirium

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41
Q

Ix in HOHG

A

Urinalysis: glycosuria +++. Ketonuria +

Capillary glucose > 30

Serum osmolality > 320mmol/L

U+E -> AKI

ABG -> normal

Blood cultures -> rule out sepsis

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42
Q

Mx of HOHG

A

ABCDE
IV access, ECG, SaO2, BP

Treat cause
Safely normalise osmolality - replace fluid and electrolytes
Normalise blood glucose

IVNaCl
IV insulin

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43
Q

Complications of Mx of HOHG

A

Cerebral oedema, central pontine myelinosis

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44
Q

What is metabolic syndrome? 2 key criteria?

A

Cluster of common abnormalities including insulin resistance, impaired glucose tol, reduced HDL, elevated triglycerides and HTN

Truncal obesity
raised BP

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45
Q

name 2 medications causing obesity

A

Glitazone, sulfonylurea
Anticonvulsants
Antidepressants: tricyclics and mirtazapine
Lithium
Progesterone only contraception
BB
Corticosteroids

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46
Q

name 2 conditions cauing obesity

A

hypothyroid, PCOS, cushings, hypogonadism

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47
Q

Ix in obesity

A

Hormone profile: sex hormones and cortisol

TFT

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48
Q

What drug can you use for obesity? when?

A

Orlistat: only after diet, behaviour and exercise

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49
Q

When would you continue orlistat

A

Continue beyond 3/12 only if lose 5%

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50
Q

Name 2 surgeries for bariatrics

A

Restrictive: gastric banding

Malabsorptive: biliopancreatic diversion

Both: roux en y gastric bypass (RYGB

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51
Q

Which 2 hormones are involved in gynaecomastia

A

Oestrogens stimulate, androgens inhibit

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52
Q

Causes of gynaecomastia. Name 3

A

Low testosterone androgen resistance, Klinefelter’s, viral orchitis (mumps), renal disease

High oestrogen
neoplasms secreting HCG (e.g. seminoma) or ectopic BCG lung, RCC, adrenal tumour (oestrogen), CAH, *liver disease - increased prod androstenedione and aromatisation to oestrogen), obesity, hyperThyroid

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53
Q

Name 2 medications causing gynaecomastia

A

Antipsychotics, TCA (increase prolactin)

Digoxin

spironnolactone (inhibits testosterone)

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54
Q

blood Ix in gynaecomastia

A

Kidney function, LFT, TFT

Hormones:\
Estradiol, testosterone, prolactin, bHCG, AFP, LH

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55
Q

gynaecomastia…

LH high + test low = ?

LH low + test low = ?

LH high + test high = ?

A

LH high + test low = testicular failure

LH low + test low = increased oestrogens

LH high + test high = androgen resistance or neoplasm

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56
Q

When would you image gynaecomastia

A

Imaging: USS or mammography if suspicious or unilateral + needle core biop

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57
Q

most common cause of hypothyroid?

Presentation?

A

Hashimotos

Iodine deficiency is more common in developing world!

Other - thyroidectomy, radioactive iodine, lithium, Amiodarone, De Quervain;s

Bradycardia, constipation, low of concentration, menorrhagia, cold intolerance, thin skin, thin hair, depressed, fatigue, weight gain, decrease appetite, carpal tunnel

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58
Q

Hypothyroid main complication ? presentation?

A

myxoedema coma

hypoventilation + seizures + hypothermia + decreased consciousness

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59
Q

Mx of myxoedema coma

A

IV levothyroxine
+ IV hydrocortisone (after blood cortisone) - this is because primary hypothyroidism can also come with primary adrenal insufficiency. Secondary hypothyroidism can be associated with hypopituitarism leading to secondary adrenal insufficiency. Additionally, levothyroxine may cause adrenal insufficiency due to the increase in the metabolism of cortisol.

+ resp support

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60
Q

2 key antibodies in hashimotos

A

Anti-TPO (anti-thyroid peroxidase)

anti-Tg (antithyroglobulin)

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61
Q

How to differentiate 1 /2 hypo thyroid disease?

A

Primary: high TSH, low T3/T4,

secondary: low TSH, low T3/T4

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62
Q

Mx of hypothyroid ? 2 comps with mx?

A

Levothyroxine (T4) for life

Osteoporosis
Arrhythmia

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63
Q

Antibody in graves

A

Anti-TSH

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64
Q

Ix in hyperthyroid ? If orbital involvement?

A

TFT: TSH low, high T3/T4

AAb: anti-TSHR (99%) at Grave’s + anti thyroglobulin + anti TPO

Anti-TPO + Anti-TSH = GRAVES!
Anti-TPO + Anti-Tg = Hashimotos!

Imaging:
- USS ?cancer

Thyroid uptake scan. This uses radioisotopes and hot = overactivity, no uptake for DeQuervain’s (subacute thyroiditis - gives hyperthyroidism for a few days then hypothyroidism for a few weeks after)

Orbital -> visual field testing, CT/MRI head

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65
Q

Usual Mx of hyperthyroid

A

BB - propanolol
Lubricating eye drops

Carbimazole
propylthiouracil - if pregnant

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66
Q

Which antithyroid drug cant be used in pregnancy?

A

carbimazole -NOT IF PREG

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67
Q

what mx is often used in Relapsed Grave’s or toxic nodular ? When can this not be used

A

radioactive iodine

preg / breastfeeding

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68
Q

2 specific complications of thyroid surgery?

A

hypoparathyroidism
damage to recurrent laryngeal nerve

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69
Q

how does a thyroid storm present

A

Hyperpyrexia > 41

CVS: HR > 140, hypotension, AF, CHF

GI: Nausea, jaundice, vomiting, diarrhoea, abdominal pain

NEURO: Confusion, agitation, delirium

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70
Q

Ix in thyroid storm?

A

Sepsis screen, TFT, ECG, CXR, ABG

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71
Q

Mx of thyroid storm

A

ABCDE
Resus: O2, IV fluids, NG tube if vomiting

Antithyroid Rx
Oral carbimazole or propylthiouracil

IV propanolol
IV hydrocortisone (treats possible relative adrenal insufficiency)

Keep cool with tepid sponging not paracetamol

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72
Q

What causes increased PTH release

A

low ca

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73
Q

PTH main organs affected?

A

Bone - increases osteoclasts -> release Ca

Kidney
1 - increases fit D metabolism by the kidneys -> this secondarily increases Ca absorbtion in GI

2 - Increases reabs Ca, decreases reabs PO4

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74
Q

Who gets primary hyperparathyroid?
Main comps?

A

postmenopausal women (benign adenoma on parathyroids)

Osteoperosis + peptic ulcers, hypercalcaemia

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75
Q

Cause of secondaery hyperparathyroid?

A

low Ca -> PT hyperplasia. However calcium still stays low.

almost always associated with kidney, liver or bowel disease

76
Q

Which hormone inhibits osteoclast activity?

A

calcitonin

Produced by para-follicular (medullary) C cells of thyroid

77
Q

What does the excess ca absorption from bone -> in hyperparathyroid?

A

osteopenia and osteoporosis

(if extreme = osteitis fibrosa cystica (salt + pepper pot skull + subperiosteal resorption )

Sx of high Ca
*Bones, stones, abdominal moans, thrones, psychic overtones

78
Q

Ix in raised Ca?

What addtional Ix might you do if you think this is longstanding?

A

Obvious cause: thiazide and lithium

Repeat plasma albumin adjusted calcium

Check renal function

Measure PTH - HyperPT often finding post raised Ca

Longstanding:
DEXA (annual)
Renal tract imaging USS
X-ray: skull and hand

79
Q

mx of mild primary HPT

A

Surveillance
Check creatinine and Ca 6 months

DEXA yearly

Vitamin D *suppresses PTH

Avoid dehydration, thiazide diuretics -
increase fluids

80
Q

Surgery is the definitive mx of primary HPT. Complications?

A

Hypothyroidism, recurrent laryngeal nerve damage

Hungry bone syndrome (due to rapid deposition of Ca in bone)

81
Q

Medical management of low bone density in HPT

A

Bisphosphonates

82
Q

Association secondary HPT

Presentation?

A

CKD (5)
vit D deficiency
High PTH, low Ca, Low vit D, high PO4

CKD pres with PROMINENT BONE PAIN

83
Q

main complications of 2ndary HPT

A

Progress to tertiary -> high Ca -> Skeletal and cardiac calcification

84
Q

Measure levels of what in secondary HPT? Whats high/low

A

High PTH,
low Ca,
PO4 high in renal disease, low in vitamin D deficiency [vit D increases PO4 absorption]

85
Q

Mx of 2ndary HPT ?

A

Correct vitamin D deficiency

In CKD: Ca supp, correct vit D, phosphate binders, calcimimetics (only at end-stage kidney disease)

86
Q

What is tertiary HPT

A

ongoing hyperplasia of PT glands after correction of underlying renal disorder CKD

i.e. after prolonged secondary hyperplasia of all 4 glands

87
Q

Mx of tertiary HPT

A

Cinacalcet [hes a cina that cal with cet]

Total or subtotal parathyroidectomy

88
Q

Appearance of people with pseudohypoparathyroid

A

Low IQ, short stature, short 4th and 5th metacarpals

89
Q

mx of hypoparathyroid

A

If tetany - urgent IV Ca

Diet: rich in Ca and vit D

Calcium and vit D

90
Q

DDx for hyperCa causes
Name 3

A

HPT

Malicnancy - squamous cell lung Ca, breast Ca

Endocrine - thyrotoxicosis, phaeo, primary adrenal insufficiency (Addison’s)

Drugs: thiazide diuretics, vitamin D

91
Q

What is meant by groans, thrones, stones, and psychic overtones

A

Abdominal groans
Anorexia, nausea and vomiting, abdo pain, PUD, acute pancreatitis

Thrones
Polyuria, polydipsia, dehydration

Stones - if long standing
Renal colic

Psychic overtones
Depression, dementia, confusion, memory

92
Q

Ix in hyperCa and why?

A

High corrected Ca (<3 = PHPT, >3 = malignancy)

Albumin - high -> with high urea = dehydration

Alk phos - normal in myeloma, raised in bony mets

Calcitonin - B cell lymphoma

PTH - high = PHPT, low = granulomatous or adrenal

*XR - bone abnormalities, cysts, pathological fractures etc

93
Q

Mx of acute high Ca (<3.5) ?

A

0.9% saline - hydration and increase urinary excretion

Loop diuretic - furosemide for fluid overload

After rehydration –> IV bisphosphinates.

94
Q

what should you give post re-hydration of acute high Ca

A

IV bisphosphonates

95
Q

Causes of hypocalcaemia?

Sx of hypoCa

A

Causes = low PTH (surgery or radiotherapy), fit D deficiency, CKD, acute pancreatitis

Paresthesia: fingers, toes, mouth

Tetany (emergency)

Carpopedal spasm (wrist flexion and fingers drawn together)

Muscle cramps

96
Q

QT in hypo vs hyper Ca

A

Hypo Prolonged QT

(shortened in hyperCa)

97
Q

What are Chvostek’s and Trousseua’s signs?

A

hypoCa

Chvostek’s sign - latent tetany
Tap facial nerve -> face spasms

Trousseua’s sign - from increased neuromuscular excitability
Inflate a BP cuff above systolic - look for carpopedal spasm

98
Q

name 3 Ix for hypoCa ? 2 more for things to exclude causes

A

Adjusted Ca

Serum Mg
Serum PO4
Serum PTH
Evaluate vit D metabolism

ECG

Exclude:
CKD (U+E), acute panc (amylase), rhabdo (check CK)

99
Q

Mx of acute hypoCa (seizures / tetany) ? What to do if hypoMg

A

10ml 10% calcium gluconate slow IV infusion, repeat as necessary

Oral calcium

Monitor Ca

If hypomagnesaemia - correct otherwise Ca will not respond

100
Q

Chronic mx of hypoCa

A

Ca
vit d

101
Q

Hormones and basic function from ant pit

A

GH: stimulates liver to produce IGF-1 and counteracts insulin

Prolactin: promotes growth of mammary glands and reproductive organs

FSH: stimulates release of sex steroids

LH: stimulates release of sex steroids

ACTH: adrenocorticotropic hormone: stimulates adrenal cortex to release glucocorticoids and androgens

TSH

102
Q

2 hormones from post pit

A

vasopressin
oxytocin

103
Q

Name 2 local effects of pit ademonas

A

Cavernous sinus = CN 3, 4, 5a, 5b, 6

Optic chiasm

Headaches: retro-orbital and bilateral worse on waking

Visual field defect: bitemporal hemianopia

Ocular nerve palsies - squint

104
Q

What is the key DDx of pit adenoma local effects

A

Craniopharyngioma
(from Rathke’s pouch, between pit and floor V3)

105
Q

General mx of pit adenoma

A

Surgery: transsphenoidal

106
Q

Key SE of pit surgery

A

pituitary dysfunction -> adrenal insufficiency, DI, SIADH

107
Q

Pharma mx of prolactinoma?

A

bromocriptine

108
Q

Pharma mx of GH adenoma

A

somatostatin

109
Q

Effect of high prolactin pn women? men?

A

Women
menstrual dysfunction + galactorrhoea -> low oestrogen

(due to inhibits GNRH -> reduced gonadotropin (FSH + LH) secretion )

Men
hypogonads, decreased libido, erectile dysfunction

110
Q

Which class of drugs causes high prolactin

A

antipsychotics - raise PL

Antidepressants

111
Q

MEN1 gene associations

A

parathyroid tumours, prolactinoma, pancreatic islet tumour

112
Q

Ix in raised prolactin

A

PRL: normal < 400, if mild el = 400-1000 - repeat before referral
> 5000 = true prolactinoma

TFT

Exclude pregnancy

Assess other pituitary function

MRI pituitary

113
Q

medical mx of prolactinaemia

A

Dopamine agonist
-bromocriptine

114
Q

Main SEs of bromocriptine

A

sleepiness, hypotension,

cardiac/retroperitoneal/pulmonary fibrosis - monitor

115
Q

With pit adenoma what sreious complication are you worried about? how does it present?

A

pituitary apoplexy
Haemorrhage / infarction of gland

Sudden onset headache, visual symptoms

116
Q

What two hormones involved in acromegaly

A

GH
IGF1

117
Q

Name 3 features of acromegaly

A

Due to tumour - headaches / visual field defect

big hands / feet

thick nose, frontal bossing , macroglossia, coarse facial features

skin - thick dark oily

carpal tunne

cardiac - HTN / LVH / arrythmia

T2DM

118
Q

Name 3 Ix for acromegaly

A

IGF1 - raised

GTT

GH

pit MRI

Glucose

Visual field testing

119
Q

mx acromegaly

A

transsphenoidal surgery

2nd line - somatostatin analouges

3rd line - bromocriptine

120
Q

Layers of adrenals

A

The deeper you get the sweeter it gets

GFR - Salt sugar sex

Zona glomerulosa - mineralocorticoids - aldosterone

Zona fasciculata - glucocorticoids - cortisol

Zona reticularis - androgens - DHEA - dehydroepiandrosterone

121
Q

Effects of cortisol?

A

RIDGE
Suppression of reproduction
Suppression of immunity
Suppression of digestion
Suppression of growth
Mobilisation of energy

122
Q

What syndrome has high cortisol

A

cushings

123
Q

What are the 2 types of cushings syndrome ?
1 cause of each?
Most common cause?

A

ACTH dependent
Excessive ACTH pit pit (Cushing’s disease),
ectopic ACTH producing tumours (due to lung cancer, small cell)

ACTH independent
Adrenal adenoma/adrenal carcinoma/excess glucocorticoids

most common is excess glucocorticoids - IATROGENIC

124
Q

Name 3 features on presentation of cushings syndrome

A

buffalo hump
moon face
wiehg t gain
proximal muscle wasting
Diabetes
hypertension
osteoperosis
infection
depression

125
Q

Ix for cushings (excluding imaging)

Treatment

A

Glucose - elevated

dexamethasone supression test

24hr urinary free cortisol

Tx = ketoconisole, metyrapone, SURGERY

126
Q

What happens in addisons

A

Destruction of adrenal cortex and subsequent reduction in output of adrenal hormones: glucocorticoids (cortisol), and mineralocorticoids (aldosterone)

127
Q

Causes of adrenal insufficiency

A

Primary
addisons (autoimmune) Surgical
Metabolic failure: CAH e.g. 21-hydroxylase deficiency

Secondary
steroids
TB

128
Q

Noticable effect of decreased cortisol in addisons

A

pigmentation of skin

129
Q

Antibody in addisons

A

Anti-21 hydroxylase

130
Q

Sx of chronic addisons

A

thin, tanned, tired, tearful and tumbling

Fatigue and weakness
GI: Anorexia, nausea, vomiting, weight loss
Cravings for salt and salty food
Muscle cramps
Faintness due to hypotension
Mood: confusion, personality change, irritable

131
Q

Signs of addisons

A

pigmental palmar crease and buccal mucosa, hypotension, postural hypotension

132
Q

how to differentiate 1/2 addisons

A

ACTH levels

High = primary, low = secondary

133
Q

Ix addisons

A

ACTH
Sodium - low, Potassium high
Cortisol - low
Renin (high), aldosterone (low)

CT adrenals

synacthen test

134
Q

What is the Dx Ix for addisons

A

Short synacthen test:

Take cortisol level
Give 250 mcg synacthen IM (synth ACTH). In 30 mins retake cortisol
If cortisol rises then exclude Addison’s >500nmol/L

135
Q

Electrolytes in addisons

A

Hyponatraemia, hyperkalaemia, hypoglycaemia, metabolic aci

136
Q

Mx addisons

A

patient education
medical emergency bracelet

Glucocorticoid - hydrocortisone
mineralcorticoid - fludrocortiosone

137
Q

What to monitor in addisons

A

symptoms, signs, BP, electrolytes

Annual
TFT, glucose + HbA1c, coeliac

138
Q

Biggest Rf for addisonian crisis

A

long term steroids

139
Q

Presentation of addisonian crisis ? progress to?

A

Malaise, fatigue, nausea/vomiting, low-grade fever, muscle cramps, confusion

Dehydration: hypotension and hypovolaemic shock

140
Q

Mx of adisonian crisis ? monitor what?

A

IV/IM hydrocortisone
rehydrate

more hydrocortisone and glucose over 24 hrs

Continuous cardiac and electrolyte monitoring (ECG, reg U+E)

141
Q

What is conns

A

primary hyperaldosteronism

142
Q

What happens in conns

A

hypernatraemia, water retention and hypokalaemia

143
Q

What might you think the cause is if someone presents with HTN, hypokalaemia, or alkalosis in someone not on diuretics

A

conns

144
Q

presentation of conns

A

Oedema

Hypertension

Hypokalaemia - weakness, cramps, parasthesia

Metabolic alkalosis - secretion of H+ in exchange for K+ (more K+ in urine) in intercalated cells

Polyuria from reduced ability of kidney to concentrate urine

145
Q

Ix in conns

A

U+E: hypernatraemia, hypokalaemia

BP: high

*Aldosterone: renin ratio (high ald, low renin - normal renin exludes Dx)
>800 = imaging required

ECG for arrhythmia

CT/MRI for adrenal adenoma

146
Q

Mx of conns

A

medical
spronolactone - aldosterone antagonist

Laparoscopic adrenalectomy (only if unilateral)

147
Q

give 3 causes of hyper K

A

Renal
AKI / CKD
Addisons
hyperkaeamia RTA

Drugs
spironolactone ACEi, ARB, NSAID, BB, Digoxin, heparin

rhabdomyolysis, burns, trauma, blood transfusion

DKA

148
Q

Presentation of hyperK

A

KEVIN!!!! Kevin is in hospital for an AKI but he also has diabetes and takes loads of meds and hes tired, flaccid and depressed.

Non-specific: weakness + fatigue, flaccid paralysis, depressed tendon reflexes

Palpitations + chest pain

149
Q

Ix in Hyper K

A

Medication review
U/E
ABG
ECG

150
Q

Seen on ECG in hyper K

A

PPRQRST
P - loss of P
PR - prolonged - ?HB ?bradycardia
QRS - widened and sinusoidal
T - peaked T waves = first thing you see

Worry —> can progress to VF

151
Q

Mx of hyperK

A

Stop drug causing

Cardiac protection
- calcium gluconate IV

Shift potassium into cells
- Insulin infusion + glucose

If needed - nebulised salbutamol/haemodialysis

Monitor ECG

152
Q

Usual cause of hypoK

A

non-K sparing diuretics / GI fluid loss (N&V)

Alkalosis or acidosis

153
Q

HypoK presentation
Investigations?

A

KAREN!!!!! Karen is weak, constipated and hypotonia.

weakness, muscle pain, constipation

Severe:
neuromuscular
(ascending weakness -> resp faulure,
hypotonia)

Ix:
- U&E
- ABG
- Glucose
- Serum Mg (also goes low)
- Serum Cl
- ECG

154
Q

Which electrolyte accompanies low K?

A

Mg

155
Q

Mx of low K - How do you give it?

A

Mild = oral K which sandoK

Severe = IV K - Dont give as a bolus as can cause fatal arrhythmia = VF

Rate should never exceed 10mmol/hr

Cardiac monitoring

156
Q

Classic 4 sx in phaeochromocytoma

A

Episodic headache + sweating + palpitations + tremor

157
Q

o/e phaeo. 3 signs

A

Hypertension, postural hypotension, tremor, flushing, tachycardia

158
Q

Ix of phaeo

A

24 hour urine catecholamines, metanephrines, VMA

Abdo CT/MRI

159
Q

2 drugs given pre surgery for phaeo

A

alpha blocker - Phenoxybenzamine

b blocker - propanolol

160
Q

What do you monitor after surgery for phaeo

A

24 hour catecholamines + VMA 2 weeks after surgery

161
Q

What is carcinoid syndrome ? usual pres?

A

Tumour of enterochromaffin cell

Flushing and diarrhoea

(Wheeze, palpitations, telangiectasia, abdominal pain)

162
Q

What is released in carcinoid syndrome?

A

serotonin / other vasoactive peptides

163
Q

Ix in carcinoid syndrome? name 2

A

Urinary 5-HT

CT CAP - to find tumour and check liver mets

Serum chromogranin A/B

164
Q

mx of carcinoid

A

Surgical resection

+ peri-operative octreotide infusion
(to prevent carcinoid crisis - continue for 48 hours post)

165
Q

What happens in diabetes insipidus?

A

large amounts of dilute urine due to hyposecretion or resistance to ADH/vasopressin (same thing) and inability to concentrate urine

166
Q

where is ADH made?

A

hypothalamus

167
Q

name 2 causes of Diabetes insipidus

A

Cranial
Damage to hypothalamus:
tumour, surgery, granulomatous disease, infection

Inherited AD vasopressin gene

Nephrogenic causes - CKD and lithium

168
Q

Ix in diabetes insipidus

A

24 urine collection

urine / serum osmolality
Desmopressin stimulation test - test urine osmolality

MRI pit/hypothalamus
water deprivation tests (can kidneys concentrate urine)

169
Q

Mx of cranial cause of diabetes insipidus

A

ADH replacement

170
Q

Mx of nephrogenic cause of diabetes insipidus

A

drink adequate fluid

171
Q

If you correct SIADH too fast what could you cause \?

A

central pontine myelinolysis

172
Q

most common cause of hyponatraemia

A

thiazine diuretics

173
Q

Name 3 causes of SIADH

A

Pulmonary processes: pneumonia, lung cancer (esp small cell)

CNS disorders: infection, trauma, MS, haemorrhage, malignancy

Malignancy: lung, GI, GU, lymphoma

Drugs: SSRIs, ACE-i, chemo drugs

174
Q

How does SIADH present

A

confusion, nausea, irritability, vomiting

175
Q

Ix in SIADH

A

Na - low
low serum osmolalaity
High urine Na
Normal renal / adrenal

176
Q

What happens to Na levels in SIADH with normal saline infusion

A

they don’t respond

177
Q

Mx SIADH

A

IV hypertonic saline

treat cause

furosemide if fluid overoad

178
Q

Big old risky with very low Na

A

cerebral oedema

179
Q

Risk of correcting low Na quickly in cerebral oedema

A

osmostic demyelination
(water moves out brain a bit fast)

180
Q

What is the dexamethasone suppression test ?

A

give steroids -> should lower cortisol

If doesnt - positive test -> pit adenoma or ectopic source eg Small cell lung Ca

181
Q

hypovolemic and hypernatraemic?

A

Give 5% dextrose

If really high Na just give normal saline as dont want to bring down too fast

182
Q

Hyperkaeamia

A

mild >5.5
severe >6.5

183
Q

Calcium normal range

A

Severe >3.5

184
Q

Malignancies causing hyperC

A

breast
myeloma
SCLC
bone mets

185
Q

signs for GRAVES

A

EYES - lid lag
ophthalmoplegia
exophthalmos/proptosis

pretibial myxoedema

clubbing

186
Q

SGLT

A

gliflozin

SE: thrust

Work by increasing excretion of glucose from urine

187
Q

GLT1 agonist

A

exenatide

Phase 4 - Katherine (26 decks)

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